Treatment of vascular risk factors is associated with slower decline in Alzheimer disease.
BACKGROUND
There is growing evidence that vascular risk factors (VRF) contribute to cognitive decline. Whether their treatment can slow down the progression of Alzheimer disease (AD) remains unsettled. The aim of this observational study was to evaluate whether the treatment of VRF is associated with a slower cognitive decline in patients who have AD without cerebrovascular disease (CVD).


METHODS
We recruited 301 consecutive patients who had AD without CVD (mean age 71.7 years; 69.4% women; first Mini-Mental State Examination [MMSE] mean score 21.6; mean follow-up 2.3 years), who had attended a memory clinic between 1997 and 2003. VRF sought were high blood pressure, dyslipidemia, diabetes mellitus, tobacco smoking, and atherosclerotic disease. Only 21 patients (7.0%) had no VRF. Others were classified as having no VRF treated (n = 72; 25.7%), some VRF treated (n = 119; 42.5%), or all VRF treated (n = 89; 31.8%). We compared MMSE progression over time among these 3 groups using a mixed random effects regression model.


RESULTS
Baseline MMSE scores were similar in the 3 groups. With adjustment for confounding factors, MMSE progression over time differed significantly between groups (p = 0.002). Patients with all their VRF treated declined less than those with none of their VRF treated. Those with some VRF treated tended to have an intermediate decline.


CONCLUSIONS
In patients who have Alzheimer disease without CVD, treatment of vascular risk factors (VRF) is associated with a slower decline in Mini-Mental State Examination score. Randomized controlled trials are needed to confirm this association, but our data suggest that dementia should not prevent treatment of VRF.
Deschaintre
Yan
Y
Université Lille Nord de France, INSERM UMR 744, Institut Pasteur de Lille, 1 rue Calmette, 59019 Lille Cedex, France.
Richard
Florence
F
Leys
Didier
D
Pasquier
Florence
F
D000368:Aged; D000544:Alzheimer Disease / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control*; D002536:Cerebral Arteries / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000150:complications / Q000503:physiopathology* / Q000628:therapy*; D018450:Disease Progression; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D002537:Intracranial Arteriosclerosis / Q000150:complications / Q000503:physiopathology / Q000628:therapy; D008137:Longitudinal Studies; D008297:Male; D009483:Neuropsychological Tests; D012307:Risk Factors; D012308:Risk Management / Q000379:methods; D040242:Risk Reduction Behavior; D013995:Time; D013997:Time Factors
D000960:Hypolipidemic Agents