Page last updated: 2024-11-08

alanine and Acute Confusional Senile Dementia

alanine has been researched along with Acute Confusional Senile Dementia in 127 studies

Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases IMMUNITY, and provides energy for muscle tissue, BRAIN, and the CENTRAL NERVOUS SYSTEM.
alanine : An alpha-amino acid that consists of propionic acid bearing an amino substituent at position 2.

Research Excerpts

ExcerptRelevanceReference
"Alaproclate, a specific inhibitor of neuronal serotonin re-uptake, was given to 12 patients with dementia of Alzheimer type."7.66Alaproclate: a pharmacokinetic and biochemical study in patients with dementia of Alzheimer type. ( Bergman, I; Bråne, G; Gottfries, CG; Jostell, KG; Karlsson, I; Svennerholm, L, 1983)
" Carnosine may be a potential therapeutic agent (neurodegenerative, metabolic, cardiovascular diseases) mainly due to its antioxidant and antiglycating activities."4.84[Carnosine--biological activity and perspectives in pharmacotherapy]. ( Zieba, R, 2007)
"To characterize clinical features of a very large pedigree with early-onset Alzheimer disease (AD) in which all affected individuals carry the identical glutamic acid-to-alanine mutation at codon 280 in the presenilin-1 gene."3.69Clinical features of early-onset Alzheimer disease in a large kindred with an E280A presenilin-1 mutation. ( Arango-Lasprilla, JC; Arango-Viana, JC; Arcos-Burgos, M; Ardilla, A; Behrens, IM; Goate, AM; Hincapíe, L; Kosik, KS; Lemere, CA; Lendon, C; Lopera, F; Madrigal, L; Martínez, A; Norton, J; Ossa, JE; Rosselli, M; Ruiz-Linares, A, 1997)
"Alaproclate, a specific inhibitor of neuronal serotonin re-uptake, was given to 12 patients with dementia of Alzheimer type."3.66Alaproclate: a pharmacokinetic and biochemical study in patients with dementia of Alzheimer type. ( Bergman, I; Bråne, G; Gottfries, CG; Jostell, KG; Karlsson, I; Svennerholm, L, 1983)
" Treatment-emergent adverse events (TEAEs) are reported by body system along with pertinent laboratory, vital sign, and ECG findings."2.79Safety profile of semagacestat, a gamma-secretase inhibitor: IDENTITY trial findings. ( Dowsett, SA; Henley, DB; May, PC; Sethuraman, G; Sundell, KL, 2014)
"Alzheimer's disease is characterized by the presence of cortical amyloid-beta (Aβ) protein plaques, which result from the sequential action of β-secretase and γ-secretase on amyloid precursor protein."2.78A phase 3 trial of semagacestat for treatment of Alzheimer's disease. ( Aisen, PS; Doody, RS; Farlow, M; He, F; Iwatsubo, T; Joffe, S; Kieburtz, K; Mohs, R; Raman, R; Sethuraman, G; Siemers, E; Sun, X; Thomas, RG; Vellas, B, 2013)
"Primary outcome measures were adverse events, plasma and cerebrospinal fluid Abeta levels, vital signs, electrocardiographic data, and laboratory safety test results."2.73Phase 2 safety trial targeting amyloid beta production with a gamma-secretase inhibitor in Alzheimer disease. ( Aisen, PS; Becerra, L; Clark, CM; Dean, RA; Farlow, MR; Fleisher, AS; Galvin, JE; Peskind, ER; Quinn, JF; Raman, R; Sherzai, A; Siemers, ER; Sowell, BB; Thal, LJ, 2008)
"Alzheimer's disease is thought to be caused by increased formations of neurotoxic amyloid beta (A beta) peptides, which give rise to the hallmark amyloid plaques."2.45Development of semagacestat (LY450139), a functional gamma-secretase inhibitor, for the treatment of Alzheimer's disease. ( Dean, RA; Henley, DB; May, PC; Siemers, ER, 2009)
"Disease-related tau protein in Alzheimer's disease is hyperphosphorylated and aggregates into neurofibrillary tangles."1.72Investigation of the role of prolines 232/233 in RTPPK motif in tau protein aggregation: An in vitro study. ( Akbari, V; Farrokhi, A; Ghobadi, S; Khodarahmi, R; Mehrabi, M; Mohammadi, S, 2022)
" As a consequence, we conclude that clinical efficacy associated with chronic administration of sodium benzoate in schizophrenic and Alzheimer's patients is likely not mediated through inhibition of DAAO."1.48Lack of Effect of Sodium Benzoate at Reported Clinical Therapeutic Concentration on d-Alanine Metabolism in Dogs. ( DeVivo, M; Popiolek, M; Steyn, SJ; Tierney, B, 2018)
"Cognition was assessed with the Alzheimer's Disease Assessment Scale-Cognitive (first 11 items, ADAS11)."1.43Changes in Neuropsychiatric Inventory Associated with Semagacestat Treatment of Alzheimer's Disease. ( Herrmann, N; Lanctôt, KL; Mintzer, JE; Porsteinsson, AP; Raman, R; Rosenberg, PB; Sun, X, 2016)
"Interpreting Alzheimer's disease (AD) clinical trial (CT) outcomes is complicated by treatment dropouts and adverse events (AEs)."1.42Adverse events and dropouts in Alzheimer's disease studies: what can we learn? ( Henley, DB; Schneider, LS; Sethuraman, G; Sundell, KL, 2015)
"An unresolved debate in Alzheimer's disease (AD) is whether amyloid plaques are pathogenic, causing overt physical disruption of neural circuits, or protective, sequestering soluble forms of amyloid-β (Aβ) that initiate synaptic damage and cognitive decline."1.40Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease. ( Chiang, AC; Cirrito, JR; Fowler, SW; Jankowsky, JL; Larson, ME; Lesné, SE; Savjani, RR; Schuler, DR; Sherman, MA, 2014)
"In the case of Alzheimer's disease, the aromatic side chains Phe19 and Phe20 in the wild-type amyloid beta (Aβ) peptide have been implicated."1.37Mutations that replace aromatic side chains promote aggregation of the Alzheimer's Aβ peptide. ( Armstrong, AH; Chen, J; Hecht, MH; McKoy, AF, 2011)
"Approximately 1% of all cases of Alzheimer's disease are inherited autosomal dominantly, and to date, three causative genes have been found, the Presenilin 1 (PSEN1) gene, the Presenilin 2 (PSEN2) gene and the Amyloid precursor protein (APP) gene."1.35Atypical early-onset Alzheimer's disease caused by the Iranian APP mutation. ( Ballegaard, M; Batbayli, M; Erdal, J; Krabbe, K; Lindquist, SG; Nielsen, JE; Schwartz, M; Stokholm, J; Waldemar, G, 2008)
"The deficits of Alzheimer's disease (AD) are believed to result, at least in part, from neurotoxicity of beta-amyloid (Abeta), a set of 38-43 amino acid fragments derived from the beta-amyloid precursor protein (APP)."1.35Long-term prevention of Alzheimer's disease-like behavioral deficits in PDAPP mice carrying a mutation in Asp664. ( Ataie, M; Banwait, S; Bredesen, DE; Galvan, V; Gorostiza, OF; Huang, W; Tang, H; Zhang, J, 2008)
" Chronic dosing of BMS-433796 in Tg2576 mice suggested a narrow therapeutic window and Notch-mediated toxicity at higher doses."1.34Discovery of (S)-2-((S)-2-(3,5-difluorophenyl)-2-hydroxyacetamido)-N-((S,Z)-3-methyl-4-oxo-4,5-dihydro-3H-benzo[d][1,2]diazepin-5-yl)propanamide (BMS-433796): a gamma-secretase inhibitor with Abeta lowering activity in a transgenic mouse model of Alzheime ( Barten, DM; Bergstrom, C; Corsa, JA; Dangler, C; Gao, Q; Guss, VL; Hendrick, JP; Loo, A; Polson, CT; Prasad, CV; Roberts, SB; Robertson, BJ; Sleczka, BG; Smith, DW; Vig, S; Wang, J; Yeola, S; Zheng, M, 2007)
"Humanin (HN) is a secretory peptide that inhibits neurotoxicity by various Alzheimer's disease-relevant insults."1.32Identification of essential amino acids in Humanin, a neuroprotective factor against Alzheimer's disease-relevant insults. ( Hashimoto, Y; Niikura, T; Nishimoto, I; Yamagishi, Y, 2003)
"One of the major clinical features of Alzheimer's disease is the presence of extracellular amyloid plaques that are associated with glycosaminoglycan-containing proteoglycans."1.31Effect of amino-acid substitutions on Alzheimer's amyloid-beta peptide-glycosaminoglycan interactions. ( Fraser, PE; McLaurin, J, 2000)
"Since Alzheimer's disease is exhibited by deterioration of the gray matter, the occurrence of elevated D-alanine levels in the gray matter of Alzheimer brains is a significant discovery and raises the question whether this enantiomer causes the degeneration of the gray matter proteins in Alzheimer's disease, or whether it is an effect of the disease."1.28Presence of D-alanine in proteins of normal and Alzheimer human brain. ( Chavez, M; Cusano, G; D'Aniello, A; Fisher, GH; Petrucelli, L; Vetere, A, 1992)

Research

Studies (127)

TimeframeStudies, this research(%)All Research%
pre-19903 (2.36)18.7374
1990's12 (9.45)18.2507
2000's36 (28.35)29.6817
2010's70 (55.12)24.3611
2020's6 (4.72)2.80

