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.
Excerpt | Relevance | Reference |
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"Alaproclate, a specific inhibitor of neuronal serotonin re-uptake, was given to 12 patients with dementia of Alzheimer type." | 7.66 | Alaproclate: 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." | 3.69 | Clinical 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." | 3.66 | Alaproclate: 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." | 2.79 | Safety 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." | 2.78 | A 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." | 2.73 | Phase 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." | 2.45 | Development 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." | 1.72 | Investigation 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." | 1.48 | Lack 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)." | 1.43 | Changes 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)." | 1.42 | Adverse 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." | 1.40 | Genetic 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." | 1.37 | Mutations 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." | 1.35 | Atypical 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)." | 1.35 | Long-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." | 1.34 | 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 ( 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." | 1.32 | Identification 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." | 1.31 | Effect 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." | 1.28 | Presence 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) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 3 (2.36) | 18.7374 |
1990's | 12 (9.45) | 18.2507 |
2000's | 36 (28.35) | 29.6817 |
2010's | 70 (55.12) | 24.3611 |
2020's | 6 (4.72) | 2.80 |
Authors | Studies |
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Akbari, V | 1 |
Mohammadi, S | 1 |
Mehrabi, M | 1 |
Ghobadi, S | 1 |
Farrokhi, A | 1 |
Khodarahmi, R | 1 |
Bacchella, C | 1 |
Gentili, S | 1 |
Mozzi, SI | 1 |
Monzani, E | 1 |
Casella, L | 1 |
Tegoni, M | 1 |
Dell'Acqua, S | 1 |
Lin, CH | 1 |
Yang, HT | 1 |
Lane, HY | 1 |
Mirkin, NG | 1 |
Krimm, S | 1 |
Vo, VG | 1 |
Pyun, JM | 1 |
Bagyinszky, E | 1 |
An, SSA | 1 |
Kim, SY | 1 |
Lu, L | 1 |
Zheng, X | 2 |
Wang, S | 1 |
Tang, C | 1 |
Zhang, Y | 1 |
Yao, G | 1 |
Zeng, J | 1 |
Ge, S | 1 |
Wen, H | 1 |
Xu, M | 1 |
Guyatt, G | 1 |
Xu, N | 1 |
Altiné-Samey, R | 1 |
Antier, D | 1 |
Mavel, S | 1 |
Dufour-Rainfray, D | 1 |
Balageas, AC | 1 |
Beaufils, E | 1 |
Emond, P | 1 |
Foucault-Fruchard, L | 1 |
Chalon, S | 1 |
Ochoa, JF | 1 |
Alonso, JF | 1 |
Duque, JE | 1 |
Tobón, CA | 1 |
Baena, A | 1 |
Lopera, F | 5 |
Mañanas, MA | 1 |
Hernández, AM | 1 |
Fukui, K | 1 |
Yachi, K | 1 |
Yoshida, H | 1 |
Tanji, K | 1 |
Matsumiya, T | 1 |
Hayakari, R | 1 |
Tsuruga, K | 1 |
Tanaka, H | 1 |
Imaizumi, T | 1 |
