alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid has been researched along with Nerve Degeneration in 77 studies
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid: An IBOTENIC ACID homolog and glutamate agonist. The compound is the defining agonist for the AMPA subtype of glutamate receptors (RECEPTORS, AMPA). It has been used as a radionuclide imaging agent but is more commonly used as an experimental tool in cell biological studies.
Nerve Degeneration: Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
| Excerpt | Relevance | Reference |
|---|---|---|
| " Previously, we showed that α-tocopherol (α-T) reduces hippocampal neuroglial activation and neurodegeneration in the rat model of kainic acid (KA)-induced status epilepticus (SE)." | 3.88 | Neurobiological Correlates of Alpha-Tocopherol Antiepileptogenic Effects and MicroRNA Expression Modulation in a Rat Model of Kainate-Induced Seizures. ( Albertini, MC; Ambrogini, P; Bartolini, D; Betti, M; Cuppini, R; Di Palma, M; Galati, C; Galli, F; Lattanzi, D; Minelli, A; Olivieri, F; Palma, E; Ruffolo, G; Saccomanno, S; Savelli, D; Torquato, P, 2018) |
| " Whereas MTA reduced the neuronal cell death in pilocarpine-induced status epilepticus and the size of the lesion in global but not focal ischemic brain damage, it was ineffective in preserving dopaminergic neurons of the substantia nigra in the 1-methyl-4-phenyl-1,2,3,6-tetrahydro-pyridine (MPTP)-mice model." | 3.80 | Differential neuroprotective effects of 5'-deoxy-5'-methylthioadenosine. ( Alberch, J; Ceña, V; Collon, KW; Domercq, M; Fernández-Díez, B; Franco, R; Giralt, A; Giralt, E; Gottlieb, M; Lopez, I; Martínez-Pinilla, E; Matute, C; Moreno, B; Parent, JM; Posadas, I; Sánchez-Gómez, MV; Teixido, M; Villoslada, P; Zhang, H, 2014) |
| "Because motoneuron degeneration is the main pathological hallmark in motoneuron diseases, and excitotoxicity is an important mechanism of neuronal death in this type of disorders, in this work we tested whether the tetanus toxin C-fragment is able to protect MN in the spinal cord in vivo." | 1.48 | Tetanus toxin C-fragment protects against excitotoxic spinal motoneuron degeneration in vivo. ( Netzahualcoyotzi, C; Tapia, R, 2018) |
| " For this purpose we conducted a dose-response study at concentrations of AMPA between 0." | 1.35 | Pattern of injury with a graded excitotoxic insult and ensuing chronic medial septal damage in the rat brain. ( Andrés, N; Batlle, M; Mahy, N; Malpesa, Y; Prats, A; Pugliese, M; Rodríguez, MJ, 2009) |
| " We investigated the effects of these cytokines on neuronal death caused by exposure of mouse organotypic hippocampal slice cultures to toxic concentrations of AMPA." | 1.33 | Modulator effects of interleukin-1beta and tumor necrosis factor-alpha on AMPA-induced excitotoxicity in mouse organotypic hippocampal slice cultures. ( Bernardino, L; Jakobsen, B; Malva, JO; Oliveira, CR; Poulsen, FR; Silva, AP; Vezzani, A; Xapelli, S; Zimmer, J, 2005) |
| "Increased seizure duration [3,522 +/- 660 sec (SEM) vs." | 1.33 | Neurodegenerative actions of interleukin-1 in the rat brain are mediated through increases in seizure activity. ( Allan, SM; Davies, RE; Heenan, LE; Patel, HC; Ross, FM; Rothwell, NJ, 2006) |
| "There was a commensurate reduction in seizure-related neuronal loss in the limbic regions of the brain." | 1.31 | In vivo, the direct and seizure-induced neuronal cytotoxicity of kainate and AMPA is modified by the non-competitive antagonist, GYKI 52466. ( Lees, GJ; Leong, W, 2001) |
| " In contrast, neither QA up to 5 mM nor trans-ACPD had a significant toxic effect in either KCl group." | 1.30 | NMDA and non-NMDA receptor-mediated excitotoxicity are potentiated in cultured striatal neurons by prior chronic depolarization. ( Chen, Q; Reiner, A; Surmeier, DJ, 1999) |
| "CGP 37849 was a weaker neuroprotectant than MK-801 (ED50 0." | 1.29 | A comparative analysis of the neuroprotective properties of competitive and uncompetitive N-methyl-D-aspartate receptor antagonists in vivo: implications for the process of excitotoxic degeneration and its therapy. ( Fagg, GE; Massieu, L; McVey, M; Thedinga, KH, 1993) |