Authors

AuthorsStudies
Akbari, V1
Mohammadi, S1
Mehrabi, M1
Ghobadi, S1
Farrokhi, A1
Khodarahmi, R1
Bacchella, C1
Gentili, S1
Mozzi, SI1
Monzani, E1
Casella, L1
Tegoni, M1
Dell'Acqua, S1
Lin, CH1
Yang, HT1
Lane, HY1
Mirkin, NG1
Krimm, S1
Vo, VG1
Pyun, JM1
Bagyinszky, E1
An, SSA1
Kim, SY1
Lu, L1
Zheng, X2
Wang, S1
Tang, C1
Zhang, Y1
Yao, G1
Zeng, J1
Ge, S1
Wen, H1
Xu, M1
Guyatt, G1
Xu, N1
Altiné-Samey, R1
Antier, D1
Mavel, S1
Dufour-Rainfray, D1
Balageas, AC1
Beaufils, E1
Emond, P1
Foucault-Fruchard, L1
Chalon, S1
Ochoa, JF1
Alonso, JF1
Duque, JE1
Tobón, CA1
Baena, A1
Lopera, F5
Mañanas, MA1
Hernández, AM1
Fukui, K1
Yachi, K1
Yoshida, H1
Tanji, K1
Matsumiya, T1
Hayakari, R1
Tsuruga, K1
Tanaka, H1
Imaizumi, T1
Tagami, S1
Yanagida, K1
Kodama, TS1
Takami, M1
Mizuta, N1
Oyama, H1
Nishitomi, K1
Chiu, YW1
Okamoto, T1
Ikeuchi, T1
Sakaguchi, G1
Kudo, T1
Matsuura, Y1
Fukumori, A1
Takeda, M1
Ihara, Y1
Okochi, M1
Villamil-Ortiz, JG1
Barrera-Ocampo, A1
Arias-Londoño, JD1
Villegas, A1
Cardona-Gómez, GP1
O'Sullivan Coyne, G1
Woodring, TS1
Lee, CR1
Chen, AP1
Kong, HH1
McAninch, EA1
Rajan, KB1
Evans, DA1
Jo, S1
Chaker, L1
Peeters, RP1
Bennett, DA1
Mash, DC1
Bianco, AC1
Ruthirakuhan, MT1
Herrmann, N2
Abraham, EH1
Chan, S1
Lanctôt, KL2
Popiolek, M1
Tierney, B1
Steyn, SJ1
DeVivo, M1
Murugan, NA1
Chiotis, K1
Rodriguez-Vieitez, E1
Lemoine, L1
Ågren, H1
Nordberg, A1
Haug, KG1
Staab, A1
Dansirikul, C1
Lehr, T1
Doody, RS2
Raman, R3
Farlow, M1
Iwatsubo, T2
Vellas, B1
Joffe, S1
Kieburtz, K1
He, F1
Sun, X2
Thomas, RG1
Aisen, PS3
Siemers, E4
Sethuraman, G4
Mohs, R2
Paban, V1
Manrique, C1
Filali, M1
Maunoir-Regimbal, S1
Fauvelle, F1
Alescio-Lautier, B1
Coskuner, O1
Wise-Scira, O1
Trechot, P1
Schmutz, JL1
Blennow, K3
Zetterberg, H3
Haass, C2
Finucane, T1
Gupta, VB1
Gupta, VK1
Martins, R1
Pomara, N1
Beggiato, S1
Giuliani, A1
Sivilia, S1
Lorenzini, L1
Antonelli, T1
Imbimbo, BP4
Giardino, L1
Calzà, L1
Ferraro, L1
Henley, DB3
Sundell, KL2
Schneider, LS1
Fowler, SW1
Chiang, AC1
Savjani, RR1
Larson, ME1
Sherman, MA1
Schuler, DR1
Cirrito, JR1
Lesné, SE1
Jankowsky, JL1
Dowsett, SA1
May, PC5
Gough, M1
Blanthorn-Hazell, S1
Parkin, ET1
De Strooper, B2
Chávez Gutiérrez, L1
Kahle-Wrobleski, K1
Fillit, H1
Kurlander, J1
Reed, C1
Belger, M1
Liu, D1
Roychaudhuri, R1
Teplow, DB3
Bowers, MT1
Paz-Y-Miño, CA1
García-Cárdenas, JM1
López-Cortés, A1
Salazar, C1
Serrano, M1
Leone, PE1
Liu-Seifert, H1
Price, K1
Han, B1
Selzler, KJ1
Henley, D1
Sundell, K1
Aisen, P1
Cummings, J2
Raskin, J1
Sydow, A1
Hochgräfe, K1
Könen, S1
Cadinu, D1
Matenia, D1
Petrova, O1
Joseph, M1
Dennissen, FJ1
Mandelkow, EM1
Liang, CT1
Huang, HB2
Wang, CC2
Chen, YR2
Chang, CF1
Shiao, MS2
Chen, YC2
Lin, TH2
Rosenberg, PB1
Mintzer, JE1
Porsteinsson, AP1
Popova, AA1
Koksharova, OA1
Liu, S1
Wu, Y1
Liu, X1
Zhou, J1
Wang, Z1
He, Z1
Huang, Z1
Das, P1
Chacko, AR1
Belfort, G1
Lombardi, G1
Berti, V1
Tedde, A1
Bagnoli, S1
Piaceri, I1
Polito, C1
Lucidi, G1
Ferrari, C1
Ginestroni, A1
Moretti, M1
Pupi, A1
Nacmias, B1
Sorbi, S1
Fleisher, AS1
Siemers, ER4
Becerra, L1
Clark, CM1
Dean, RA5
Farlow, MR2
Galvin, JE2
Peskind, ER1
Quinn, JF2
Sherzai, A1
Sowell, BB1
Thal, LJ1
Schroeder, A1
Fahrenholz, F1
Schmitt, U1
Rönnbäck, A1
Zhu, S1
Dillner, K1
Aoki, M1
Lilius, L1
Näslund, J1
Winblad, B1
Graff, C1
Ito, K1
Ishibashi, K1
Tomiyama, T1
Umeda, T1
Yamamoto, K1
Kitajima, E1
Idomoto, T1
Nagatomo, T1
Mori, H2
Drew, SC1
Masters, CL2
Barnham, KJ2
Peretto, I1
Hureau, C1
Coppel, Y1
Dorlet, P1
Solari, PL1
Sayen, S1
Guillon, E1
Sabater, L1
Faller, P1
Shitaka, Y1
Mitani, Y1
Nagakura, A1
Miyake, A1
Matsuoka, N1
Giaccone, G1
Morbin, M1
Moda, F1
Botta, M1
Mazzoleni, G1
Uggetti, A1
Catania, M1
Moro, ML1
Redaelli, V1
Spagnoli, A1
Rossi, RS1
Salmona, M1
Di Fede, G1
Tagliavini, F1
Yamamoto-Watanabe, Y1
Watanabe, M1
Jackson, M1
Akimoto, H1
Sugimoto, K1
Yasujima, M1
Wakasaya, Y1
Matsubara, E1
Kawarabayashi, T1
Harigaya, Y1
Lyndon, AR1
Shoji, M1
Extance, A1
Samson, K1
Kelleher, RJ1
Shen, J1
Lo, CJ1
Su, CL1
Liu, HT1
Gandy, S1
Wustman, B1
Schor, NF1
Armstrong, AH1
Chen, J1
McKoy, AF1
Hecht, MH1
Cooper, AJ1
Pinto, JT1
Callery, PS1
Lachno, DR1
Romeo, MJ1
Vanderstichele, H1
Coart, E1
Konrad, RJ1
Zajac, JJ1
Talbot, JA1
Jensen, HF1
Demattos, RB1
Gravitz, L1
Carlson, C1
Estergard, W1
Oh, J1
Suhy, J1
Jack, CR1
Barakos, J1
Jämsä, A1
Belda, O1
Edlund, M1
Lindström, E1
Borghys, H1
Tuefferd, M1
Van Broeck, B1
Clessens, E1
Dillen, L1
Cools, W1
Vinken, P1
Straetemans, R1
De Ridder, F1
Gijsen, H1
Mercken, M1
Panza, F2
Frisardi, V2
Solfrizzi, V2
Logroscino, G1
Santamato, A1
Greco, A1
Seripa, D3
Pilotto, A3
MacPherson, SE1
Parra, MA1
Moreno, S1
Della Sala, S1
Portelius, E2
Gustavsson, MK1
Andreasson, U2
Shahpasand, K1
Uemura, I1
Saito, T1
Asano, T1
Hata, K1
Shibata, K1
Toyoshima, Y1
Hasegawa, M1
Hisanaga, S1
Cotella, D1
Hernandez-Enriquez, B1
Wu, X1
Li, R1
Pan, Z1
Leveille, J1
Link, CD1
Oddo, S1
Sesti, F1
D'Onofrio, G1
Paroni, G1
Cascavilla, L1
Svedružić, ZM1
Popović, K1
Smoljan, I1
Sendula-Jengić, V1
Marcil, A1
Bourgeois, P1
Nutu, M1
Mawuenyega, KG1
Sigurdson, WC1
Paul, SM1
Holtzman, DM2
Bateman, RJ1
Busche, MA1
Chen, X1
Henning, HA1
Reichwald, J1
Staufenbiel, M1
Sakmann, B1
Konnerth, A1
Vélez, JI1
Chandrasekharappa, SC1
Henao, E1
Martinez, AF1
Harper, U1
Jones, M1
Solomon, BD1
Lopez, L1
Garcia, G1
Aguirre-Acevedo, DC1
Acosta-Baena, N1
Correa, JC1
Lopera-Gómez, CM1
Jaramillo-Elorza, MC1
Rivera, D1
Kosik, KS2
Schork, NJ1
Swanson, JM1
Arcos-Burgos, M2
Xia, W1
Wong, ST1
Hanlon, E1
Morin, P1
Iwai, A1
Hopkins, CR1
McKee, TD1
Loureiro, RM1
Dumin, JA1
Zarayskiy, V1
Tate, B1
Hsu, CK1
Hsu, CC1
Lee, JY1
Kuo, YM1
Pai, MC1
García-Lozano, JR1
Mir, P1
Alberca, R1
Aguilera, I1
Gil Néciga, E1
Fernández-López, O1
Cayuela, A1
Núñez-Roldan, A1
Yamagishi, Y1
Hashimoto, Y3
Niikura, T2
Nishimoto, I2
Beyer, K1
Lao, JI1
Latorre, P1
Riutort, N1
Matute, B1
Fernández-Figueras, MT1
Mate, JL1
Ariza, A1
Yang, JD1
Feng, GY1
Zhang, J2
Cheung, J1
St Clair, D1
He, L1
Ichimura, K1
Culpan, D1
MacGowan, SH1
Ford, JM1
Nicoll, JA1
Griffin, WS1
Dewar, D1
Cairns, NJ1
Hughes, A1
Kehoe, PG1
Wilcock, GK1
Ikonen, M1
Liu, B1
Ma, L1
Lee, KW1
Cohen, P1
Orlacchio, A2
Kawarai, T2
Polidoro, M1
Paterson, AD1
Rogaeva, E2
St George-Hyslop, PH1
Bernardi, G1
Craig, D1
Hart, DJ1
Carson, R1
McIlroy, SP1
Passmore, AP1
Haeffner, F1
Ciccotosto, GD1
Curtain, CC1
Tew, D1
Mavros, C1
Beyreuther, K1
Carrington, D1
Cherny, RA1
Cappai, R1
Bush, AI1
Helisalmi, S1
Hiltunen, M1
Vepsäläinen, S1
Iivonen, S1
Corder, EH1
Lehtovirta, M1
Mannermaa, A1
Koivisto, AM1
Soininen, H1
Saarela, MS1
Lehtimäki, T1
Rinne, JO1
Hervonen, A1
Jylhä, M1
Röyttä, M1
Ahonen, JP1
Mattila, KM1
Kitazume, S1
Suzuki, M1
Saido, TC1
Armstrong, J1
Boada, M1
Rey, MJ1
Vidal, N1
Ferrer, I1
Navaneetham, D1
Jin, L1
Pandey, P1
Strickler, JE1
Babine, RE1
Abdel-Meguid, SS1
Walsh, PN1
He, Y1
Zhou, H1
Tang, H2
Luo, Y1
Ragnarsson, L1
Yasuda, T1
Lewis, RJ1
Dodd, PR1
Adams, DJ1
Kaye, J1
Porsteinsson, A1
Tariot, P1
Zoulnouni, P1
Knopman, DS1
Satterwhite, J1
Gonzales, C1
Li, T1
Paudel, HK1
Mariani, E1
Ingegni, T1
Nocentini, G1
Mangialasche, F1
Ercolani, S1
Cherubini, A1
Metastasio, A1
Senin, U1
Mecocci, P1
Prasad, CV1
Zheng, M1
Vig, S1
Bergstrom, C1
Smith, DW1
Gao, Q1
Yeola, S1
Polson, CT1
Corsa, JA1
Guss, VL1
Loo, A1
Wang, J1
Sleczka, BG1
Dangler, C1
Robertson, BJ1
Hendrick, JP1
Roberts, SB1
Barten, DM1
Zieba, R1
Lindquist, SG1
Nielsen, JE1
Stokholm, J1
Schwartz, M1
Batbayli, M1
Ballegaard, M1
Erdal, J1
Krabbe, K1
Waldemar, G1
Masuda, Y1
Uemura, S1
Nakanishi, A1
Ohashi, R1
Takegoshi, K1
Shimizu, T1
Shirasawa, T1
Irie, K1
Galvan, V1
Gorostiza, OF1
Banwait, S1
Huang, W1
Ataie, M1
Bredesen, DE1
Bergman, I1
Bråne, G1
Gottfries, CG1
Jostell, KG1
Karlsson, I1
Svennerholm, L1
Clements, A1
Walsh, DM2
Williams, CH1
Allsop, D1
Hung, AY1
Selkoe, DJ2
Shen, ZM1
Perczel, A1
Hollósi, M1
Nagypál, I1
Fasman, GD1
Rosenberg, RN1
Ardilla, A1
Martínez, A1
Madrigal, L1
Arango-Viana, JC1
Lemere, CA1
Arango-Lasprilla, JC1
Hincapíe, L1
Ossa, JE1
Behrens, IM1
Norton, J1
Lendon, C1
Goate, AM1
Ruiz-Linares, A1
Rosselli, M1
Hong, M1
Chen, DC1
Klein, PS1
Lee, VM1
Akiyama, H1
Sahara, N1
Kondo, H1
Ikeda, K1
Nishimura, T1
Oda, T1
McGeer, PL1
Tomita, S1
Kirino, Y1
Suzuki, T1
Papassotiropoulos, A1
Bagli, M1
Feder, O1
Jessen, F1
Maier, W1
Rao, ML1
Ludwig, M1
Schwab, SG1
Heun, R1
McLaurin, J1
Fraser, PE1
Hartley, DM1
Condron, MM1
Athan, ES1
Williamson, J1
Ciappa, A1
Santana, V1
Romas, SN1
Lee, JH1
Rondon, H1
Lantigua, RA1
Medrano, M1
Torres, M1
Arawaka, S1
Song, YQ1
Sato, C1
Fafel, KC1
Boss, MA1
Seltzer, WK1
Stern, Y1
St George-Hyslop, P1
Tycko, B1
Mayeux, R1
Lleó, A1
Blesa, R1
Gendre, J1
Castellví, M1
Pastor, P1
Queralt, R1
Oliva, R1
D'Aniello, A2
Vetere, A2
Fisher, GH2
Cusano, G1
Chavez, M1
Petrucelli, L1
Padula, L1
Cusano, GP1
Man, EH1
Ellison, DW1
Beal, MF1
Mazurek, MF1
Bird, ED1
Martin, JB1
Hollander, E1
Mohs, RC1
Davis, KL1