Tagami, S | 1 |
Yanagida, K | 1 |
Kodama, TS | 1 |
Takami, M | 1 |
Mizuta, N | 1 |
Oyama, H | 1 |
Nishitomi, K | 1 |
Chiu, YW | 1 |
Okamoto, T | 1 |
Ikeuchi, T | 1 |
Sakaguchi, G | 1 |
Kudo, T | 1 |
Matsuura, Y | 1 |
Fukumori, A | 1 |
Takeda, M | 1 |
Ihara, Y | 1 |
Okochi, M | 1 |
Villamil-Ortiz, JG | 1 |
Barrera-Ocampo, A | 1 |
Arias-Londoño, JD | 1 |
Villegas, A | 1 |
Cardona-Gómez, GP | 1 |
O'Sullivan Coyne, G | 1 |
Woodring, TS | 1 |
Lee, CR | 1 |
Chen, AP | 1 |
Kong, HH | 1 |
McAninch, EA | 1 |
Rajan, KB | 1 |
Evans, DA | 1 |
Jo, S | 1 |
Chaker, L | 1 |
Peeters, RP | 1 |
Bennett, DA | 1 |
Mash, DC | 1 |
Bianco, AC | 1 |
Ruthirakuhan, MT | 1 |
Herrmann, N | 2 |
Abraham, EH | 1 |
Chan, S | 1 |
Lanctôt, KL | 2 |
Popiolek, M | 1 |
Tierney, B | 1 |
Steyn, SJ | 1 |
DeVivo, M | 1 |
Murugan, NA | 1 |
Chiotis, K | 1 |
Rodriguez-Vieitez, E | 1 |
Lemoine, L | 1 |
Ågren, H | 1 |
Nordberg, A | 1 |
Haug, KG | 1 |
Staab, A | 1 |
Dansirikul, C | 1 |
Lehr, T | 1 |
Doody, RS | 2 |
Raman, R | 3 |
Farlow, M | 1 |
Iwatsubo, T | 2 |
Vellas, B | 1 |
Joffe, S | 1 |
Kieburtz, K | 1 |
He, F | 1 |
Sun, X | 2 |
Thomas, RG | 1 |
Aisen, PS | 3 |
Siemers, E | 4 |
Sethuraman, G | 4 |
Mohs, R | 2 |
Paban, V | 1 |
Manrique, C | 1 |
Filali, M | 1 |
Maunoir-Regimbal, S | 1 |
Fauvelle, F | 1 |
Alescio-Lautier, B | 1 |
Coskuner, O | 1 |
Wise-Scira, O | 1 |
Trechot, P | 1 |
Schmutz, JL | 1 |
Blennow, K | 3 |
Zetterberg, H | 3 |
Haass, C | 2 |
Finucane, T | 1 |
Gupta, VB | 1 |
Gupta, VK | 1 |
Martins, R | 1 |
Pomara, N | 1 |
Beggiato, S | 1 |
Giuliani, A | 1 |
Sivilia, S | 1 |
Lorenzini, L | 1 |
Antonelli, T | 1 |
Imbimbo, BP | 4 |
Giardino, L | 1 |
Calzà, L | 1 |
Ferraro, L | 1 |
Henley, DB | 3 |
Sundell, KL | 2 |
Schneider, LS | 1 |
Fowler, SW | 1 |
Chiang, AC | 1 |
Savjani, RR | 1 |
Larson, ME | 1 |
Sherman, MA | 1 |
Schuler, DR | 1 |
Cirrito, JR | 1 |
Lesné, SE | 1 |
Jankowsky, JL | 1 |
Dowsett, SA | 1 |
May, PC | 5 |
Gough, M | 1 |
Blanthorn-Hazell, S | 1 |
Parkin, ET | 1 |
De Strooper, B | 2 |
Chávez Gutiérrez, L | 1 |
Kahle-Wrobleski, K | 1 |
Fillit, H | 1 |
Kurlander, J | 1 |
Reed, C | 1 |
Belger, M | 1 |
Liu, D | 1 |
Roychaudhuri, R | 1 |
Teplow, DB | 3 |
Bowers, MT | 1 |
Paz-Y-Miño, CA | 1 |
García-Cárdenas, JM | 1 |
López-Cortés, A | 1 |
Salazar, C | 1 |
Serrano, M | 1 |
Leone, PE | 1 |
Liu-Seifert, H | 1 |
Price, K | 1 |
Han, B | 1 |
Selzler, KJ | 1 |
Henley, D | 1 |
Sundell, K | 1 |
Aisen, P | 1 |
Cummings, J | 2 |
Raskin, J | 1 |
Sydow, A | 1 |
Hochgräfe, K | 1 |
Könen, S | 1 |
Cadinu, D | 1 |
Matenia, D | 1 |
Petrova, O | 1 |
Joseph, M | 1 |
Dennissen, FJ | 1 |
Mandelkow, EM | 1 |
Liang, CT | 1 |
Huang, HB | 2 |
Wang, CC | 2 |
Chen, YR | 2 |
Chang, CF | 1 |
Shiao, MS | 2 |
Chen, YC | 2 |
Lin, TH | 2 |
Rosenberg, PB | 1 |
Mintzer, JE | 1 |
Porsteinsson, AP | 1 |
Popova, AA | 1 |
Koksharova, OA | 1 |
Liu, S | 1 |
Wu, Y | 1 |
Liu, X | 1 |
Zhou, J | 1 |
Wang, Z | 1 |
He, Z | 1 |
Huang, Z | 1 |
Das, P | 1 |
Chacko, AR | 1 |
Belfort, G | 1 |
Lombardi, G | 1 |
Berti, V | 1 |