| "The nifedipine response was reproduced by isradipine and by verapamil with IC50 values of 9 and 100 nM, respectively." | 1.28 | Various Ca2+ entry blockers prevent glutamate-induced neurotoxicity. ( Memo, M; Pizzi, M; Ribola, M; Spano, P; Valerio, A, 1991) |
| "Kainic acid treatment did not alter resting mean arterial pressure or heart rate." | 1.28 | Excitotoxin-induced degeneration of rat vagal afferent neurons. ( Beart, PM; Jarrott, B; Lewis, SJ; Louis, CJ; Louis, WJ; Verberne, AJ, 1990) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 3 (3.90) | 18.7374 |
| 1990's | 34 (44.16) | 18.2507 |
| 2000's | 26 (33.77) | 29.6817 |
| 2010's | 14 (18.18) | 24.3611 |
| 2020's | 0 (0.00) | 2.80 |
| Authors | Studies |
|---|---|
| Ambrogini, P | 1 |
| Albertini, MC | 1 |
| Betti, M | 1 |
| Galati, C | 1 |
| Lattanzi, D | 1 |
| Savelli, D | 1 |
| Di Palma, M | 1 |
| Saccomanno, S | 1 |
| Bartolini, D | 1 |
| Torquato, P | 1 |
| Ruffolo, G | 1 |
| Olivieri, F | 1 |
| Galli, F | 1 |
| Palma, E | 1 |
| Minelli, A | 1 |
| Cuppini, R | 1 |
| Netzahualcoyotzi, C | 2 |
| Tapia, R | 10 |
| Beppu, K | 1 |
| Kosai, Y | 1 |
| Kido, MA | 1 |
| Akimoto, N | 1 |
| Mori, Y | 1 |
| Kojima, Y | 1 |
| Fujita, K | 1 |
| Okuno, Y | 1 |
| Yamakawa, Y | 1 |
| Ifuku, M | 1 |
| Shinagawa, R | 1 |
| Nabekura, J | 1 |
| Sprengel, R | 1 |
| Noda, M | 1 |
| Santa-Cruz, LD | 2 |
| Moreno, B | 1 |
| Lopez, I | 1 |
| Fernández-Díez, B | 1 |
| Gottlieb, M | 1 |
| Matute, C | 1 |
| Sánchez-Gómez, MV | 1 |
| Domercq, M | 1 |
| Giralt, A | 1 |
| Alberch, J | 1 |
| Collon, KW | 1 |
| Zhang, H | 1 |
| Parent, JM | 1 |
| Teixido, M | 1 |
| Giralt, E | 1 |
| Ceña, V | 1 |
| Posadas, I | 1 |
| Martínez-Pinilla, E | 1 |
| Villoslada, P | 1 |
| Franco, R | 1 |
| Guerrero-Castillo, S | 1 |
| Uribe-Carvajal, S | 1 |
| Ramírez-Jarquín, UN | 2 |
| Yan, B | 1 |
| Li, L | 1 |
| Harden, SW | 1 |
| Gozal, D | 1 |
| Lin, Y | 1 |
| Wead, WB | 1 |
| Wurster, RD | 1 |
| Cheng, ZJ | 1 |
| Rodríguez, MJ | 1 |
| Prats, A | 1 |
| Malpesa, Y | 1 |
| Andrés, N | 1 |
| Pugliese, M | 1 |
| Batlle, M | 1 |
| Mahy, N | 2 |
| Pitt, D | 1 |
| Gonzales, E | 1 |
| Cross, AH | 1 |
| Goldberg, MP | 1 |
| Tovar-Y-Romo, LB | 2 |
| Finn, R | 1 |
| Kovács, AD | 1 |
| Pearce, DA | 1 |
| Bliss, RM | 2 |
| Finckbone, VL | 1 |
| Trice, J | 1 |
| Strahlendorf, H | 4 |
| Strahlendorf, J | 4 |
| Lisý, V | 1 |
| Stastný, F | 1 |
| Li, J | 1 |
| Zheng, S | 1 |
| Zuo, Z | 1 |
| Silva, AP | 2 |
| Pinheiro, PS | 1 |
| Carvalho, AP | 1 |
| Carvalho, CM | 1 |
| Jakobsen, B | 2 |
| Zimmer, J | 2 |
| Malva, JO | 2 |
| Frandsen, A | 1 |
| Schousboe, A | 1 |
| Box, C | 1 |
| Attridge, J | 1 |
| Diertien, J | 1 |
| Finckbone, V | 2 |
| Henne, WM | 2 |
| Medina, MS | 1 |
| Miles, R | 3 |
| Oomman, S | 1 |
| Schneider, M | 1 |
| Singh, H | 1 |
| Veliyaparambil, M | 1 |
| Kieran, D | 1 |
| Greensmith, L | 1 |
| Kim, SJ | 1 |
| Han, Y | 1 |
| Platania, P | 1 |
| Seminara, G | 1 |
| Aronica, E | 1 |
| Troost, D | 1 |
| Vincenza Catania, M | 1 |
| Angela Sortino, M | 1 |
| Bernardino, L | 1 |
| Xapelli, S | 1 |
| Poulsen, FR | 1 |
| Oliveira, CR | 1 |
| Vezzani, A | 2 |
| Patel, HC | 1 |
| Ross, FM | 1 |
| Heenan, LE | 1 |
| Davies, RE | 1 |
| Rothwell, NJ | 6 |
| Allan, SM | 5 |
| Lai, C | 1 |
| Xie, C | 1 |
| McCormack, SG | 1 |
| Chiang, HC | 1 |
| Michalak, MK | 1 |
| Lin, X | 1 |
| Chandran, J | 1 |
| Shim, H | 1 |
| Shimoji, M | 1 |
| Cookson, MR | 1 |
| Huganir, RL | 1 |
| Rothstein, JD | 1 |
| Price, DL | 1 |
| Wong, PC | 1 |
| Martin, LJ | 1 |
| Zhu, JJ | 1 |
| Cai, H | 1 |
| Corona, JC | 1 |
| Slemmer, JE | 1 |
| Haasdijk, ED | 1 |
| Engel, DC | 1 |
| Plesnila, N | 1 |
| Weber, JT | 1 |
| Lecrux, C | 1 |
| Nicole, O | 1 |
| Chazalviel, L | 1 |
| Catone, C | 1 |
| Chuquet, J | 1 |
| MacKenzie, ET | 1 |
| Touzani, O | 1 |
| Sato, Y | 1 |
| Nakanishi, K | 1 |
| Tokita, Y | 1 |