Clinical Trials (6)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Effect of γ-Secretase Inhibition on the Progression of Alzheimer's Disease: LY450139 Versus Placebo[NCT00594568]Phase 31,537 participants (Actual)Interventional2008-03-31Completed
Effect of LY450139 a y-Secretase Inhibitor, on the Progression of Alzheimer's Disease as Compared With Placebo[NCT00762411]Phase 31,111 participants (Actual)Interventional2008-09-30Completed
Effect of LY2062430, an Anti-Amyloid Beta Monoclonal Antibody, on the Progression of Alzheimer's Disease as Compared With Placebo[NCT00905372]Phase 31,000 participants (Anticipated)Interventional2009-05-31Completed
Effect of Passive Immunization on the Progression of Alzheimer's Disease: LY2062430 Versus Placebo[NCT00904683]Phase 31,040 participants (Actual)Interventional2009-05-31Completed
LY450139: Tolerability and Biomarker Assessment in Subjects With Mild to Moderate Alzheimer's Disease[NCT00244322]Phase 245 participants Interventional2005-10-31Completed
Levetiracetam for Alzheimer's Disease Neuropsychiatric Symptoms Related to Epilepsy Trial (LAPSE) - A Phase II Exploratory Study[NCT04004702]Phase 265 participants (Anticipated)Interventional2020-01-31Not yet recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog11) Score at 16 Weeks After Cessation of Study Drug

ADAS-Cog11 consists of 11 items assessing areas of function most typically impaired in Alzheimer's disease (AD): orientation, verbal memory, language, and praxis. The scale ranges from 0 to 70, with higher scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
Placebo6.59
100 mg LY4501397.57
140 mg LY4501397.90

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog11) Score at 76 Weeks

ADAS-Cog11 was used as a primary efficacy measure. It consists of 11 items assessing areas of function most typically impaired in Alzheimer's disease (AD): orientation, verbal memory, language, and praxis. The scale ranges from 0 to 70, with higher scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo6.19
100 mg LY4501397.29
140 mg LY4501397.68

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog12) Score at 16 Weeks After Cessation of Study Drug

ADAS-Cog12 is ADAS-Cog11 augmented with delayed free recall measure, resulting in a total score ranging from 0 to 80. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
Placebo6.97
100 mg LY4501398.27
140 mg LY4501398.41

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog12) Score at 76 Weeks

ADAS-Cog12 is ADAS-Cog11 augmented with delayed free recall measure, resulting in a total score ranging from 0 to 80. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo6.52
100 mg LY4501397.98
140 mg LY4501398.33

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog14) Score at 16 Weeks After Cessation of Study Drug

ADAS-Cog14 is ADAS-Cog11 augmented with delayed free recall, digit cancellation, and maze completion measures. A score of 0 to 10 for delayed free recall and a conversion code of 0 to 5 for digit cancellation and maze completion provide total score ranges for this extended ADAS-Cog14 of 0 to 90. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
Placebo7.90
100 mg LY4501399.30
140 mg LY4501399.89

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog14) Score at 76 Weeks

ADAS-Cog14 is ADAS-Cog11 augmented with delayed free recall, digit cancellation, and maze completion measures. A score of 0 to 10 for delayed free recall and a conversion code of 0 to 5 for digit cancellation and maze completion provide total score ranges for this extended ADAS-Cog14 of 0 to 90. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo7.42
100 mg LY4501398.97
140 mg LY4501399.48

Change From Baseline in Alzheimer's Disease Cooperative Study Activities of Daily Living (ADCS-ADL) Inventory Score at 16 Weeks After Cessation of Study Drug

ADCS-ADL is a 23-item inventory developed as a Rater-administered questionnaire answered by the participant's caregiver. It measures performance of basic and instrumental activities of daily living by participants. The total score ranges from 0 to 78, with lower scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
Placebo-9.26
100 mg LY450139-9.15
140 mg LY450139-11.73

Change From Baseline in Alzheimer's Disease Cooperative Study Activities of Daily Living (ADCS-ADL) Inventory Score at 76 Weeks

ADCS-ADL is a 23-item inventory developed as a Rater-administered questionnaire answered by the participant's caregiver. It measures performance of basic and instrumental activities of daily living by participants. The total score ranges from 0 to 78, with lower scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo-8.76
100 mg LY450139-10.13
140 mg LY450139-12.70

Change From Baseline in Amyloid Beta (Aβ) 1-42 Concentration in Spinal Fluid up to 76 Weeks

