All Relations between Alzheimer Disease and ache

Publication Sentence Publish Date Extraction Date Species
D Kaufe. Beyond the cholinergic hypothesis: the effect of metrifonate and other cholinesterase inhibitors on neuropsychiatric symptoms in Alzheimer's disease. Dementia and geriatric cognitive disorders. vol 9 Suppl 2. 1998-11-06. PMID:9718229. preliminary studies suggest that non-cognitive behavioural and personality alterations in alzheimer's disease may benefit from agents which inhibit central acetylcholinesterase (ache). 1998-11-06 2023-08-12 Not clear
D Kaufe. Beyond the cholinergic hypothesis: the effect of metrifonate and other cholinesterase inhibitors on neuropsychiatric symptoms in Alzheimer's disease. Dementia and geriatric cognitive disorders. vol 9 Suppl 2. 1998-11-06. PMID:9718229. these data are consistent with previous studies and are believed to represent the first large prospective, controlled study demonstrating a beneficial effect of ache inhibitor therapy on neuropsychiatric symptoms in alzheimer's disease. 1998-11-06 2023-08-12 Not clear
A Rampa, A Bisi, P Valenti, M Recanatini, A Cavalli, V Andrisano, V Cavrini, L Fin, A Buriani, P Giust. Acetylcholinesterase inhibitors: synthesis and structure-activity relationships of omega-[N-methyl-N-(3-alkylcarbamoyloxyphenyl)- methyl]aminoalkoxyheteroaryl derivatives. Journal of medicinal chemistry. vol 41. issue 21. 1998-11-03. PMID:9767635. acetylcholinesterase (ache) inhibitors are one of the most actively investigated classes of compounds in the search for an effective treatment of alzheimer's disease. 1998-11-03 2023-08-12 rat
L E Tune, T Sunderlan. New cholinergic therapies: treatment tools for the psychiatrist. The Journal of clinical psychiatry. vol 59 Suppl 13. 1998-10-20. PMID:9771828. the focus is on pivotal articles investigating the role of cholinergic augmentation strategies, including precursor loading and acetylcholinesterase (ache) inhibitors, in the management of cognitive and noncognitive symptoms of alzheimer's disease. 1998-10-20 2023-08-12 Not clear
L E Tune, T Sunderlan. New cholinergic therapies: treatment tools for the psychiatrist. The Journal of clinical psychiatry. vol 59 Suppl 13. 1998-10-20. PMID:9771828. therapy with ache inhibitors provides modest significant symptomatic improvement in patients with mild to moderate alzheimer's disease. 1998-10-20 2023-08-12 Not clear
F H Calderón, R von Bernhardi, G De Ferrari, S Luza, R Aldunate, N C Inestros. Toxic effects of acetylcholinesterase on neuronal and glial-like cells in vitro. Molecular psychiatry. vol 3. issue 3. 1998-10-08. PMID:9672900. acetylcholinesterase (ache), the enzyme involved in the hydrolysis of the neurotransmitter acetylcholine, has been implicated in non-cholinergic actions which may play a role in neurodegenerative diseases such as alzheimer's disease. 1998-10-08 2023-08-12 Not clear
F H Calderón, R von Bernhardi, G De Ferrari, S Luza, R Aldunate, N C Inestros. Toxic effects of acetylcholinesterase on neuronal and glial-like cells in vitro. Molecular psychiatry. vol 3. issue 3. 1998-10-08. PMID:9672900. considering that we have previously shown that ache promotes the assembly of beta-amyloid peptide into neurotoxic amyloid fibrils, it is conceivable that the neurotoxicity of ache shown here may play a role in the neuronal degeneration observed in alzheimer's disease. 1998-10-08 2023-08-12 Not clear
T Mant, W M Troetel, B P Imbimb. Maximum tolerated dose and pharmacodynamics of eptastigmine in elderly healthy volunteers. Journal of clinical pharmacology. vol 38. issue 7. 1998-10-05. PMID:9702845. eptastigmine is a new acetylcholinesterase (ache) inhibitor currently under development for the symptomatic treatment of alzheimer disease. 1998-10-05 2023-08-12 human
Z J Zhang, D A Lappi, C C Wrenn, T A Milner, R G Wile. Selective lesion of the cholinergic basal forebrain causes a loss of cortical neuropeptide Y and somatostatin neurons. Brain research. vol 800. issue 2. 1998-09-04. PMID:9685641. these findings indicate that: (1) cholinergic denervation of the nbm is associated with an irreversible loss of neocortical npy and ss immunoreactive neurons analogous to that observed in alzheimer's disease and aging; (2) the degree of the loss of cortical npy and ss immunoreactive neurons seems to be related to the extent of the reduction of cortical ache intensity in both toxin-injected and normal aged rats. 1998-09-04 2023-08-12 rat
P N Tario. Evaluating response to metrifonate. The Journal of clinical psychiatry. vol 59 Suppl 9. 1998-08-28. PMID:9720485. metrifonate, administered orally to patients with probable alzheimer's disease in a once-daily dose, readily enters the brain and inhibits brain acetylcholinesterase (ache) activity in a dose-dependent fashion. 1998-08-28 2023-08-12 Not clear