| Kakizawa, H | 1 |
| Ida, M | 1 |
| Maeda, H | 1 |
| Matsui, F | 1 |
| Aono, S | 1 |
| Saito, A | 1 |
| Kuroda, Y | 1 |
| Hayakawa, M | 1 |
| Kojima, S | 1 |
| Oohira, A | 1 |
| Nishimoto, T | 1 |
| Kihara, T | 1 |
| Akaike, A | 2 |
| Niidome, T | 1 |
| Sugimoto, H | 1 |
| Coles, J | 1 |
| Oomman, SK | 1 |
| Hoffman, TC | 1 |
| Tsuji, K | 1 |
| Nakamura, Y | 1 |
| Ogata, T | 1 |
| Mitani, A | 1 |
| Kataoka, K | 1 |
| Shibata, T | 1 |
| Ishida, M | 1 |
| Shinozaki, H | 2 |
| Chen, Q | 2 |
| Harris, C | 1 |
| Brown, CS | 1 |
| Howe, A | 1 |
| Surmeier, DJ | 2 |
| Reiner, A | 2 |
| Willis, CL | 1 |
| Meldrum, BS | 2 |
| Nunn, PB | 1 |
| Anderton, BH | 1 |
| Leigh, PN | 1 |
| Weiss, JH | 6 |
| Turetsky, D | 1 |
| Wilke, G | 1 |
| Choi, DW | 3 |
| Tamura, Y | 1 |
| Yokota, T | 1 |
| Shimohama, S | 1 |
| Kimura, J | 1 |
| Massieu, L | 2 |
| Hans, P | 1 |
| Bonhomme, V | 1 |
| Collette, J | 1 |
| Albert, A | 1 |
| Moonen, G | 1 |
| Duvoisin, RM | 1 |
| Zhang, C | 1 |
| Hamassaki-Britto, DE | 1 |
| Britto, LR | 1 |
| Strijbos, PJ | 1 |
| Bendahan, G | 1 |
| Boatell, ML | 1 |
| Bjelke, B | 1 |
| Tinner, B | 1 |
| Olson, L | 1 |
| Fuxe, K | 1 |
| McAlonan, GM | 1 |
| Dawson, GR | 1 |
| Wilkinson, LO | 1 |
| Robbins, TW | 1 |
| Everitt, BJ | 1 |
| Lu, YM | 2 |
| Yin, HZ | 3 |
| Hartley, DM | 1 |
| Kurth, MC | 1 |
| Bjerkness, L | 1 |
| Thedinga, KH | 1 |
| McVey, M | 1 |
| Fagg, GE | 1 |
| Bruno, V | 1 |
| Battaglia, G | 1 |
| Copani, A | 1 |
| Giffard, RG | 1 |
| Raciti, G | 1 |
| Raffaele, R | 1 |
| Nicoletti, F | 1 |
| Chiang, J | 1 |
| Kwak, S | 1 |
| Nakamura, R | 1 |
| Strahlendorf, JC | 3 |
| Acosta, S | 2 |
| Strahlendorf, HK | 3 |
| Ikonomidou, C | 1 |
| Turski, L | 1 |
| Pasinetti, GM | 1 |
| Tocco, G | 1 |
| Sakhi, S | 1 |
| Musleh, WD | 1 |
| DeSimoni, MG | 1 |
| Mascarucci, P | 1 |
| Schreiber, S | 1 |
| Baudry, M | 1 |
| Finch, CE | 1 |
| Ha, DH | 1 |
| Carriedo, SG | 1 |
| Lawrence, CB | 1 |
| Brandon, T | 1 |
| Kim, EY | 1 |
| Koh, JY | 2 |
| Kim, YH | 1 |
| Sohn, S | 1 |
| Joe, E | 1 |
| Gwag, BJ | 1 |
| Mennini, T | 1 |
| Cagnotto, A | 1 |
| Carvelli, L | 1 |
| Comoletti, D | 1 |
| Manzoni, C | 1 |
| Muzio, V | 1 |
| Rizzi, M | 1 |
| Loddick, SA | 1 |
| Vandenberghe, W | 1 |
| Robberecht, W | 1 |
| Brorson, JR | 1 |
| Lees, GJ | 1 |
| Leong, W | 1 |
| Barenberg, P | 1 |
| Harrison, DC | 1 |
| Read, S | 1 |
| Collins, B | 1 |
| Parsons, AA | 1 |
| Philpott, K | 1 |
| Grundy, RI | 1 |
| Palmer, E | 1 |
| Lin, A | 1 |
| Cotman, CW | 1 |
| Stewart, GR | 1 |
| Olney, JW | 1 |
| Pathikonda, M | 1 |
| Snider, WD | 1 |
| Pizzi, M | 1 |
| Ribola, M | 1 |
| Valerio, A | 1 |
| Memo, M | 1 |
| Spano, P | 1 |
| Moncada, C | 1 |
| Arvin, B | 1 |
| Le Peillet, E | 1 |
| Schoepp, DD | 1 |
| Ornstein, PL | 1 |
| Salhoff, CR | 1 |
| Leander, JD | 1 |
| Koh, J | 1 |
| Baimbridge, KG | 1 |
| Lewis, SJ | 1 |
| Verberne, AJ | 1 |
| Louis, CJ | 1 |
| Jarrott, B | 1 |
| Beart, PM | 1 |
| Louis, WJ | 1 |
| Morgan, IG | 1 |
| Benavides, J | 1 |
| Fage, D | 1 |
| Carter, C | 1 |
| Scatton, B | 1 |
| Foster, AC | 1 |
| Gill, R | 1 |
| Woodruff, GN | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| The Relationship Between Neuropsychological Testing and MRI, PET and Blood Biomarkers in Neurodegenerative Disease (COBRE - Project 1): AIM 2[NCT03702816] | Phase 2 | 24 participants (Actual) | Interventional | 2018-12-13 | Terminated (stopped due to GE180 has limited Blood - brain barrier permeation, reducing its utility in neuroinflammation. COVID19 created supply chain issues, impacting enrollment.) | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Cingulate SUVR- GE180 binding potential in the cingulate ROI, as a marker of cingulate neuroinflammation. Cingulate neuroinflammation would be expected to relate to cingulate AD pathology, and given known cingulate lobe role in executive system function, is hypothesized to relate to measures of executive function in particular, with greater cingulate GE180 relating to poorer cognitive function. (NCT03702816)