Tedde, A | 1 |
Bagnoli, S | 1 |
Piaceri, I | 1 |
Polito, C | 1 |
Lucidi, G | 1 |
Ferrari, C | 1 |
Ginestroni, A | 1 |
Moretti, M | 1 |
Pupi, A | 1 |
Nacmias, B | 1 |
Sorbi, S | 1 |
Fleisher, AS | 1 |
Siemers, ER | 4 |
Becerra, L | 1 |
Clark, CM | 1 |
Dean, RA | 5 |
Farlow, MR | 2 |
Galvin, JE | 2 |
Peskind, ER | 1 |
Quinn, JF | 2 |
Sherzai, A | 1 |
Sowell, BB | 1 |
Thal, LJ | 1 |
Schroeder, A | 1 |
Fahrenholz, F | 1 |
Schmitt, U | 1 |
Rönnbäck, A | 1 |
Zhu, S | 1 |
Dillner, K | 1 |
Aoki, M | 1 |
Lilius, L | 1 |
Näslund, J | 1 |
Winblad, B | 1 |
Graff, C | 1 |
Ito, K | 1 |
Ishibashi, K | 1 |
Tomiyama, T | 1 |
Umeda, T | 1 |
Yamamoto, K | 1 |
Kitajima, E | 1 |
Idomoto, T | 1 |
Nagatomo, T | 1 |
Mori, H | 2 |
Drew, SC | 1 |
Masters, CL | 2 |
Barnham, KJ | 2 |
Peretto, I | 1 |
Hureau, C | 1 |
Coppel, Y | 1 |
Dorlet, P | 1 |
Solari, PL | 1 |
Sayen, S | 1 |
Guillon, E | 1 |
Sabater, L | 1 |
Faller, P | 1 |
Shitaka, Y | 1 |
Mitani, Y | 1 |
Nagakura, A | 1 |
Miyake, A | 1 |
Matsuoka, N | 1 |
Giaccone, G | 1 |
Morbin, M | 1 |
Moda, F | 1 |
Botta, M | 1 |
Mazzoleni, G | 1 |
Uggetti, A | 1 |
Catania, M | 1 |
Moro, ML | 1 |
Redaelli, V | 1 |
Spagnoli, A | 1 |
Rossi, RS | 1 |
Salmona, M | 1 |
Di Fede, G | 1 |
Tagliavini, F | 1 |
Yamamoto-Watanabe, Y | 1 |
Watanabe, M | 1 |
Jackson, M | 1 |
Akimoto, H | 1 |
Sugimoto, K | 1 |
Yasujima, M | 1 |
Wakasaya, Y | 1 |
Matsubara, E | 1 |
Kawarabayashi, T | 1 |
Harigaya, Y | 1 |
Lyndon, AR | 1 |
Shoji, M | 1 |
Extance, A | 1 |
Samson, K | 1 |
Kelleher, RJ | 1 |
Shen, J | 1 |
Lo, CJ | 1 |
Su, CL | 1 |
Liu, HT | 1 |
Gandy, S | 1 |
Wustman, B | 1 |
Schor, NF | 1 |
Armstrong, AH | 1 |
Chen, J | 1 |
McKoy, AF | 1 |
Hecht, MH | 1 |
Cooper, AJ | 1 |
Pinto, JT | 1 |
Callery, PS | 1 |
Lachno, DR | 1 |
Romeo, MJ | 1 |
Vanderstichele, H | 1 |
Coart, E | 1 |
Konrad, RJ | 1 |
Zajac, JJ | 1 |
Talbot, JA | 1 |
Jensen, HF | 1 |
Demattos, RB | 1 |
Gravitz, L | 1 |
Carlson, C | 1 |
Estergard, W | 1 |
Oh, J | 1 |
Suhy, J | 1 |
Jack, CR | 1 |
Barakos, J | 1 |
Jämsä, A | 1 |
Belda, O | 1 |
Edlund, M | 1 |
Lindström, E | 1 |
Borghys, H | 1 |
Tuefferd, M | 1 |
Van Broeck, B | 1 |
Clessens, E | 1 |
Dillen, L | 1 |
Cools, W | 1 |
Vinken, P | 1 |
Straetemans, R | 1 |
De Ridder, F | 1 |
Gijsen, H | 1 |
Mercken, M | 1 |
Panza, F | 2 |
Frisardi, V | 2 |
Solfrizzi, V | 2 |
Logroscino, G | 1 |
Santamato, A | 1 |
Greco, A | 1 |
Seripa, D | 3 |
Pilotto, A | 3 |
MacPherson, SE | 1 |
Parra, MA | 1 |
Moreno, S | 1 |
Della Sala, S | 1 |
Portelius, E | 2 |
Gustavsson, MK | 1 |
Andreasson, U | 2 |
Shahpasand, K | 1 |
Uemura, I | 1 |
Saito, T | 1 |
Asano, T | 1 |
Hata, K | 1 |
Shibata, K | 1 |
Toyoshima, Y | 1 |
Hasegawa, M | 1 |
Hisanaga, S | 1 |
Cotella, D | 1 |
Hernandez-Enriquez, B | 1 |
Wu, X | 1 |
Li, R | 1 |
Pan, Z | 1 |
Leveille, J | 1 |
Link, CD | 1 |
Oddo, S | 1 |
Sesti, F | 1 |
D'Onofrio, G | 1 |
Paroni, G | 1 |
Cascavilla, L | 1 |
Svedružić, ZM | 1 |
Popović, K | 1 |
Smoljan, I | 1 |
Sendula-Jengić, V | 1 |
Marcil, A | 1 |
Bourgeois, P | 1 |