Concentration of an amino peptide known as Aβ 1-42 in spinal fluid. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00594568)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
Placebo-86.16
100 mg LY45013923.27
140 mg LY450139-40.51

Change From Baseline in Amyloid Imaging Positron Emission Tomography (AV-45 PET) up to 76 Weeks

A radioactive tracer for PET that is a ligand for amyloid called AV-45. This permits the visualization of amyloid in the brains of Alzheimer's participants. The outcome reported is the composite summary of the standard uptake value ratio (SUVR) normalized to the cerebellar gray matter. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00594568)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionratio (Least Squares Mean)
Placebo0.08
100 mg LY4501390.06
140 mg LY4501390.09

Change From Baseline in Clinical Dementia Rating-Sum of Boxes (CDR-SB) Score at 76 Weeks

CDR-SB is a semi-structured interview of participants and their caregivers. Participant's cognitive status is rated across 6 domains of functioning, including memory, orientation, judgment/problem solving, community affairs, home/hobbies, and personal care. Severity score assigned for each of 6 domains; Total score (SB) ranges from 0 to 18. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo2.31
100 mg LY4501392.73
140 mg LY4501393.04

Change From Baseline in EuroQol 5-Dimensional Health-Related Quality of Life Scale Proxy Version (EQ-5D Proxy) Visual Analog Scale (VAS) Score at 76 Weeks

EQ-5D (proxy version) measures mobility, self-care, usual activities, pain/discomfort, anxiety/depression; each has 3 severity levels (no, some, severe problems) coded to a 1-digit number (1-3). Digits are combined into 5-digit number describing health state. Numerals 1-3 are not added for total score. VAS assesses caregiver's impression of participant's overall health state; scores range from 0 to 100; Lower scores indicate greater disease severity. Least Squares (LS) Mean value controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo-1.41
100 mg LY450139-7.49
140 mg LY450139-5.33

Change From Baseline in Mini Mental State Examination (MMSE) Score at 76 Weeks

MMSE is a brief screening instrument used to assess cognitive function (orientation, memory, attention, and ability to name objects, follow verbal and written commands, write a sentence, and copy figures) in elderly participants. The total score ranges from 0 to 30; Lower score indicates greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo-2.95
100 mg LY450139-3.14
140 mg LY450139-3.71

Change From Baseline in Neuropsychiatric Inventory (NPI) Score at 76 Weeks

NPI assesses psychopathology in participants with dementia and other neurologic disorders. Information is obtained from a caregiver familiar with the participant's behavior. Total score ranges from 12 to 144; Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
Placebo1.92
100 mg LY4501393.31
140 mg LY4501394.15

Change From Baseline in Phosphorylated-Tau (P-Tau) Concentration in Spinal Fluid

Concentration of p-tau in spinal fluid. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00594568)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
Placebo9.75
100 mg LY450139-6.26
140 mg LY450139-5.13

Change From Baseline in Positron Emission Tomography (PET) Using Fluorine-18 Fluorodeoxyglucose (18F-FDG) at 76 Weeks

Measurement of local cerebral glucose metabolism by PET using the radioactive tracer 18F-FDG. The outcome reported is the composite summary of the standard uptake value ratio (SUVR) normalized to the Pons. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00594568)
Timeframe: Baseline (randomization), 76 weeks

Interventionratio (Least Squares Mean)
Placebo-0.08
100 mg LY450139-0.12
140 mg LY450139-0.11

Change From Baseline in Resource Utilization in Dementia-Lite (RUD-Lite) Score (Number of Hospitalizations) up to 76 Weeks

Assesses healthcare resource utilization (formal and informal care). Information gathered on both caregivers (caregiving time, work status) and participants (accommodation and healthcare resource utilization) was collected from baseline and follow-up interviews; Reported number of hospitalizations per participant up to 76 weeks. Least Squares (LS) Mean value was controlled for age and investigator. (NCT00594568)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionhospitalizations/participant (Least Squares Mean)
Placebo0.55
100 mg LY4501390.66
140 mg LY4501390.83

Change From Baseline in Tau Concentration in Spinal Fluid up to 76 Weeks

Concentration of total tau in spinal fluid. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00594568)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
Placebo75.11
100 mg LY45013920.50
140 mg LY45013961.00

LY450139 Population Pharmacokinetics: Clearance of LY450139

Model estimated apparent oral clearance. Clearance is defined as the volume of plasma that is completely cleared of drug (LY450139) per unit time. (NCT00594568)
Timeframe: 6 weeks, 12 weeks, and 52 weeks

Interventionliter per hour (L/h) (Geometric Mean)
LY45013918.8

LY450139 Population Pharmacokinetics: Volume of Distribution of LY450139

Model-estimated apparent volume of distribution. Volume of distribution is a measure of the extent to which the drug distributes in the body. (NCT00594568)
Timeframe: 6 weeks, 12 weeks, and 52 weeks

Interventionliter (L) (Geometric Mean)
LY45013966.8

Percent Change From Baseline in Amyloid Beta (Aβ) 1-42 Plasma Concentration at 52 Weeks

Concentration of amino acid peptide, known as Aβ 1-42, in plasma. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00594568)
Timeframe: Baseline (randomization), 52 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
Placebo3.86
100 mg LY450139-5.97
140 mg LY450139-19.95

Change From Baseline in Hippocampal Volume Using Volumetric Magnetic Resonance Imaging (vMRI) up to 76 Weeks

The vMRI assessment of left and right hippocampal volume is reported. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00594568)
Timeframe: Baseline (randomization), up to 76 weeks

,,
Interventioncubic millimeter (mm^3) (Least Squares Mean)
Left Hippocampal VolumeRight Hippocampal Volume
100 mg LY450139-75.34-93.89
140 mg LY450139-107.62-112.40
Placebo-96.54-108.69

Change From Baseline in Alzheimer's Disease Assessment Scale (ADAS-Cog14) at 16 Weeks After Cessation of Study Drug

ADAS-Cog14 is ADAS-Cog11 augmented with delayed free recall, digit cancellation, and maze completion measures. A score of 0 to 10 for delayed free recall and a conversion code of 0 to 5 for digit cancellation and maze completion provide total score ranges for this extended ADAS-Cog14 of 0 to 90. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
140 mg LY4501396.00
Placebo5.89

Change From Baseline in Alzheimer's Disease Assessment Scale (ADAS-Cog14) at 76 Weeks

ADAS-Cog14 is ADAS-Cog11 augmented with delayed free recall, digit cancellation, and maze completion measures. A score of 0 to 10 for delayed free recall and a conversion code of 0 to 5 for digit cancellation and maze completion provide total score ranges for this extended ADAS-Cog14 of 0 to 90. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY4501399.23
Placebo8.32

Change From Baseline in Alzheimer's Disease Assessment Scale- Cognitive Subscale (ADAS-Cog11) at 16 Weeks After Cessation of Study Drug

The cognitive subscale of ADAS (ADAS Cog11) consists of 11 items assessing areas of function most typically impaired in Alzheimer's disease (AD): orientation, verbal memory, language, and praxis. The scale ranges from 0 to 70, with higher scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
140 mg LY4501394.81
Placebo4.85

Change From Baseline in Alzheimer's Disease Assessment Scale- Cognitive Subscale (ADAS-Cog11) at 76 Weeks

The cognitive subscale of the ADAS (ADAS Cog11) was used as a primary efficacy measure and consists of 11 items assessing areas of function most typically impaired in Alzheimer's disease (AD): orientation, verbal memory, language, and praxis. The scale ranges from 0 to 70, with higher scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY4501397.37
Placebo6.77

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog12) at 16 Weeks After Cessation of Study Drug

ADAS-Cog12 is ADAS-Cog11 augmented with delayed free recall measure, resulting in a total score ranging from 0 to 80. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
140 mg LY4501395.33
Placebo5.14

Change From Baseline in Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog12) at 76 Weeks

ADAS-Cog12 is ADAS-Cog11 augmented with delayed free recall measure, resulting in a total score ranging from 0 to 80. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY45013910.09
Placebo10.34

Change From Baseline in Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory (ADCS-ADL) at 16 Weeks After Cessation of Study Drug

The ADCS-ADL is a 23-item inventory developed as a rater-administered questionnaire answered by the participant's caregiver. The ADCS-ADL measures both basic and instrumental activities of daily living by participants. The total score ranges from 0 to 78, with lower scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 16 weeks following treatment cessation

Interventionunits on a scale (Least Squares Mean)
140 mg LY450139-8.88
Placebo-7.68

Change From Baseline in Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory (ADCS-ADL) at 76 Weeks

The ADCS-ADL is a 23-item inventory developed as a rater-administered questionnaire answered by the participant's caregiver. The ADCS-ADL measures both basic and instrumental activities of daily living by participants. The total score ranges from 0 to 78, with lower scores indicating greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY450139-10.49
Placebo-9.77

Change From Baseline in Amyloid Beta (Aβ) 1-42 Concentration in Spinal Fluid up to 76 Weeks

Concentration of an amino acid peptide known as Aβ 1-42 in spinal fluid. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00762411)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
140 mg LY45013919.20
Placebo-21.39

Change From Baseline in Amyloid Imaging Positron Emission Tomography (AV-45 PET) up to 76 Weeks

A radioactive tracer for PET that is a ligand for amyloid called [18F]-AV-45. This permits the visualization of amyloid in the brains of Alzheimer's participants. The outcome reported is the composite summary of the standard uptake value ratio (SUVR) normalized to the cerebellar gray matter. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00762411)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionratio (Least Squares Mean)
140 mg LY450139-0.36
Placebo0.16

Change From Baseline in Clinical Dementia Rating Sum of Boxes (CDR-SB) at 76 Weeks

CDR-SB is a semi-structured interview of participants and their caregivers. Participant's cognitive status is rated across 6 domains of functioning, including memory, orientation, judgment/problem solving, community affairs, home/hobbies, and personal care. Severity score assigned for each of 6 domains; total score (SB) ranges from 0 to 18. Higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY4501393.05
Placebo4.00