Timeframe: Baseline (Single scan)
| Intervention | SUVR (Mean) |
|---|---|
| Control | 0.9994 |
| Mild Cognitive Impairment | 1.0387 |
| Alzheimer's Disease | 1.0554 |
| Parkinson's Disease | 0.9893 |
DRS- The Dementia Rating Scale is a comprehensive, but relatively brief assessment of overall cognitive functioning. The measure consists of items testing memory, attention, executive skills, and visuospatial skill, for a total of 144 points. A score of less than 124 is indicative of dementia level cognitive functioning. A higher score indicates a better outcome. (NCT03702816)
Timeframe: Baseline (Pre-scan)
| Intervention | score on a scale (Mean) |
|---|---|
| Control | 139.2 |
| Mild Cognitive Impairment | 130.4 |
| Alzheimer's Disease | 120.3 |
| Parkinson's Disease | 139.3 |
The executive function composite score is comprised from data from two gold-standard clinical measures of set-shifting and inhibition (Trail Making Test, part B; Delis Kaplan Executive Functioning Scale Color Word Inhibition, inhibition score). The raw score for each individual assessment is corrected for age based on published normative data for each test. These adjusted scores (T scores and/or scaled scores) are converted to z-scores, then the two z-scores are averaged together to create the composite score. A higher value is indicative of better executive function, a lower value is indicative of worse executive function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
| Intervention | z score (Mean) |
|---|---|
| Control | 0.572 |
| Mild Cognitive Impairment | -0.011 |
| Alzheimer's Disease | -1.361 |
| Parkinson's Disease | 0.029 |
Frontal SUVR- GE180 binding potential in the frontal cortical ROI, as a marker of frontal neuroinflammation. Frontal neuroinflammation would be expected to relate to frontal lobe AD pathology, and given known frontal lobe role in executive system function, is hypothesized to relate to measures of executive function in particular, and also to memory and language dysfunction, as these have executive components. Greater frontal lobe GE180 is expected to relate to poorer cognitive function. (NCT03702816)
Timeframe: Baseline (Single scan)
| Intervention | SUVR (Mean) |
|---|---|
| Control | 0.8893 |
| Mild Cognitive Impairment | 0.9436 |
| Alzheimer's Disease | 0.8855 |
| Parkinson's Disease | 0.8850 |
The language composite score is comprised from data from two gold-standard clinical measures of confrontation naming and semantic fluency (Boston Naming Test; Animal Naming Test). The raw score for the Animal Naming Test is converted directly to a z-score based on published normative data. The Boston Naming Test is corrected for age based on published normative data, resulting in a scaled score, which is then converted to a z-score. Then the two z-scores are averaged together to create the composite score. A higher value is indicative of better language function, a lower value is indicative of worse language function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
| Intervention | z score (Mean) |
|---|---|
| Control | 0.584 |
| Mild Cognitive Impairment | -0.234 |
| Alzheimer's Disease | -0.7272 |
| Parkinson's Disease | 0.541 |
The memory composite score is comprised from data from two gold-standard clinical measures of verbal and nonverbal memory (Rey Auditory Verbal Learning Test, delayed recall score; Brief Visuospatial Memory Test, Revised, delayed recall score). The raw score for each individual assessment is corrected for age based on published normative data for each test. These adjusted scores (T scores and/or scaled scores) are converted to z-scores, then the two z-scores are averaged together to create the composite score. A higher value is indicative of better memory function, a lower value is indicative of worse memory function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
| Intervention | z score (Mean) |
|---|---|
| Control | 0.367 |
| Mild Cognitive Impairment | -0.675 |
