
DOI . ORG {
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Title[redir]:
Statin therapy for Alzheimer’s disease | Journal of Molecular Neuroscience
Description:
Disease-modifying therapies are being developed for Alzheimer’s disease (AD). These are expected to slow the clinical progression of the disease or delay its onset. Cerebral accumulation of amyloid β (Aβ) peptides is an early and perhaps necessary event for establishing AD pathology. Consequently therapies aimed at attenuating brain amyloidosis are expected to be disease modifying. Based on the epidemiological evidence pointing to a link between cholesterol metabolism and AD and the numerous laboratory studies implicating cholesterol in the process of Aβ production and accumulation, it is now believed that cholesterol-lowering therapies will be of value as disease modifying agents. Several epidemiological studies revealed that statin use for the treatment of coronary arterial disease is associated with a decreased prevalence or a decreased risk of developing AD. These observations require both preclinical and clinical validation. The former involves testing statins in one or more animal models of AD in order to establish which disease features are affected by statin treatment, the relative efficacy with which different statins modify these features and the mechanism(s) by which statins affect AD phenotypes. The latter requires prospective, randomized, placebo controlled trials to evaluate the effect of statin treatment on cognitive and AD biomarker outcomes. We have initiated a study aimed at determining the effects of atorvastatin (LipitorR), a statin with the largest US market share, on brain Aβ deposition in the PSAPP transgenic mouse model of Alzheimer’s amyloidosis. Our results indicate that Lipitor treatment markedly attenuates Aβ deposition in this animal model.
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Keywords {🔍}
article, google, scholar, cas, pubmed, disease, alzheimers, cholesterol, amyloid, statins, statin, sci, therapy, betaamyloid, privacy, cookies, content, journal, research, pathology, treatment, risk, study, model, access, neurol, publish, search, petanceska, pappolla, refolo, clinical, effects, transgenic, dementia, precursor, protein, acad, usa, data, information, log, august, suzana, derosa, olm, therapies, brain, link, decreased,
Topics {✒️}
month download article/chapter putative disease-modifying therapy unique amyloid beta-protein beta-amyloid immunore-activity low-density lipoprotein-cholesterol tara thomas-bryant hmg-coa reductase inhibitors accelerated alzheimer-type phenotype amyloid precursor protein effective antiatherosclerotic therapy full article pdf cholesterol-lowering therapies privacy choices/manage cookies molecular neuroscience aims transgenic mouse model placebo controlled trials human beta-amyloid amyloid beta proteins cholesterol acyltransferase modulates epidemiological studies revealed epidemiological evidence pointing amyloid beta-peptide serum total cholesterol august 2002 volume 19 transgenic mice carrying disease modifying agents statin therapy animal model cholesterol depletion inhibits european economic area brain aβ deposition 3-hydroxy-3-methylglutaryl coenzyme 3-hydroxy3-methylglutaryl coenzyme total cholesterol level conditions privacy policy coronary arterial disease coronary artery disease dietary fat intake subjects taking statins case-control study ad biomarker outcomes accepting optional cookies preclinical development published related subjects age-related change article journal establishing ad pathology involves testing statins journal finder publish cholesterol-dependent generation
Questions {❓}
- (1997) Coronary artery disease, hypertension, ApoE, and cholesterol: a link to Alzheimer’s disease?
- Will it work?
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headline:Statin therapy for Alzheimer’s disease
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description:Disease-modifying therapies are being developed for Alzheimer’s disease (AD). These are expected to slow the clinical progression of the disease or delay its onset. Cerebral accumulation of amyloid β (Aβ) peptides is an early and perhaps necessary event for establishing AD pathology. Consequently therapies aimed at attenuating brain amyloidosis are expected to be disease modifying. Based on the epidemiological evidence pointing to a link between cholesterol metabolism and AD and the numerous laboratory studies implicating cholesterol in the process of Aβ production and accumulation, it is now believed that cholesterol-lowering therapies will be of value as disease modifying agents. Several epidemiological studies revealed that statin use for the treatment of coronary arterial disease is associated with a decreased prevalence or a decreased risk of developing AD. These observations require both preclinical and clinical validation. The former involves testing statins in one or more animal models of AD in order to establish which disease features are affected by statin treatment, the relative efficacy with which different statins modify these features and the mechanism(s) by which statins affect AD phenotypes. The latter requires prospective, randomized, placebo controlled trials to evaluate the effect of statin treatment on cognitive and AD biomarker outcomes. We have initiated a study aimed at determining the effects of atorvastatin (LipitorR), a statin with the largest US market share, on brain Aβ deposition in the PSAPP transgenic mouse model of Alzheimer’s amyloidosis. Our results indicate that Lipitor treatment markedly attenuates Aβ deposition in this animal model.
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