Nutu, M | 1 |
Mawuenyega, KG | 1 |
Sigurdson, WC | 1 |
Paul, SM | 1 |
Holtzman, DM | 2 |
Bateman, RJ | 1 |
Busche, MA | 1 |
Chen, X | 1 |
Henning, HA | 1 |
Reichwald, J | 1 |
Staufenbiel, M | 1 |
Sakmann, B | 1 |
Konnerth, A | 1 |
Vélez, JI | 1 |
Chandrasekharappa, SC | 1 |
Henao, E | 1 |
Martinez, AF | 1 |
Harper, U | 1 |
Jones, M | 1 |
Solomon, BD | 1 |
Lopez, L | 1 |
Garcia, G | 1 |
Aguirre-Acevedo, DC | 1 |
Acosta-Baena, N | 1 |
Correa, JC | 1 |
Lopera-Gómez, CM | 1 |
Jaramillo-Elorza, MC | 1 |
Rivera, D | 1 |
Kosik, KS | 2 |
Schork, NJ | 1 |
Swanson, JM | 1 |
Arcos-Burgos, M | 2 |
Xia, W | 1 |
Wong, ST | 1 |
Hanlon, E | 1 |
Morin, P | 1 |
Iwai, A | 1 |
Hopkins, CR | 1 |
McKee, TD | 1 |
Loureiro, RM | 1 |
Dumin, JA | 1 |
Zarayskiy, V | 1 |
Tate, B | 1 |
Hsu, CK | 1 |
Hsu, CC | 1 |
Lee, JY | 1 |
Kuo, YM | 1 |
Pai, MC | 1 |
García-Lozano, JR | 1 |
Mir, P | 1 |
Alberca, R | 1 |
Aguilera, I | 1 |
Gil Néciga, E | 1 |
Fernández-López, O | 1 |
Cayuela, A | 1 |
Núñez-Roldan, A | 1 |
Yamagishi, Y | 1 |
Hashimoto, Y | 3 |
Niikura, T | 2 |
Nishimoto, I | 2 |
Beyer, K | 1 |
Lao, JI | 1 |
Latorre, P | 1 |
Riutort, N | 1 |
Matute, B | 1 |
Fernández-Figueras, MT | 1 |
Mate, JL | 1 |
Ariza, A | 1 |
Yang, JD | 1 |
Feng, GY | 1 |
Zhang, J | 2 |
Cheung, J | 1 |
St Clair, D | 1 |
He, L | 1 |
Ichimura, K | 1 |
Culpan, D | 1 |
MacGowan, SH | 1 |
Ford, JM | 1 |
Nicoll, JA | 1 |
Griffin, WS | 1 |
Dewar, D | 1 |
Cairns, NJ | 1 |
Hughes, A | 1 |
Kehoe, PG | 1 |
Wilcock, GK | 1 |
Ikonen, M | 1 |
Liu, B | 1 |
Ma, L | 1 |
Lee, KW | 1 |
Cohen, P | 1 |
Orlacchio, A | 2 |
Kawarai, T | 2 |
Polidoro, M | 1 |
Paterson, AD | 1 |
Rogaeva, E | 2 |
St George-Hyslop, PH | 1 |
Bernardi, G | 1 |
Craig, D | 1 |
Hart, DJ | 1 |
Carson, R | 1 |
McIlroy, SP | 1 |
Passmore, AP | 1 |
Haeffner, F | 1 |
Ciccotosto, GD | 1 |
Curtain, CC | 1 |
Tew, D | 1 |
Mavros, C | 1 |
Beyreuther, K | 1 |
Carrington, D | 1 |
Cherny, RA | 1 |
Cappai, R | 1 |
Bush, AI | 1 |
Helisalmi, S | 1 |
Hiltunen, M | 1 |
Vepsäläinen, S | 1 |
Iivonen, S | 1 |
Corder, EH | 1 |
Lehtovirta, M | 1 |
Mannermaa, A | 1 |
Koivisto, AM | 1 |
Soininen, H | 1 |
Saarela, MS | 1 |
Lehtimäki, T | 1 |
Rinne, JO | 1 |
Hervonen, A | 1 |
Jylhä, M | 1 |
Röyttä, M | 1 |
Ahonen, JP | 1 |
Mattila, KM | 1 |
Kitazume, S | 1 |
Suzuki, M | 1 |
Saido, TC | 1 |
Armstrong, J | 1 |
Boada, M | 1 |
Rey, MJ | 1 |
Vidal, N | 1 |
Ferrer, I | 1 |
Navaneetham, D | 1 |
Jin, L | 1 |
Pandey, P | 1 |
Strickler, JE | 1 |
Babine, RE | 1 |
Abdel-Meguid, SS | 1 |
Walsh, PN | 1 |
He, Y | 1 |
Zhou, H | 1 |
Tang, H | 2 |
Luo, Y | 1 |
Ragnarsson, L | 1 |
Yasuda, T | 1 |
Lewis, RJ | 1 |
Dodd, PR | 1 |
Adams, DJ | 1 |
Kaye, J | 1 |
Porsteinsson, A | 1 |
Tariot, P | 1 |
Zoulnouni, P | 1 |
Knopman, DS | 1 |
Satterwhite, J | 1 |
Gonzales, C | 1 |
Li, T | 1 |
Paudel, HK | 1 |
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Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