| Alzheimer's Disease | -2.483 |
| Parkinson's Disease | -0.404 |
MoCA -The Montreal Cognitive Assessment is a brief screening tool, originally designed to detect patients with MCI in a memory disorders clinic [10]. Standard administration consists of 12 individual tasks grouped into seven cognitive domains (visuospatial/executive, naming; attention, language, abstraction, memory, and orientation). Task performance is summed generating both domain and a total score. An education correction of one point is added to the total score for individuals with 12 years of education or less. Scores range from 0-30, with a score of 26 or less indicating cognitive impairment. (NCT03702816)
Timeframe: Baseline (Pre-scan)
| Intervention | score on a scale (Mean) |
|---|---|
| Control | 26.0 |
| Mild Cognitive Impairment | 23.4 |
| Alzheimer's Disease | 18.3 |
| Parkinson's Disease | 27.5 |
Parietal SUVR - GE180 binding potential in the parietal cortical ROI, as a marker of parietal neuroinflammation. Parietal neuroinflammation would be expected to relate to parietal lobe AD pathology, and given known parietal lobe role in visual and executive system function, is hypothesized to relate to measures of visuospatial and executive skills in particular, with greater parietal lobe GE180 relating to poorer cognitive function. (NCT03702816)
Timeframe: Baseline (Single scan)
| Intervention | SUVR (Mean) |
|---|---|
| Control | 0.8701 |
| Mild Cognitive Impairment | 0.9241 |
| Alzheimer's Disease | 0.8847 |
| Parkinson's Disease | 0.8562 |
The speed composite score is comprised from data from two gold-standard clinical measures of speeded attention and psychomotor speed (Trail Making Test, part A; Symbol Digit Modalities Test, oral version). The raw score for the Symbol Digit Modalities Test, oral version is converted directly to a z-score based on published normative data. The Trail making Test, part A is corrected for age based on published normative data, resulting in a T-score, which is then converted to a z-score. Then the two z-scores are averaged together to create the composite score. A higher value is indicative of better speed function, a lower value is indicative of worse speed function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
| Intervention | z score (Mean) |
|---|---|
| Control | 0.285 |
| Mild Cognitive Impairment | -0.013 |
| Alzheimer's Disease | -1.585 |
| Parkinson's Disease | -0.731 |
Temporal SUVR-- GE180 binding potential in the temporal cortical ROI, as a marker of temporal neuroinflammation. Temporal neuroinflammation would be expected to relate to temporal lobe AD pathology, and given known temporal lobe role in memory and language system function, is hypothesized to relate to measures of memory in particular, with greater temporal lobe GE180 relating to poorer memory and language function. (NCT03702816)
Timeframe: Baseline (Single scan)
| Intervention | SUVR (Mean) |
|---|---|
| Control | 0.9127 |
| Mild Cognitive Impairment | 0.9779 |
| Alzheimer's Disease | 0.9146 |
| Parkinson's Disease | 0.8899 |
Whole Brain GE180- GE180 binding potential in the whole brain, as a marker of global neuroinflammation. Global neuroinflammation would be expected to relate to more widespread pathology on average, and is hypothesized to relate to global measures of cognition, including the MoCA and DRS, with greater whole brain GE180 relating to poorer cognitive function overall. (NCT03702816)
Timeframe: Baseline (Single scan)
| Intervention | SUVR (Mean) |
|---|---|
| Control | 0.9179 |
| Mild Cognitive Impairment | 0.9711 |
| Alzheimer's Disease | 0.9351 |
| Parkinson's Disease | 0.9051 |
3 reviews available for alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and Nerve Degeneration
| Article | Year |
|---|---|
AMPA receptor-mediated neurotoxicity: role of Ca2+ and desensitization.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Nerve Degeneration; Perm | 2003 |
Neurodegenerative disorders: clues from glutamate and energy metabolism.
