1. Lipid lowering agents are associated with a slower cognitive decline in Alzheimer's disease
- Author
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Régis Bordet, A Al Khedr, C. Libersa, Florence Richard, Dominique Deplanque, I. Masse, and Florence Pasquier
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Male ,Paper ,medicine.medical_specialty ,Placebo ,chemistry.chemical_compound ,Alzheimer Disease ,Internal medicine ,medicine ,Humans ,Dementia ,Senile plaques ,Cognitive decline ,Psychiatry ,Aged ,Hypolipidemic Agents ,Memory Disorders ,Cholesterol ,Cognitive disorder ,Odds ratio ,medicine.disease ,Editorial Commentary ,Psychiatry and Mental health ,Treatment Outcome ,chemistry ,Disease Progression ,Female ,lipids (amino acids, peptides, and proteins) ,Surgery ,Neurology (clinical) ,Alzheimer's disease ,Mental Status Schedule ,Cognition Disorders ,Psychology - Abstract
disease. Methods: An observational study in 342 Alzheimer patients followed in a memory clinic for 34.8 months (mean age 73.5 years, mini-mental state examination score (MMSE) 21.3 at entry); 129 were dyslipaemic treated with LLAs (47% with statins), 105 were untreated dyslipaemic, and 108 were normolipaemic. The rate of cognitive decline was calculated as the difference between the first and last MMSE score, divided by the time between the measurements, expressed by year. Patients were divided into slow and fast decliners according to their annual rate of decline (lower or higher than the median annual rate of decline in the total population). Results: Patients treated with LLAs had a slower decline on the MMSE (1.5 point/year, p = 0.0102) than patients with untreated dyslipaemia (2.4 points/year), or normolipaemic patients (2.6 points/year). Patients with a slower decline were more likely to be treated with LLAs. Logistic regression analysis, with low annual cognitive decline as the dependent variable, showed that the independent variable LLA (treated with or not) was positively associated with the probability of lower cognitive decline (odds ratio = 0.45, p = 0.002). Conclusions: LLAs may slow cognitive decline in Alzheimer's disease and have a neuroprotective effect. This should be confirmed by placebo controlled randomised trials in patients with Alzheimer's disease and no dyslipaemia. a hallmark of Alzheimer's disease. In transgenic animal models of Alzheimer's disease, hypercholesterolaemia accelerates the development of Alzheimer amyloid pathology. 91 0 Cholesterol- fed rabbits develop extracellular deposits of b-amyloid, and when they are placed subsequently on a control diet, a significant reduction in identifiable b-amyloid immunoreac- tivity is observed. 11 A strong association of late life high density lipoprotein (HDL) cholesterol levels with the number of neuritic plaques and neurofibrillary tangles in a population based necropsy series also support the view that cholesterol plays a role in the formation of Alzheimer's disease pathology.
- Published
- 2005
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