Effect of γ-Secretase Inhibition on the Progression of Alzheimer's Disease: LY450139 Versus Placebo[NCT00594568] | Phase 3 | 1,537 participants (Actual) | Interventional | 2008-03-31 | Completed | ||
Effect of LY450139 a y-Secretase Inhibitor, on the Progression of Alzheimer's Disease as Compared With Placebo[NCT00762411] | Phase 3 | 1,111 participants (Actual) | Interventional | 2008-09-30 | Completed | ||
Effect of LY2062430, an Anti-Amyloid Beta Monoclonal Antibody, on the Progression of Alzheimer's Disease as Compared With Placebo[NCT00905372] | Phase 3 | 1,000 participants (Anticipated) | Interventional | 2009-05-31 | Completed | ||
Effect of Passive Immunization on the Progression of Alzheimer's Disease: LY2062430 Versus Placebo[NCT00904683] | Phase 3 | 1,040 participants (Actual) | Interventional | 2009-05-31 | Completed | ||
LY450139: Tolerability and Biomarker Assessment in Subjects With Mild to Moderate Alzheimer's Disease[NCT00244322] | Phase 2 | 45 participants | Interventional | 2005-10-31 | Completed | ||
Levetiracetam for Alzheimer's Disease Neuropsychiatric Symptoms Related to Epilepsy Trial (LAPSE) - A Phase II Exploratory Study[NCT04004702] | Phase 2 | 65 participants (Anticipated) | Interventional | 2020-01-31 | Not yet recruiting | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 6.59 |
100 mg LY450139 | 7.57 |
140 mg LY450139 | 7.90 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 6.19 |
100 mg LY450139 | 7.29 |
140 mg LY450139 | 7.68 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 6.97 |
100 mg LY450139 | 8.27 |
140 mg LY450139 | 8.41 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 6.52 |
100 mg LY450139 | 7.98 |
140 mg LY450139 | 8.33 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 7.90 |
100 mg LY450139 | 9.30 |
140 mg LY450139 | 9.89 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 7.42 |
100 mg LY450139 | 8.97 |
140 mg LY450139 | 9.48 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | -9.26 |
100 mg LY450139 | -9.15 |
140 mg LY450139 | -11.73 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | -8.76 |
100 mg LY450139 | -10.13 |
140 mg LY450139 | -12.70 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
Placebo | -86.16 |
100 mg LY450139 | 23.27 |
140 mg LY450139 | -40.51 |
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
Intervention | ratio (Least Squares Mean) |
---|---|
Placebo | 0.08 |
100 mg LY450139 | 0.06 |
140 mg LY450139 | 0.09 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 2.31 |
100 mg LY450139 | 2.73 |
140 mg LY450139 | 3.04 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | -1.41 |
100 mg LY450139 | -7.49 |
140 mg LY450139 | -5.33 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | -2.95 |
100 mg LY450139 | -3.14 |
140 mg LY450139 | -3.71 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
Placebo | 1.92 |
100 mg LY450139 | 3.31 |
140 mg LY450139 | 4.15 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
Placebo | 9.75 |
100 mg LY450139 | -6.26 |
140 mg LY450139 | -5.13 |
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