Topics: Aging; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Brain Damage, Chronic; Bra | 1996 |
Mechanisms of tumor necrosis factor alpha action on neurodegeneration: interaction with insulin-like growth factor-1.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Brain; Excitatory Amino Acid Agon | 1999 |
74 other studies available for alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and Nerve Degeneration
| Article | Year |
|---|---|
Neurobiological Correlates of Alpha-Tocopherol Antiepileptogenic Effects and MicroRNA Expression Modulation in a Rat Model of Kainate-Induced Seizures.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; alpha-Tocopherol; Animals; Blood-Brain Bar | 2018 |
Tetanus toxin C-fragment protects against excitotoxic spinal motoneuron degeneration in vivo.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Disease Models, Animal; Injection | 2018 |
Expression, subunit composition, and function of AMPA-type glutamate receptors are changed in activated microglia; possible contribution of GluA2 (GluR-B)-deficiency under pathological conditions.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Genotype; Glutamic Acid; | 2013 |
Role of energy metabolic deficits and oxidative stress in excitotoxic spinal motor neuron degeneration in vivo.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Antioxidants; Cell Death; Disease | 2014 |
Differential neuroprotective effects of 5'-deoxy-5'-methylthioadenosine.
Topics: Acute Disease; Adrenergic Antagonists; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Ani | 2014 |
Degeneration of spinal motor neurons by chronic AMPA-induced excitotoxicity in vivo and protection by energy substrates.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Antioxidants; Ascorbic Acid; Cell | 2015 |
Mitochondrial Dysfunction during the Early Stages of Excitotoxic Spinal Motor Neuron Degeneration in Vivo.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Disease Models, Animal; Excitator | 2016 |
Neuropathological characterization of spinal motor neuron degeneration processes induced by acute and chronic excitotoxic stimulus in vivo.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Apoptosis; Astrocytes; Caspase 3; | 2016 |
Chronic GABAergic blockade in the spinal cord in vivo induces motor alterations and neurodegeneration.
Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Anim | 2017 |
Chronic intermittent hypoxia impairs heart rate responses to AMPA and NMDA and induces loss of glutamate receptor neurons in nucleus ambiguous of F344 rats.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Baroreflex; Blood Pressure; Brain | 2009 |
Pattern of injury with a graded excitotoxic insult and ensuing chronic medial septal damage in the rat brain.
Topics: Acetylcholine; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Astrocytes; Atroph | 2009 |
Dysmyelinated axons in shiverer mice are highly vulnerable to alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor-mediated toxicity.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Biomarkers; Brain; Disease Models | 2010 |
VEGF protects spinal motor neurons against chronic excitotoxic degeneration in vivo by activation of PI3-K pathway and inhibition of p38MAPK.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Analysis of Variance; Animals; Choline O-A | 2010 |
Altered sensitivity to excitotoxic cell death and glutamate receptor expression between two commonly studied mouse strains.
Topics: Alanine; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Animals, Newborn; Cell D | 2010 |
Tumor necrosis factor-α (TNF-α) augments AMPA-induced Purkinje neuron toxicity.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Animals, Newborn; Calcium; Calciu | 2011 |
Delayed administration of VEGF rescues spinal motor neurons from death with a short effective time frame in excitotoxic experimental models in vivo.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Analysis of Variance; Animals; Brain-Deriv | 2012 |
Nitric oxide synthase inhibition and glutamate binding in quinolinate-lesioned rat hippocampus.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Binding, Competitive; Cell Membra | 2002 |
Isoflurane decreases AMPA-induced dark cell degeneration and edematous damage of Purkinje neurons in the rat cerebellar slices.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cell Size; Cerebellum; Female; Is | 2002 |
Activation of neuropeptide Y receptors is neuroprotective against excitotoxicity in organotypic hippocampal slice cultures.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Dentate Gyrus; Hippocampus; Kaini | 2003 |
AMPA-induced dark cell degeneration of cerebellar Purkinje neurons involves activation of caspases and apparent mitochondrial dysfunction.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Animals, Newborn; bcl-2-Associate | 2003 |
Inhibition of calpains, by treatment with leupeptin, improves motoneuron survival and muscle function in models of motoneuron degeneration.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Animals, Newborn; Calpain; Cell C | 2004 |
Insulin inhibits AMPA-induced neuronal damage via stimulation of protein kinase B (Akt).
