Volume 903, Issue 1 p. 437-441

The Renin Angiotensin System and Alzheimer's Disease

PHILIPPE AMOUYEL

Corresponding Author

PHILIPPE AMOUYEL

INSERM U508, Institut Pasteur de Lille, Lille, France

Address for correspondence: Prof. Philippe Amouyel, INSERM U508, Institut Pasteur de Lille, 1 rue Calmette, F-59019 Lille, France. Tel.: +33 3 20 87 77 10; fax: +33 3 20 87 78 94. e-mail: [email protected]Search for more papers by this author
FLORENCE RICHARD

FLORENCE RICHARD

INSERM U508, Institut Pasteur de Lille, Lille, France

Search for more papers by this author
CLAUDINE BERR

CLAUDINE BERR

INSERM U360, Hôpital de la Salpétrière, Paris, France

Search for more papers by this author
ISABELLE DAVID-FROMENTIN

ISABELLE DAVID-FROMENTIN

Gérontologie Clinique, Centre Hospitalier Emile Roux, Limeil Brévannes, France

Search for more papers by this author
NICOLE HELBECQUE

NICOLE HELBECQUE

INSERM U508, Institut Pasteur de Lille, Lille, France

Search for more papers by this author
First published: 30 January 2006
Citations: 47

Abstract

Abstract: Recent reports sustain the hypothesis of tight links between vascular and neurodegenerative diseases: associations between atherosclerosis lesions and Alzheimer's disease (AD), increased risk of AD for hypertensive subjects, decreased risk of dementia for elderly treated with hypotensive drugs, and a major impact of apolipoprotein E polymorphism, a protein of the lipid metabolism, on the occurrence of AD. All these results suggest that vascular determinants, both environmental and genetic, may predispose to or speed up dementia. As a major player of vascular homeostasis, the renin angiotensin system (RAS) proteins constitute an interesting source of candidate genes. Among these, the angiotensin I-converting enzyme gene (ACE), a central enzyme of the RAS, presents in its sequence a deletion (D)/insertion (I) polymorphism associated with variations of plasma ACE levels and with the risk of myocardial infarction. We explored the impact of this genetic polymorphism on the risk of cognitive impairment and of dementia in several epidemiological studies. Physiopathological hypotheses suggest a possible involvement of the RAS proteins in the occurrence and evolution of AD. Moreover, although inconsistent, several results of case-control studies tend to suggest that the ACE I/D genetic polymorphism may constitute a genetic susceptibility factor for dementia, reinforcing the hypothesis of a major implication of vascular risk factors in the occurrence of dementia.