Intervention | ratio (Least Squares Mean) |
---|---|
Placebo | -0.08 |
100 mg LY450139 | -0.12 |
140 mg LY450139 | -0.11 |
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
Intervention | hospitalizations/participant (Least Squares Mean) |
---|---|
Placebo | 0.55 |
100 mg LY450139 | 0.66 |
140 mg LY450139 | 0.83 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
Placebo | 75.11 |
100 mg LY450139 | 20.50 |
140 mg LY450139 | 61.00 |
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
Intervention | liter per hour (L/h) (Geometric Mean) |
---|---|
LY450139 | 18.8 |
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
Intervention | liter (L) (Geometric Mean) |
---|---|
LY450139 | 66.8 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
Placebo | 3.86 |
100 mg LY450139 | -5.97 |
140 mg LY450139 | -19.95 |
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
Intervention | cubic millimeter (mm^3) (Least Squares Mean) | |
---|---|---|
Left Hippocampal Volume | Right Hippocampal Volume | |
100 mg LY450139 | -75.34 | -93.89 |
140 mg LY450139 | -107.62 | -112.40 |
Placebo | -96.54 | -108.69 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 6.00 |
Placebo | 5.89 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 9.23 |
Placebo | 8.32 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 4.81 |
Placebo | 4.85 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 7.37 |
Placebo | 6.77 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 5.33 |
Placebo | 5.14 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 10.09 |
Placebo | 10.34 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | -8.88 |
Placebo | -7.68 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | -10.49 |
Placebo | -9.77 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
140 mg LY450139 | 19.20 |
Placebo | -21.39 |
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
Intervention | ratio (Least Squares Mean) |
---|---|
140 mg LY450139 | -0.36 |
Placebo | 0.16 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 3.05 |
Placebo | 4.00 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | -3.56 |
Placebo | -3.35 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | 2.94 |
Placebo | 3.84 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
140 mg LY450139 | 7.94 |
Placebo | 14.75 |
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
Intervention | ratio (Least Squares Mean) |
---|---|
140 mg LY450139 | -0.13 |
Placebo | -0.08 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | -1.83 |
Placebo | -1.05 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
140 mg LY450139 | -11.60 |
Placebo | 117.88 |
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
Intervention | units on a scale (Least Squares Mean) |
---|---|
140 mg LY450139 | -4.46 |
Placebo | -3.38 |
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
Intervention | number of hospitalizations (Least Squares Mean) |
---|---|
140 mg LY450139 | 0.72 |
Placebo | 0.82 |
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