G Sberna, J Sáez-Valero, Q X Li, C Czech, K Beyreuther, C L Masters, C A McLean, D H Smal. Acetylcholinesterase is increased in the brains of transgenic mice expressing the C-terminal fragment (CT100) of the beta-amyloid protein precursor of Alzheimer's disease. Journal of neurochemistry. vol 71. issue 2. 1998-08-19. PMID:9681463. acetylcholinesterase (ache) expression is markedly affected in alzheimer's disease (ad). 1998-08-19 2023-08-12 mouse
Z Henderson, P S Harrison, E Jagger, J H Beeb. Density of choline acetyltransferase-immunoreactive terminals in the rat dentate gyrus after entorhinal cortex lesions: a quantitative light microscope study. Experimental neurology. vol 152. issue 1. 1998-08-17. PMID:9682012. lesion of the entorhinal cortex in the adult rat is a model for alzheimer's disease and produces a marked increase in acetylcholinesterase (ache) activity in the outer molecular layer (oml) of the dentate gyrus. 1998-08-17 2023-08-12 rat
S Darvesh, D L Grantham, D A Hopkin. Distribution of butyrylcholinesterase in the human amygdala and hippocampal formation. The Journal of comparative neurology. vol 393. issue 3. 1998-07-15. PMID:9548556. because of the importance of buche and ache in alzheimer's disease, we have studied the distribution of buche in the normal human amygdala and hippocampal formation and compared it with that of ache by using histochemical techniques. 1998-07-15 2023-08-12 human
N R Cutler, R J Polinsky, J J Sramek, A Enz, S S Jhee, L Mancione, J Hourani, P Zolnoun. Dose-dependent CSF acetylcholinesterase inhibition by SDZ ENA 713 in Alzheimer's disease. Acta neurologica Scandinavica. vol 97. issue 4. 1998-06-23. PMID:9576639. this study evaluates the activity of sdz ena 713, a centrally-selective acetylcholinesterase (ache) inhibitor, in the cerebral spinal fluid (csf) of patients with alzheimer's disease (ad), and its relationship to central and peripheral pharmacokinetic parameters. 1998-06-23 2023-08-12 Not clear
N R Cutler, S S Jhee, P Cyrus, F Bieber, P TanPiengco, J J Sramek, B Gulansk. Safety and tolerability of metrifonate in patients with Alzheimer's disease: results of a maximum tolerated dose study. Life sciences. vol 62. issue 16. 1998-05-26. PMID:9585171. a pilot study, and phase i and phase ii studies of metrifonate in alzheimer's disease (ad) patients conducted prior to the current study showed benign, dose-dependent adverse event profiles consisting primarily of gastrointestinal events, optimal daily dosing with a loading phase (in the absence of a loading dose phase, 6-8 weeks were required to attain steady-state ache inhibition levels), and an improvement in alzheimer's disease assessment scale (adas) scores. 1998-05-26 2023-08-12 Not clear
K Otoguro, F Kuno, S Omur. Arisugacins, selective acetylcholinesterase inhibitors of microbial origin. Pharmacology & therapeutics. vol 76. issue 1-3. 1998-05-21. PMID:9535168. synthetic inhibitors of acetylcholinesterase (ache) recently have attracted particular attention for treatment of alzheimer's disease. 1998-05-21 2023-08-12 Not clear
A Alvarez, R Alarcón, C Opazo, E O Campos, F J Muñoz, F H Calderón, F Dajas, M K Gentry, B P Doctor, F G De Mello, N C Inestros. Stable complexes involving acetylcholinesterase and amyloid-beta peptide change the biochemical properties of the enzyme and increase the neurotoxicity of Alzheimer's fibrils. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 18. issue 9. 1998-05-05. PMID:9547230. brain acetylcholinesterase (ache) forms stable complexes with amyloid-beta peptide (abeta) during its assembly into filaments, in agreement with its colocalization with the abeta deposits of alzheimer's brain. 1998-05-05 2023-08-12 Not clear
A Alvarez, R Alarcón, C Opazo, E O Campos, F J Muñoz, F H Calderón, F Dajas, M K Gentry, B P Doctor, F G De Mello, N C Inestros. Stable complexes involving acetylcholinesterase and amyloid-beta peptide change the biochemical properties of the enzyme and increase the neurotoxicity of Alzheimer's fibrils. The Journal of neuroscience : the official journal of the Society for Neuroscience. vol 18. issue 9. 1998-05-05. PMID:9547230. thus, in addition to its possible role as a heterogeneous nucleator during amyloid formation, ache, by forming such stable complexes, may increase the neurotoxicity of abeta fibrils and thus may determine the selective neuronal loss observed in alzheimer's brain. 1998-05-05 2023-08-12 Not clear
C Opazo, N C Inestros. Crosslinking of amyloid-beta peptide to brain acetylcholinesterase. Molecular and chemical neuropathology. vol 33. issue 1. 1998-04-21. PMID:9493175. recently, we have found that ache promotes the assembly of amyloid-beta peptides (a beta) into alzheimer fibrils. 1998-04-21 2023-08-12 Not clear
C Opazo, N C Inestros. Crosslinking of amyloid-beta peptide to brain acetylcholinesterase. Molecular and chemical neuropathology. vol 33. issue 1. 1998-04-21. PMID:9493175. our results suggest that ache and the a beta peptide may be involved in physiologically relevant interactions, related to the pathogenesis of alzheimer disease (ad). 1998-04-21 2023-08-12 Not clear