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cell Line; Dose-Response Relation | 2005 |
17beta-estradiol rescues spinal motoneurons from AMPA-induced toxicity: a role for glial cells.
Topics: Adult; Aged; Aged, 80 and over; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amyotrophi | 2005 |
Modulator effects of interleukin-1beta and tumor necrosis factor-alpha on AMPA-induced excitotoxicity in mouse organotypic hippocampal slice cultures.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cell Death; Cell Survival; Dose-R | 2005 |
Neurodegenerative actions of interleukin-1 in the rat brain are mediated through increases in seizure activity.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Analysis of Variance; Animals; Anticonvuls | 2006 |
Amyotrophic lateral sclerosis 2-deficiency leads to neuronal degeneration in amyotrophic lateral sclerosis through altered AMPA receptor trafficking.
Topics: Adaptor Proteins, Signal Transducing; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amyo | 2006 |
Ca2+-permeable AMPA receptors and intracellular Ca2+ determine motoneuron vulnerability in rat spinal cord in vivo.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amino Acids; Animals; Calcium; Calcium Sig | 2007 |
Aldolase C-positive cerebellar Purkinje cells are resistant to delayed death after cerebral trauma and AMPA-mediated excitotoxicity.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Biomarkers; Brain Injuries; Calbi | 2007 |
Spontaneously hypertensive rats are highly vulnerable to AMPA-induced brain lesions.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Blood Pressure; Brain Damage, Chr | 2007 |
A highly sulfated chondroitin sulfate preparation, CS-E, prevents excitatory amino acid-induced neuronal cell death.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Caspase 3; Cell Death; Cell Survi | 2008 |
alpha-Amino-3-hydroxy-5-methyl-4-isoxazole propionate attenuates glutamate-induced caspase-3 cleavage via regulation of glycogen synthase kinase 3beta.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Binding Sites; Brain Ischemia; Ca | 2008 |
AMPA-induced dark cell degeneration is associated with activation of caspases in pyramidal neurons of the rat hippocampus.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Animals, Newborn; Aspartic Acid; | 2008 |
Neurotoxicity of acromelic acid in cultured neurons from rat spinal cord.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amino Acids; Animals; Cells, Cultured; Kai | 1995 |
Glutamate-mediated excitotoxic death of cultured striatal neurons is mediated by non-NMDA receptors.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Basal Ganglia; Cell Death; Cells, | 1995 |
Neuronal damage induced by beta-N-oxalylamino-L-alanine, in the rat hippocampus, can be prevented by a non-NMDA antagonist, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amino Acids, Diamino; Animals; beta-Alanin | 1993 |
AMPA/kainate receptor-mediated damage to NADPH-diaphorase-containing neurons is Ca2+ dependent.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Cells, Cultured; Cerebra | 1994 |
Nicotine-induced protection of cultured cortical neurons against N-methyl-D-aspartate receptor-mediated glutamate cytotoxicity.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cells, Cultured; Cerebral Cortex; | 1994 |
2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline protects against both AMPA and kainate-induced lesions in rat striatum in vivo.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Biomarkers; Choline O-Acetyltrans | 1994 |
Propofol protects cultured rat hippocampal neurons against N-methyl-D-aspartate receptor-mediated glutamate toxicity.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Brain Ischemia; Cells, Cultured; | 1994 |
Changes in expression of glutamate receptor subunits following photoreceptor degeneration in the rd mouse retina.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Gene Expression; In Situ Hybridiz | 1995 |
Interleukin-1 beta attenuates excitatory amino acid-induced neurodegeneration in vitro: involvement of nerve growth factor.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Analysis of Variance; Animals; Antibodies, | 1995 |
Differential brain area vulnerability to long-term subcortical excitotoxic lesions.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Brain Damage, Chronic; Calcium; I | 1995 |
The effects of AMPA-induced lesions of the medial septum and vertical limb nucleus of the diagonal band of Broca on spatial delayed non-matching to sample and spatial learning in the water maze.
Topics: Acetylcholine; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Choline O-Acetyltr | 1995 |
Ca2+ permeable AMPA/kainate channels permit rapid injurious Ca2+ entry.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Calcium Channels; Cell C | 1995 |
Glutamate receptor-induced 45Ca2+ accumulation in cortical cell culture correlates with subsequent neuronal degeneration.
Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Anim | 1993 |
A comparative analysis of the neuroprotective properties of competitive and uncompetitive N-methyl-D-aspartate receptor antagonists in vivo: implications for the process of excitotoxic degeneration and its therapy.