Intervention | liters per hour (L/h) (Geometric Mean) |
---|---|
140 mg LY450139 | 18.9 |
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
Intervention | liters (L) (Geometric Mean) |
---|---|
140 mg LY450139 | 66.1 |
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
Intervention | picogram per milliliter (pg/mL) (Least Squares Mean) |
---|---|
140 mg LY450139 | -16.03 |
Placebo | 76.37 |
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
Intervention | cubic millimeter (mm^3) (Least Squares Mean) | |
---|---|---|
Right Hippocampal Volume | Left Hippocampal Volume | |
140 mg LY450139 | -158.50 | -84.41 |
Placebo | -73.60 | -111.27 |
19 reviews available for alanine and Acute Confusional Senile Dementia
Article | Year |
---|---|
Anti-Aβ agents for mild to moderate Alzheimer's disease: systematic review and meta-analysis.
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.
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.
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.
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.
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.
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.
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.
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.].
Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor | 2010 |
Reversible and irreversible protein glutathionylation: biological and clinical aspects.
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Amyloid Precursor | 2012 |
γ-Secretase modulator in Alzheimer's disease: shifting the end.
Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Amyloid Precursor Protein Secretases; Animals; Az | 2012 |
[Gamma-secretase inhibitors and modulators].
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.
Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Aminopeptidases; Amyloid Precursor Protein Secretas | 2004 |
[Carnosine--biological activity and perspectives in pharmacotherapy].
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.
Topics: Alanine; Alzheimer Disease; Amino Acid Sequence; Amyloid beta-Peptides; Amyloid beta-Protein Precurs | 1993 |
Cholinergic approaches to the treatment of Alzheimer's disease.
Topics: 4-Aminopyridine; Alanine; Alzheimer Disease; Aminopyridines; Arecoline; Clinical Trials as Topic; Hu | 1986 |
9 trials available for alanine and Acute Confusional Senile Dementia
Article | Year |
---|---|
A phase 3 trial of semagacestat for treatment of Alzheimer's disease.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Aspartic Acid Endopeptidases; Azep | 2006 |
Cholinergic approaches to the treatment of Alzheimer's disease.
Topics: 4-Aminopyridine; Alanine; Alzheimer Disease; Aminopyridines; Arecoline; Clinical Trials as Topic; Hu | 1986 |
100 other studies available for alanine and Acute Confusional Senile Dementia
Article | Year |
---|---|
Investigation of the role of prolines 232/233 in RTPPK motif in tau protein aggregation: An in vitro study.