Change From Baseline in Mini Mental State Examination (MMSE) at 76 Weeks

MMSE is a brief screening instrument used to assess cognitive function (orientation, memory, attention, ability to name objects, follow verbal/written commands, write a sentence, and copy figures) in elderly participants. Total score ranges from 0 to 30; lower score indicates greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY450139-3.56
Placebo-3.35

Change From Baseline in Neuropsychiatric Inventory (NPI) at 76 Weeks

NPI assesses psychopathology in participants with dementia and other neurologic disorders. Information is obtained from a caregiver familiar with the participant's behavior. Total score ranges from 12 to 144; higher scores indicate greater disease severity. Least Squares (LS) Mean value was controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY4501392.94
Placebo3.84

Change From Baseline in Phosphorylated-Tau (P-tau) Concentration in Spinal Fluid up to 76 Weeks

Concentration of p-tau in spinal fluid. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00762411)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
140 mg LY4501397.94
Placebo14.75

Change From Baseline in Positron Emission Tomography (PET) Using Fluorine-18 Fluorodeoxyglucose (18F-FDG) at 76 Weeks

Measurement of local cerebral glucose metabolism by PET using the radioactive tracer 18F-FDG. The outcome reported is the composite summary of the standard uptake value ratio (SUVR) normalized to the Pons. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionratio (Least Squares Mean)
140 mg LY450139-0.13
Placebo-0.08

Change From Baseline in Quality of Life in Alzheimer's Disease (QoL-AD) at 76 Weeks

Assess QoL for AD: participant rates mood, relationships, memory, finances, physical condition, and overall QoL assessment. Each of 13 items, rated on a 4-point scale. Sum of items=total score (range: 13 to 52). Higher scores indicate greater QoL. Participant's primary caregiver asked to complete same measure. Least Squares (LS) Mean value controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY450139-1.83
Placebo-1.05

Change From Baseline in Tau Concentration in Spinal Fluid up to 76 Weeks

Concentration of total tau in spinal fluid. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00762411)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
140 mg LY450139-11.60
Placebo117.88

Change From Baseline in the EuroQol 5-Dimensional Health-Related Quality of Life Scale Proxy Version (EQ-5D Proxy) Visual Analog Scale (VAS) at 76 Weeks

EQ-5D (proxy version) measures mobility, self-care, usual activities, pain/discomfort, anxiety/depression; each has 3 severity levels (no, some, severe problems) coded to a 1-digit number (1-3). Digits are combined into 5-digit number describing health state. Numerals 1-3 are not added for total score. VAS assesses caregiver's impression of participant's overall health state; scores range: 0 to 100. Lower scores indicate greater disease severity. Least Squares (LS) Mean value controlled for baseline value, age, investigator, visit, and concomitant standard of care (SOC) medication. (NCT00762411)
Timeframe: Baseline (randomization), 76 weeks

Interventionunits on a scale (Least Squares Mean)
140 mg LY450139-4.46
Placebo-3.38

Change From Baseline in the Resource Utilization in Dementia-Lite (RUD-Lite) up to 76 Weeks

Assesses healthcare resource utilization (formal and informal care). Information gathered on both caregivers (care-giving time, work status) and participants (accommodation and healthcare resource utilization) was gathered from baseline and follow-up interviews. Reported number of hospitalizations per participant up to 76 weeks. Least Squares (LS) Mean value was controlled for age and investigator. (NCT00762411)
Timeframe: Baseline (randomization), up to 76 weeks

Interventionnumber of hospitalizations (Least Squares Mean)
140 mg LY4501390.72
Placebo0.82

LY450139 Population Pharmacokinetics: Clearance of LY450139

Model estimated apparent oral clearance. Clearance is defined as the volume of plasma which is completely cleared of drug (LY450139) per unit time. (NCT00762411)
Timeframe: 6 weeks, 12 weeks, and 52 weeks

Interventionliters per hour (L/h) (Geometric Mean)
140 mg LY45013918.9

LY450139 Population Pharmacokinetics: Volume of Distribution of LY450139

Model-estimated apparent volume of distribution. Volume of distribution is a measure of the extent to which drug distributes in the body. (NCT00762411)
Timeframe: 6 weeks, 12 weeks, and 52 weeks

Interventionliters (L) (Geometric Mean)
140 mg LY45013966.1

Percent Change From Baseline in Amyloid Beta (Aβ) 1-42 Plasma Concentration at 52 Weeks

Concentration of amino acid peptide known as Aβ 1-42 in plasma. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00762411)
Timeframe: Baseline (randomization), 52 weeks

Interventionpicogram per milliliter (pg/mL) (Least Squares Mean)
140 mg LY450139-16.03
Placebo76.37

Change From Baseline in Hippocampal Volume Using Volumetric Magnetic Resonance Imaging (vMRI) up to 76 Weeks

The vMRI assessment of right and left hippocampal volume is reported. Least Squares (LS) Mean value was controlled for baseline value, age, and investigator. (NCT00762411)
Timeframe: Baseline (randomization), up to 76 weeks

,
Interventioncubic millimeter (mm^3) (Least Squares Mean)
Right Hippocampal VolumeLeft Hippocampal Volume
140 mg LY450139-158.50-84.41
Placebo-73.60-111.27

Reviews

19 reviews available for alanine and Acute Confusional Senile Dementia

ArticleYear
Anti-Aβ agents for mild to moderate Alzheimer's disease: systematic review and meta-analysis.
    Journal of neurology, neurosurgery, and psychiatry, 2020, Volume: 91, Issue:12

    Topics: Acitretin; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Antibodies, Monoclonal, Humanized; Anx

2020
The contributions of metabolomics in the discovery of new therapeutic targets in Alzheimer's disease.
    Fundamental & clinical pharmacology, 2021, Volume: 35, Issue:3

    Topics: Alanine; Alzheimer Disease; Animals; Arginine; Aspartic Acid; Biomarkers; Disease Models, Animal; Gl

2021
A Common DIO2 Polymorphism and Alzheimer Disease Dementia in African and European Americans.
    The Journal of clinical endocrinology and metabolism, 2018, 05-01, Volume: 103, Issue:5

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Amino Acid Substitution; Black or African Ameri

2018
Pharmacological interventions for apathy in Alzheimer's disease.
    The Cochrane database of systematic reviews, 2018, May-04, Volume: 5

    Topics: Alanine; Alzheimer Disease; Antidepressive Agents; Apathy; Azepines; Benzhydryl Compounds; Biphenyl

2018
Learning by failing: ideas and concepts to tackle γ-secretases in Alzheimer's disease and beyond.
    Annual review of pharmacology and toxicology, 2015, Volume: 55

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; An

2015
Neurotoxic Non-proteinogenic Amino Acid β-N-Methylamino-L-alanine and Its Role in Biological Systems.
    Biochemistry. Biokhimiia, 2016, Volume: 81, Issue:8

    Topics: Alanine; Alzheimer Disease; Amino Acids, Diamino; Amyotrophic Lateral Sclerosis; Animals; Humans; Ne

2016
Lack of association between MTHFR A1298C variant and Alzheimer's disease: evidence from a systematic review and cumulative meta-analysis.
    Neurological research, 2017, Volume: 39, Issue:5

    Topics: Alanine; Alzheimer Disease; Cysteine; Genetic Association Studies; Genetic Predisposition to Disease

2017
Development of semagacestat (LY450139), a functional gamma-secretase inhibitor, for the treatment of Alzheimer's disease.
    Expert opinion on pharmacotherapy, 2009, Volume: 10, Issue:10

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Azepines; Cholinesterase

2009
[Progress in the development of anti-amyloid drugs for treatment of Alzheimer's disease.].
    Nihon yakurigaku zasshi. Folia pharmacologica Japonica, 2010, Volume: 136, Issue:1

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor

2010
Reversible and irreversible protein glutathionylation: biological and clinical aspects.
    Expert opinion on drug metabolism & toxicology, 2011, Volume: 7, Issue:7

    Topics: Alanine; Aldehydes; Alzheimer Disease; Apoptosis; Busulfan; Cataract; Cell Cycle; Cystic Fibrosis; D

2011
Interacting with γ-secretase for treating Alzheimer's disease: from inhibition to modulation.
    Current medicinal chemistry, 2011, Volume: 18, Issue:35

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; Az

2011
Evaluation of the performance of novel Aβ isoforms as theragnostic markers in Alzheimer's disease: from the cell to the patient.
    Neuro-degenerative diseases, 2012, Volume: 10, Issue:1-4

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; An

2012
Advances in the identification of γ-secretase inhibitors for the treatment of Alzheimer's disease.
    Expert opinion on drug discovery, 2012, Volume: 7, Issue:1

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor

2012
γ-Secretase modulator in Alzheimer's disease: shifting the end.
    Journal of Alzheimer's disease : JAD, 2012, Volume: 31, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; Az

2012
[Gamma-secretase inhibitors and modulators].
    Nihon rinsho. Japanese journal of clinical medicine, 2011, Volume: 69 Suppl 10 Pt 2

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Flurbiprofen; Humans

2011
Involvement of proteases in glycosyltransferase secretion: Alzheimer's beta-secretase-dependent cleavage and a following processing by an aminopeptidase.
    Glycoconjugate journal, 2004, Volume: 21, Issue:1-2

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Aminopeptidases; Amyloid Precursor Protein Secretas

2004
[Carnosine--biological activity and perspectives in pharmacotherapy].
    Wiadomosci lekarskie (Warsaw, Poland : 1960), 2007, Volume: 60, Issue:1-2

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Animals; Antioxidants; Calcium Channels; Cardiova

2007
A causal role for amyloid in Alzheimer's disease: the end of the beginning.
    Neurology, 1993, Volume: 43, Issue:5

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Amyloid beta-Peptides; Amyloid beta-Protein Precurs

1993
Cholinergic approaches to the treatment of Alzheimer's disease.
    British medical bulletin, 1986, Volume: 42, Issue:1

    Topics: 4-Aminopyridine; Alanine; Alzheimer Disease; Aminopyridines; Arecoline; Clinical Trials as Topic; Hu