Topics: 2-Amino-5-phosphonovalerate; Acetylcholine; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid | 1993 |
Activation of class II or III metabotropic glutamate receptors protects cultured cortical neurons against excitotoxic degeneration.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Astrocytes; Biotransformation; Ce | 1995 |
Ca(2+)-permeable AMPA/kainate and NMDA channels: high rate of Ca2+ influx underlies potent induction of injury.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Calcium Channels; Intrac | 1996 |
Selective degeneration of inhibitory interneurons in the rat spinal cord induced by intrathecal infusion of acromelic acid.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Dose-Response Relationship, Drug; | 1995 |
Diazoxide and cyclothiazide convert AMPA-induced dark cell degeneration of Purkinje cells to edematous damage in the cerebellar slice.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Benzothiadiazines; Cerebellum; Di | 1996 |
Hereditary deficiencies in complement C5 are associated with intensified neurodegenerative responses that implicate new roles for the C-system in neuronal and astrocytic functions.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Astrocytes; Cell Death; Cells, Cu | 1996 |
Kainate-stimulated Zn2+ uptake labels cortical neurons with Ca2+-permeable AMPA/kainate channels.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Cells, Cultured; Cerebra | 1998 |
Interleukin-1 beta and interleukin-1 receptor antagonist do not affect glutamate release or calcium entry in rat striatal synaptosomes.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Calcium; Cerebral Cortex; Chelati | 1998 |
AMPA receptor-mediated alterations of intracellular calcium homeostasis in rat cerebellar Purkinje cells in vitro: correlates to dark cell degeneration.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Aniline Compounds; Animals; Anti-Anxiety A | 1998 |
Zn2+ entry produces oxidative neuronal necrosis in cortical cell cultures.
Topics: 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; 6-Cyano-7-nitroquinoxaline-2,3-dione; al | 1999 |
Biochemical and pharmacological evidence of a functional role of AMPA receptors in motor neuron dysfunction in mnd mice.
Topics: 2-Amino-5-phosphonovalerate; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amyotrophic L | 1999 |
NMDA and non-NMDA receptor-mediated excitotoxicity are potentiated in cultured striatal neurons by prior chronic depolarization.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Anti-Anxiety Agents; Benzodiazepi | 1999 |
AMPA receptor calcium permeability, GluR2 expression, and selective motoneuron vulnerability.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amyotrophic Lateral Sclerosis; Animals; Ca | 2000 |
In vivo, the direct and seizure-induced neuronal cytotoxicity of kainate and AMPA is modified by the non-competitive antagonist, GYKI 52466.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Anti-Anxiety Agents; Benzodiazepi | 2001 |
Choline blocks AMPA-induced dark cell degeneration of Purkinje neurons: potential role of the alpha7 nicotinic receptor.
Topics: Aconitine; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; alpha7 Nicotinic Acetylcholine | 2001 |
Hypoxia induces an excitotoxic-type of dark cell degeneration in cerebellar Purkinje neurons.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cell Death; Chromatin; DNA Fragme | 2001 |
Selective increases in cytokine expression in the rat brain in response to striatal injection of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate and interleukin-1.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Apoptosis; Cerebral Cortex; Corpu | 2001 |
Site-specific actions of interleukin-1 on excitotoxic cell death in the rat striatum.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cell Death; Cerebral Cortex; Drug | 2002 |
Varied actions of proinflammatory cytokines on excitotoxic cell death in the rat central nervous system.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cell Death; Central Nervous Syste | 2002 |
A metabotropic glutamate receptor agonist does not mediate neuronal degeneration in cortical culture.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Cells, Cultured; Cerebral Cortex; | 1991 |
Excitotoxicity in the embryonic chick spinal cord.
Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amin | 1991 |
Various Ca2+ entry blockers prevent glutamate-induced neurotoxicity.
Topics: 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl e | 1991 |
Non-NMDA antagonists protect against kainate more than AMPA toxicity in the rat hippocampus.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Anti-Anxiety Agents; Benzodiazepi | 1991 |
Neuroprotectant effects of LY274614, a structurally novel systemically active competitive NMDA receptor antagonist.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Anticonvulsants; Binding, Competi | 1991 |
Cortical neurons containing somatostatin- or parvalbumin-like immunoreactivity are atypically vulnerable to excitotoxic injury in vitro.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Aspartic Acid; Cell Survival; Cel | 1990 |
Excitotoxin-induced degeneration of rat vagal afferent neurons.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Blood Pressure; Dose-Response Rel | 1990 |
AMPA is a powerful neurotoxin in the chicken retina.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Aspartic Acid; Chickens; Choline | 1987 |
Peripheral type benzodiazepine binding sites are a sensitive indirect index of neuronal damage.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Animals; Aspartic Acid; Binding Sites; Cho | 1987 |
Neuroprotective effects of MK-801 in vivo: selectivity and evidence for delayed degeneration mediated by NMDA receptor activation.
Topics: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Anesthesia; Animals; Aspartic Acid; Brain; | 1988 |