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.
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.
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.
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Cell Line, Tumor; Cell Survival; Cyclooxygenase 2 | 2017 |
Semagacestat Is a Pseudo-Inhibitor of γ-Secretase.
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.
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.
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.
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.
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Amyloid beta-Peptides; Arginine; Humans; Models, Theoretical; Molecular | 2013 |
[Exacerbation of psoriasiform lesions by a gamma-secretase inhibitor].
Topics: Adrenal Cortex Hormones; Aged; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Aze | 2013 |
Semagacestat's fall: where next for AD therapies?
Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Humans | 2013 |
Semagacestat for treatment of Alzheimer's disease.
Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Female; Humans; Male | 2013 |
Semagacestat for treatment of Alzheimer's disease.
Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Azepines; Female; Humans; Male | 2013 |
Semagacestat for treatment of Alzheimer's disease.
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.
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?
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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.
Topics: ADAM Proteins; ADAM10 Protein; Age Factors; Alanine; Alzheimer Disease; Amyloid beta-Protein Precurs | 2009 |
Molecule of the month. Semagacestat.
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.
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.
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.
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.
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.
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.
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.
Topics: Aged; Aged, 80 and over; Alanine; Alzheimer Disease; Amyotrophic Lateral Sclerosis; Biomarkers; Case | 2010 |
Alzheimer's failure raises questions about disease-modifying strategies.
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.
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?
Topics: Alanine; Alzheimer Disease; Amyloid; Amyloid Precursor Protein Secretases; Azepines; Cognition Disor | 2010 |
Genetics. Gamma-secretase and human disease.
Topics: Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Animals; Azepines; Hidradenitis Su | 2010 |
Aβ40(L17A/F19A) mutant diminishes the aggregation and neurotoxicity of Aβ40.
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.
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.
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.
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.
Topics: Aged; Alanine; Alzheimer Disease; Amyloid Precursor Protein Secretases; Antibodies, Monoclonal; Anti | 2011 |
Drugs: a tangled web of targets.
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.
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Animals; Aspartic Acid; Biological Transport; Cells, Cultured; Chloroceb | 2012 |
Toxic role of K+ channel oxidation in mammalian brain.
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.
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.
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.
Topics: Age of Onset; Alanine; Alzheimer Disease; Cohort Studies; Databases, Factual; Female; Founder Effect | 2013 |
ACS chemical neuroscience molecule spotlight on semagacestat (LY450139).
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Amino Acids; Amyloid beta-Protein Precursor; Animals; Arginine; Culture | 2003 |
Methionine synthase polymorphism is a risk factor for Alzheimer disease.
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.
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.
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.
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Amyloid beta-Peptides; Catalysis; Copper; Elect | 2004 |
Genetic variation in apolipoprotein D and Alzheimer's disease.
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.
Topics: Aged; Aged, 80 and over; Alanine; Alleles; Alzheimer Disease; Apolipoprotein E4; Apolipoproteins E; | 2004 |
Familial Alzheimer disease associated with A713T mutation in APP.
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.
Topics: Alanine; Alzheimer Disease; Arginine; Binding Sites; Carrier Proteins; Catalytic Domain; Crystallogr | 2005 |
Deficiency of disulfide bonds facilitating fibrillogenesis of endostatin.
Topics: Alanine; Alzheimer Disease; Animals; Benzothiazoles; Cell Survival; Circular Dichroism; Disulfides; | 2006 |
NMDA receptor subunit-dependent modulation by conantokin-G and Ala7-conantokin-G.
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.
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.
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
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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.
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.
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.
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.
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.
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.
Topics: Alanine; Alzheimer Disease; Amino Acid Substitution; Aspartic Acid; Genetic Carrier Screening; Human | 2001 |
Split verdict on schizophrenia.
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.
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.
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.
Topics: Aged; Aging; Alanine; Alzheimer Disease; Amino Acids; Aspartic Acid; Brain; gamma-Aminobutyric Acid; | 1986 |