1986

Trials

9 trials available for alanine and Acute Confusional Senile Dementia

ArticleYear
A phase 3 trial of semagacestat for treatment of Alzheimer's disease.
    The New England journal of medicine, 2013, Jul-25, Volume: 369, Issue:4

    Topics: Activities of Daily Living; Aged; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precurs

2013
Safety profile of semagacestat, a gamma-secretase inhibitor: IDENTITY trial findings.
    Current medical research and opinion, 2014, Volume: 30, Issue:10

    Topics: Aged; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Clinical Trials, P

2014
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Cognitive Impairment Precedes and Predicts Functional Impairment in Mild Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 47, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Antibodies, Monoclonal, Humanized; Antipsychoti

2015
Phase 2 safety trial targeting amyloid beta production with a gamma-secretase inhibitor in Alzheimer disease.
    Archives of neurology, 2008, Volume: 65, Issue:8

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Amnesia; Amyloid beta-Peptides; Amyloid Precurs

2008
Prevalence of asymptomatic vasogenic edema in pretreatment Alzheimer's disease study cohorts from phase 3 trials of semagacestat and solanezumab.
    Alzheimer's & dementia : the journal of the Alzheimer's Association, 2011, Volume: 7, Issue:4

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protei

2011
Amyloid-β(1-15/16) as a marker for γ-secretase inhibition in Alzheimer's disease.
    Journal of Alzheimer's disease : JAD, 2012, Volume: 31, Issue:2

    Topics: Adult; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Azep

2012
Exacerbation of psoriatic skin lesions in a patient with Alzheimer disease receiving gamma-secretase inhibitor.
    Journal of the American Academy of Dermatology, 2013, Volume: 68, Issue:2

    Topics: Aged; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Humans; Middle Age

2013
Effects of a gamma-secretase inhibitor in a randomized study of patients with Alzheimer disease.
    Neurology, 2006, Feb-28, Volume: 66, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Aspartic Acid Endopeptidases; Azep

2006
Cholinergic approaches to the treatment of Alzheimer's disease.
    British medical bulletin, 1986, Volume: 42, Issue:1

    Topics: 4-Aminopyridine; Alanine; Alzheimer Disease; Aminopyridines; Arecoline; Clinical Trials as Topic; Hu

1986

Other Studies

100 other studies available for alanine and Acute Confusional Senile Dementia

ArticleYear
Investigation of the role of prolines 232/233 in RTPPK motif in tau protein aggregation: An in vitro study.
    International journal of biological macromolecules, 2022, Oct-31, Volume: 219

    Topics: Alanine; Alzheimer Disease; Humans; Mutant Proteins; Proline; Protein Aggregates; tau Proteins

2022
Role of the Cysteine in R3 Tau Peptide in Copper Binding and Reactivity.
    International journal of molecular sciences, 2022, Sep-14, Volume: 23, Issue:18

    Topics: Alanine; Alzheimer Disease; Copper; Cysteine; Disulfides; Dopamine; Humans; Peptides; Protein Aggreg

2022
D-glutamate, D-serine, and D-alanine differ in their roles in cognitive decline in patients with Alzheimer's disease or mild cognitive impairment.
    Pharmacology, biochemistry, and behavior, 2019, Volume: 185

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Behavioral Symptoms; Chromatography, Liquid; Co

2019
Hydrogen sulfide concentration in the milieu of the hydrated alanine dipeptide determines its polyproline II-beta propensity: Main chain contribution to the energetic origin of the formation of amyloid.
    Biopolymers, 2020, Volume: 111, Issue:7

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Dipeptides; Humans; Hydrogen Sulfide; Peptides; P

2020
Identification of a Pathogenic PSEN1 Ala285Val Mutation Associated with Early-Onset Alzheimer's Disease.
    Current Alzheimer research, 2020, Volume: 17, Issue:5

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Female; Humans; Middle Aged; Mutation; Pedigree; Pr

2020
Precuneus Failures in Subjects of the PSEN1 E280A Family at Risk of Developing Alzheimer's Disease Detected Using Quantitative Electroencephalography.
    Journal of Alzheimer's disease : JAD, 2017, Volume: 58, Issue:4

    Topics: Adult; Alanine; Alzheimer Disease; Brain Mapping; Brain Waves; Cognition Disorders; Electroencephalo

2017
Rebamipide reduces amyloid-β 1-42 (Aβ42) production and ameliorates Aβ43-lowered cell viability in cultured SH-SY5Y human neuroblastoma cells.
    Neuroscience research, 2017, Volume: 124

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Cell Line, Tumor; Cell Survival; Cyclooxygenase 2

2017
Semagacestat Is a Pseudo-Inhibitor of γ-Secretase.
    Cell reports, 2017, Oct-03, Volume: 21, Issue:1

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; An

2017
Differential Pattern of Phospholipid Profile in the Temporal Cortex from E280A-Familiar and Sporadic Alzheimer's Disease Brains.
    Journal of Alzheimer's disease : JAD, 2018, Volume: 61, Issue:1

    Topics: Adult; Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Analysis of Variance; Fatty Acids; Femal

2018
Hidradenitis Suppurativa-Like Lesions Associated with Pharmacologic Inhibition of Gamma-Secretase.
    The Journal of investigative dermatology, 2018, Volume: 138, Issue:4

    Topics: Adult; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Azepines; Biopsy;

2018
Lack of Effect of Sodium Benzoate at Reported Clinical Therapeutic Concentration on d-Alanine Metabolism in Dogs.
    ACS chemical neuroscience, 2018, 11-21, Volume: 9, Issue:11

    Topics: Alanine; Alzheimer Disease; Animals; Benzoic Acid; Cognitive Dysfunction; D-Amino-Acid Oxidase; Dogs

2018
Cross-interaction of tau PET tracers with monoamine oxidase B: evidence from in silico modelling and in vivo imaging.
    European journal of nuclear medicine and molecular imaging, 2019, Volume: 46, Issue:6

    Topics: Aged; Alanine; Alzheimer Disease; Benzylamines; Binding Sites; Brain; Computational Biology; Compute

2019
A semi-physiological model of amyloid-β biosynthesis and clearance in human cerebrospinal fluid: a tool for alzheimer's disease research and drug development.
    Journal of clinical pharmacology, 2013, Volume: 53, Issue:7

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Azepines; C

2013
Therapeutic and preventive effects of methylene blue on Alzheimer's disease pathology in a transgenic mouse model.
    Neuropharmacology, 2014, Volume: 76 Pt A

    Topics: Administration, Oral; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Animals; Avoidance Learning

2014
Arginine and disordered amyloid-β peptide structures: molecular level insights into the toxicity in Alzheimer's disease.
    ACS chemical neuroscience, 2013, Dec-18, Volume: 4, Issue:12

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Arginine; Humans; Models, Theoretical; Molecular

2013
[Exacerbation of psoriasiform lesions by a gamma-secretase inhibitor].
    Annales de dermatologie et de venereologie, 2013, Volume: 140, Issue:10

    Topics: Adrenal Cortex Hormones; Aged; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Aze

2013
Semagacestat's fall: where next for AD therapies?
    Nature medicine, 2013, Volume: 19, Issue:10

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Humans

2013
Semagacestat for treatment of Alzheimer's disease.
    The New England journal of medicine, 2013, 10-24, Volume: 369, Issue:17

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Female; Humans; Male

2013
Semagacestat for treatment of Alzheimer's disease.
    The New England journal of medicine, 2013, 10-24, Volume: 369, Issue:17

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Female; Humans; Male

2013
Semagacestat for treatment of Alzheimer's disease.
    The New England journal of medicine, 2013, 10-24, Volume: 369, Issue:17

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Female; Humans; Male

2013
CHF5074 and LY450139 sub-acute treatments differently affect cortical extracellular glutamate levels in pre-plaque Tg2576 mice.
    Neuroscience, 2014, Apr-25, Volume: 266

    Topics: Alanine; Alzheimer Disease; Animals; Azepines; Cyclopropanes; Disease Models, Animal; Extracellular

2014
Adverse events and dropouts in Alzheimer's disease studies: what can we learn?
    Alzheimer's & dementia : the journal of the Alzheimer's Association, 2015, Volume: 11, Issue:1

    Topics: Accidental Falls; Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Atrial Fibrillation; Azepines

2015
Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014, Jun-04, Volume: 34, Issue:23

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; An

2014
The histidine composition of the amyloid-β domain, but not the E1 copper binding domain, modulates β-secretase processing of amyloid-β protein precursor in Alzheimer's disease.
    Journal of Alzheimer's disease : JAD, 2015, Volume: 43, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; Ce

2015
Methodological challenges in assessing the impact of comorbidities on costs in Alzheimer's disease clinical trials.
    The European journal of health economics : HEPAC : health economics in prevention and care, 2015, Volume: 16, Issue:9

    Topics: Activities of Daily Living; Age Factors; Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Azepin

2015
Lessons from a failed γ-secretase Alzheimer trial.
    Cell, 2014, Nov-06, Volume: 159, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Azepines; B

2014
Amyloid β-Protein Assembly: Differential Effects of the Protective A2T Mutation and Recessive A2V Familial Alzheimer's Disease Mutation.
    ACS chemical neuroscience, 2015, Oct-21, Volume: 6, Issue:10

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Peptides; Humans; Hydrophobic and

2015
Positive Association of the Cathepsin D Ala224Val Gene Polymorphism With the Risk of Alzheimer's Disease.
    The American journal of the medical sciences, 2015, Volume: 350, Issue:4

    Topics: Aged; Alanine; Alleles; Alzheimer Disease; Case-Control Studies; Cathepsin D; Cystatin C; Ecuador; F

2015
Age-dependent neuroinflammation and cognitive decline in a novel Ala152Thr-Tau transgenic mouse model of PSP and AD.
    Acta neuropathologica communications, 2016, Feb-25, Volume: 4

    Topics: Age Factors; Aging; Alanine; Alzheimer Disease; Animals; Astrocytes; Cognition Disorders; Cytokines;

2016
L17A/F19A Substitutions Augment the α-Helicity of β-Amyloid Peptide Discordant Segment.
    PloS one, 2016, Volume: 11, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Circular Dichroism; Humans; Isotopes; Magnetic Re

2016
Changes in Neuropsychiatric Inventory Associated with Semagacestat Treatment of Alzheimer's Disease.
    Journal of Alzheimer's disease : JAD, 2016, 08-10, Volume: 54, Issue:1

    Topics: Aged; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Apathy; Appetite; Azepines;

2016
Alzheimer's Protective Cross-Interaction between Wild-Type and A2T Variants Alters Aβ
    ACS chemical neuroscience, 2017, 03-15, Volume: 8, Issue:3

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Peptides; Animals; Humans; Kinetic

2017
Low Florbetapir PET Uptake and Normal Aβ1-42 Cerebrospinal Fluid in an APP Ala713Thr Mutation Carrier.
    Journal of Alzheimer's disease : JAD, 2017, Volume: 57, Issue:3

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Aniline Compounds

2017
Effect of a dominant-negative form of ADAM10 in a mouse model of Alzheimer's disease.
    Journal of Alzheimer's disease : JAD, 2009, Volume: 16, Issue:2

    Topics: ADAM Proteins; ADAM10 Protein; Age Factors; Alanine; Alzheimer Disease; Amyloid beta-Protein Precurs

2009
Molecule of the month. Semagacestat.
    Drug news & perspectives, 2008, Volume: 21, Issue:7

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Azepines; C

2008
Progressive neuropathology and cognitive decline in a single Arctic APP transgenic mouse model.
    Neurobiology of aging, 2011, Volume: 32, Issue:2

    Topics: Age Factors; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Anim

2011
Oligomeric amyloid beta-protein as a therapeutic target in Alzheimer's disease: its significance based on its distinct localization and the occurrence of a familial variant form.
    Current Alzheimer research, 2009, Volume: 6, Issue:2

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Animals; Antibodies; Antibody Specificity; Glutam

2009
Alanine-2 carbonyl is an oxygen ligand in Cu2+ coordination of Alzheimer's disease amyloid-beta peptide--relevance to N-terminally truncated forms.
    Journal of the American Chemical Society, 2009, Jul-01, Volume: 131, Issue:25

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Copper; Humans; Hydrogen-Ion Concentration; Ligan

2009
Semagacestat, a gamma-secretase inhibitor for the potential treatment of Alzheimer's disease.
    Current opinion in investigational drugs (London, England : 2000), 2009, Volume: 10, Issue:7

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Azepines; Clinical Trials

2009
Deprotonation of the Asp1-Ala2 peptide bond induces modification of the dynamic copper(II) environment in the amyloid-beta peptide near physiological pH.
    Angewandte Chemie (International ed. in English), 2009, Volume: 48, Issue:50

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Aspartic Acid; Binding Sites; Copper; Dipeptides;

2009
Neuropathology of the recessive A673V APP mutation: Alzheimer disease with distinctive features.
    Acta neuropathologica, 2010, Volume: 120, Issue:6

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Peptides; Amyloid beta-Protein Pre

2010
Quantification of cystatin C in cerebrospinal fluid from various neurological disorders and correlation with G73A polymorphism in CST3.
    Brain research, 2010, Nov-18, Volume: 1361

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Amyotrophic Lateral Sclerosis; Biomarkers; Case

2010
Alzheimer's failure raises questions about disease-modifying strategies.
    Nature reviews. Drug discovery, 2010, Volume: 9, Issue:10

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Clinical Trials, Phase I

2010
NerveCenter: Phase III Alzheimer trial halted: Search for therapeutic biomarkers continues.
    Annals of neurology, 2010, Volume: 68, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid; Amyloid Precursor Protein Secretases; Azepines; Biomarkers; Cli

2010
What can be inferred from the interruption of the semagacestat trial for treatment of Alzheimer's disease?
    Biological psychiatry, 2010, Nov-15, Volume: 68, Issue:10

    Topics: Alanine; Alzheimer Disease; Amyloid; Amyloid Precursor Protein Secretases; Azepines; Cognition Disor

2010
Genetics. Gamma-secretase and human disease.
    Science (New York, N.Y.), 2010, Nov-19, Volume: 330, Issue:6007

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Azepines; Hidradenitis Su

2010
Aβ40(L17A/F19A) mutant diminishes the aggregation and neurotoxicity of Aβ40.
    Biochemical and biophysical research communications, 2011, Feb-04, Volume: 405, Issue:1

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Peptides; Animals; Cell Survival;

2011
New pathway links γ-secretase to inflammation and memory while sparing notch.
    Annals of neurology, 2011, Volume: 69, Issue:1

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Azepines; CREB-Binding Pr

2011
What the halted phase III γ-secretase inhibitor trial may (or may not) be telling us.
    Annals of neurology, 2011, Volume: 69, Issue:2

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Azepines; E

2011
Mutations that replace aromatic side chains promote aggregation of the Alzheimer's Aβ peptide.
    Biochemistry, 2011, May-17, Volume: 50, Issue:19

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Amino Acids, Aromatic; Amyloid beta-Peptides; Human

2011
Validation of ELISA methods for quantification of total tau and phosporylated-tau181 in human cerebrospinal fluid with measurement in specimens from two Alzheimer's disease studies.
    Journal of Alzheimer's disease : JAD, 2011, Volume: 26, Issue:3

    Topics: Aged; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Antibodies, Monoclonal; Anti

2011
Drugs: a tangled web of targets.
    Nature, 2011, Jul-13, Volume: 475, Issue:7355

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; An

2011
BACE-1 inhibition prevents the γ-secretase inhibitor evoked Aβ rise in human neuroblastoma SH-SY5Y cells.
    Journal of biomedical science, 2011, Oct-21, Volume: 18

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Aspartic Ac

2011
A canine model to evaluate efficacy and safety of γ-secretase inhibitors and modulators.
    Journal of Alzheimer's disease : JAD, 2012, Volume: 28, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Azepines; Dogs; Drug Eval

2012
Dual task abilities as a possible preclinical marker of Alzheimer's disease in carriers of the E280A presenilin-1 mutation.
    Journal of the International Neuropsychological Society : JINS, 2012, Volume: 18, Issue:2

    Topics: Adult; Alanine; Alzheimer Disease; Analysis of Variance; Biomarkers; Cognition Disorders; Female; Gl

2012
Regulation of mitochondrial transport and inter-microtubule spacing by tau phosphorylation at the sites hyperphosphorylated in Alzheimer's disease.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012, Feb-15, Volume: 32, Issue:7

    Topics: Alanine; Alzheimer Disease; Animals; Aspartic Acid; Biological Transport; Cells, Cultured; Chloroceb

2012
Toxic role of K+ channel oxidation in mammalian brain.
    The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012, Mar-21, Volume: 32, Issue:12

    Topics: 2,2'-Dipyridyl; Age Factors; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein

2012
Modulation of γ-secretase activity by multiple enzyme-substrate interactions: implications in pathogenesis of Alzheimer's disease.
    PloS one, 2012, Volume: 7, Issue:3

    Topics: Alanine; Algorithms; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amylo

2012
Critical role of soluble amyloid-β for early hippocampal hyperactivity in a mouse model of Alzheimer's disease.
    Proceedings of the National Academy of Sciences of the United States of America, 2012, May-29, Volume: 109, Issue:22

    Topics: Age Factors; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases

2012
Pooling/bootstrap-based GWAS (pbGWAS) identifies new loci modifying the age of onset in PSEN1 p.Glu280Ala Alzheimer's disease.
    Molecular psychiatry, 2013, Volume: 18, Issue:5

    Topics: Age of Onset; Alanine; Alzheimer Disease; Cohort Studies; Databases, Factual; Female; Founder Effect

2013
ACS chemical neuroscience molecule spotlight on semagacestat (LY450139).
    ACS chemical neuroscience, 2010, Aug-18, Volume: 1, Issue:8

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor

2010
An improved cell-based method for determining the γ-secretase enzyme activity against both Notch and APP substrates.
    Journal of neuroscience methods, 2013, Feb-15, Volume: 213, Issue:1

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Protein Precursor; Amyloid Precursor Protein Secretases; Az

2013
Mitochondrial DNA A4336G mutation in Alzheimer's and Parkinson's diseases.
    European neurology, 2002, Volume: 48, Issue:1

    Topics: Aged; Alanine; Alzheimer Disease; Case-Control Studies; DNA, Mitochondrial; Female; Glycine; Humans;

2002
Identification of essential amino acids in Humanin, a neuroprotective factor against Alzheimer's disease-relevant insults.
    Peptides, 2003, Volume: 24, Issue:4

    Topics: Alanine; Alzheimer Disease; Amino Acids; Amyloid beta-Protein Precursor; Animals; Arginine; Culture

2003
Methionine synthase polymorphism is a risk factor for Alzheimer disease.
    Neuroreport, 2003, Jul-18, Volume: 14, Issue:10

    Topics: 5-Methyltetrahydrofolate-Homocysteine S-Methyltransferase; Age of Onset; Aged; Aged, 80 and over; Ag

2003
Apolipoprotein E -491 promoter polymorphism is an independent risk factor for Alzheimer's disease in the Chinese population.
    Neuroscience letters, 2003, Oct-16, Volume: 350, Issue:1

    Topics: Aged; Alanine; Alleles; Alzheimer Disease; Apolipoproteins E; Asian People; Case-Control Studies; Ch

2003
Tumour necrosis factor-alpha gene polymorphisms and Alzheimer's disease.
    Neuroscience letters, 2003, Oct-16, Volume: 350, Issue:1

    Topics: Aged; Aged, 80 and over; Alanine; Alleles; Alzheimer Disease; Case-Control Studies; Cohort Studies;

2003
Interaction between the Alzheimer's survival peptide humanin and insulin-like growth factor-binding protein 3 regulates cell survival and apoptosis.
    Proceedings of the National Academy of Sciences of the United States of America, 2003, Oct-28, Volume: 100, Issue:22

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Apoptosis; Cell Survival; Humans; Insulin-Like Grow

2003
Lack of association between Alzheimer's disease and the promoter region polymorphisms of the nicastrin gene.
    Neuroscience letters, 2004, Jun-03, Volume: 363, Issue:1

    Topics: Adult; Age of Onset; Aged; Alanine; Alleles; Alzheimer Disease; Amyloid Precursor Protein Secretases

2004
Allelic variation at the A218C tryptophan hydroxylase polymorphism influences agitation and aggression in Alzheimer's disease.
    Neuroscience letters, 2004, Jun-17, Volume: 363, Issue:3

    Topics: Aged; Aged, 80 and over; Aggression; Alanine; Alzheimer Disease; Chi-Square Distribution; Cohort Stu

2004
Tyrosine gated electron transfer is key to the toxic mechanism of Alzheimer's disease beta-amyloid.
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2004, Volume: 18, Issue:12

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Peptides; Catalysis; Copper; Elect

2004
Genetic variation in apolipoprotein D and Alzheimer's disease.
    Journal of neurology, 2004, Volume: 251, Issue:8

    Topics: Age of Onset; Aged; Alanine; Alzheimer Disease; Apolipoproteins; Apolipoproteins D; Case-Control Stu

2004
Interaction between matrix metalloproteinase 3 and the epsilon4 allele of apolipoprotein E increases the risk of Alzheimer's disease in Finns.
    Neuroscience letters, 2004, Sep-09, Volume: 367, Issue:3

    Topics: Aged; Aged, 80 and over; Alanine; Alleles; Alzheimer Disease; Apolipoprotein E4; Apolipoproteins E;

2004
Familial Alzheimer disease associated with A713T mutation in APP.
    Neuroscience letters, 2004, Nov-11, Volume: 370, Issue:2-3

    Topics: Alanine; Alzheimer Disease; Cerebral Cortex; DNA Mutational Analysis; Exons; Humans; Immunohistochem

2004
Structural and mutational analyses of the molecular interactions between the catalytic domain of factor XIa and the Kunitz protease inhibitor domain of protease nexin 2.
    The Journal of biological chemistry, 2005, Oct-28, Volume: 280, Issue:43

    Topics: Alanine; Alzheimer Disease; Arginine; Binding Sites; Carrier Proteins; Catalytic Domain; Crystallogr

2005
Deficiency of disulfide bonds facilitating fibrillogenesis of endostatin.
    The Journal of biological chemistry, 2006, Jan-13, Volume: 281, Issue:2

    Topics: Alanine; Alzheimer Disease; Animals; Benzothiazoles; Cell Survival; Circular Dichroism; Disulfides;

2006
NMDA receptor subunit-dependent modulation by conantokin-G and Ala7-conantokin-G.
    Journal of neurochemistry, 2006, Volume: 96, Issue:1

    Topics: Alanine; Alzheimer Disease; Animals; Concanavalin A; Conotoxins; Electrophysiology; Excitatory Amino

2006
Glycogen synthase kinase 3beta phosphorylates Alzheimer's disease-specific Ser396 of microtubule-associated protein tau by a sequential mechanism.
    Biochemistry, 2006, Mar-14, Volume: 45, Issue:10

    Topics: Alanine; Alzheimer Disease; Animals; Brain; Cattle; Cells, Cultured; Glycogen Synthase Kinase 3; Gly

2006
Interaction of CTSD and A2M polymorphisms in the risk for Alzheimer's disease.
    Journal of the neurological sciences, 2006, Sep-25, Volume: 247, Issue:2

    Topics: Aged; Aged, 80 and over; Alanine; alpha-Macroglobulins; Alzheimer Disease; Cathepsin D; DNA Mutation

2006
Discovery of (S)-2-((S)-2-(3,5-difluorophenyl)-2-hydroxyacetamido)-N-((S,Z)-3-methyl-4-oxo-4,5-dihydro-3H-benzo[d][1,2]diazepin-5-yl)propanamide (BMS-433796): a gamma-secretase inhibitor with Abeta lowering activity in a transgenic mouse model of Alzheime
    Bioorganic & medicinal chemistry letters, 2007, Jul-15, Volume: 17, Issue:14

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; Be

2007
Atypical early-onset Alzheimer's disease caused by the Iranian APP mutation.
    Journal of the neurological sciences, 2008, May-15, Volume: 268, Issue:1-2

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Blood Pressure; D

2008
Verification of the C-terminal intramolecular beta-sheet in Abeta42 aggregates using solid-state NMR: implications for potent neurotoxicity through the formation of radicals.
    Bioorganic & medicinal chemistry letters, 2008, Jun-01, Volume: 18, Issue:11

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Free Radicals; Methionine; Models, Biological; Mo

2008
Long-term prevention of Alzheimer's disease-like behavioral deficits in PDAPP mice carrying a mutation in Asp664.
    Behavioural brain research, 2008, Aug-22, Volume: 191, Issue:2

    Topics: Age Factors; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Anal

2008
Alaproclate: a pharmacokinetic and biochemical study in patients with dementia of Alzheimer type.
    Psychopharmacology, 1983, Volume: 80, Issue:3

    Topics: Aged; Alanine; Alzheimer Disease; Dementia; Female; Humans; Kinetics; Male; Serotonin

1983
Effects of the mutations Glu22 to Gln and Ala21 to Gly on the aggregation of a synthetic fragment of the Alzheimer's amyloid beta/A4 peptide.
    Neuroscience letters, 1993, Oct-14, Volume: 161, Issue:1

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Amyloid; Amyloid beta-Peptides; Glutamates; Glutami

1993
Mutations associated with a locus for familial Alzheimer's disease result in alternative processing of amyloid beta-protein precursor.
    The Journal of biological chemistry, 1994, Jul-01, Volume: 269, Issue:26

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Amyloid beta-Protein Precursor; Base Sequence; Cell

1994
Study of Al3+ binding and conformational properties of the alanine-substituted C-terminal domain of the NF-M protein and its relevance to Alzheimer's disease.
    Biochemistry, 1994, Aug-16, Volume: 33, Issue:32

    Topics: Alanine; Aluminum; Alzheimer Disease; Calcium; Cations; Circular Dichroism; Humans; Neurofilament Pr

1994
Clinical features of early-onset Alzheimer disease in a large kindred with an E280A presenilin-1 mutation.
    JAMA, 1997, Mar-12, Volume: 277, Issue:10

    Topics: Adult; Age of Onset; Alanine; Alzheimer Disease; Autopsy; Brain; Codon; Female; Glutamic Acid; Heada

1997
Lithium reduces tau phosphorylation by inhibition of glycogen synthase kinase-3.
    The Journal of biological chemistry, 1997, Oct-03, Volume: 272, Issue:40

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Calcium-Calmodulin-Dependent Protein Kinases; Carci

1997
Variable deposition of amyloid beta-protein (A beta) with the carboxy-terminus that ends at residue valine40 (A beta 40) in the cerebral cortex of patients with Alzheimer's disease: a double-labeling immunohistochemical study with antibodies specific for
    Neurochemical research, 1997, Volume: 22, Issue:12

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Amyloid beta-Peptides; Antibodies; Antibody Spe

1997
A basic amino acid in the cytoplasmic domain of Alzheimer's beta-amyloid precursor protein (APP) is essential for cleavage of APP at the alpha-site.
    The Journal of biological chemistry, 1998, Jul-24, Volume: 273, Issue:30

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Protein Precursor; Binding Sites;

1998
Genetic polymorphism of cathepsin D is strongly associated with the risk for developing sporadic Alzheimer's disease.
    Neuroscience letters, 1999, Mar-12, Volume: 262, Issue:3

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Amino Acid Substitution; Apolipoprotein E4; Apo

1999
Effect of amino-acid substitutions on Alzheimer's amyloid-beta peptide-glycosaminoglycan interactions.
    European journal of biochemistry, 2000, Volume: 267, Issue:21

    Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Amino Acid Substitution; Amyloid beta-Peptides; Cho

2000
In vitro studies of amyloid beta-protein fibril assembly and toxicity provide clues to the aetiology of Flemish variant (Ala692-->Gly) Alzheimer's disease.
    The Biochemical journal, 2001, May-01, Volume: 355, Issue:Pt 3

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Peptides; Animals; Cells, Cultured

2001
A founder mutation in presenilin 1 causing early-onset Alzheimer disease in unrelated Caribbean Hispanic families.
    JAMA, 2001, Nov-14, Volume: 286, Issue:18

    Topics: Age of Onset; Aged; Alanine; Alzheimer Disease; Amyloid beta-Protein Precursor; Apolipoproteins E; C

2001
A novel presenilin 2 gene mutation (D439A) in a patient with early-onset Alzheimer's disease.
    Neurology, 2001, Nov-27, Volume: 57, Issue:10

    Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Aspartic Acid; Genetic Carrier Screening; Human

2001
Split verdict on schizophrenia.
    Nature genetics, 1992, Volume: 1, Issue:4

    Topics: Alanine; Alzheimer Disease; Amyloid beta-Protein Precursor; Chromosomes, Human, Pair 11; Codon; DNA;

1992
Presence of D-alanine in proteins of normal and Alzheimer human brain.
    Brain research, 1992, Oct-02, Volume: 592, Issue:1-2

    Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Brain; Humans; Methods; Middle Aged; Nerve Tiss

1992
Free D-aspartate and D-alanine in normal and Alzheimer brain.
    Brain research bulletin, 1991, Volume: 26, Issue:6

    Topics: Adult; Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Aspartic Acid; Brain Chemistry; Humans;

1991
A postmortem study of amino acid neurotransmitters in Alzheimer's disease.
    Annals of neurology, 1986, Volume: 20, Issue:5

    Topics: Aged; Aging; Alanine; Alzheimer Disease; Amino Acids; Aspartic Acid; Brain; gamma-Aminobutyric Acid;

1986