rain atherosclerosis was the term historicallyused in an attempt to provide a rational explanation
forthe progressive cognitive decline observed in manybutnot allelderly people. The term was derived
from theobservation that the vasculature of the brain was dis-rupted in the elderly, like that of the rest of
the organs,and that manybut not alldemented individualsshowed brain infarcts at postmortem examination.Despite the fact that Alois Alzheimer published hisdescription of a demented individual with no significantunderlying vascular pathology 100 years ago, the
effortsto distinguish between vascular and nonvascular demen-tia were mostly undertaken in the 1970s.1-3 The
impetusto distinguish between the two types of dementia,Alzheimers disease (AD) and the entity initially
termedmulti-infarct dementia (MID) and later on vasculardementia (VD), had both scientific and pragmaticunderpinning (the change from MID to VD was neces-sary, since the term MID did not cover the full
range ofcerebrovascular pathology).Reasoning for differentiation between AD and VDThe scientific reasoning for the distinction between
ADand VD was based on evidence collected during the1970s and 1980s, leading investigators to conclude
that avascular pathology was not the main underlying pathol-ogy for most demented individuals. First, manydemented individuals had diffuse amyloid deposits orplaques and neurofibrillary tangles as the predominantpostmortem pathology, with no or minimal vascularpathology or infarcts.1 Second, in some of thesedemented individuals with predominantly plaques andtangles, the counts of the cholinergic cells in
the nucleusbasalis of Meynert were diminished, as was the
activityof the neurotransmitter acetylcholine in the cortex.4-8S t a t e o f t h e a r t7Is the distinction between Alzheimers
diseaseand vascular dementia possible and
relevant?Ramit Ravona-Springer, MD; Michael
Davidson, MD;Shlomo Noy, MD, PhDKeywords: Alzheimers disease; vascular dementia; cardiovascular risk factor; cholesterol;
apolipoprotein E; diabetes;
hyperhomocysteinemiaAuthor affiliations: Sackler
School of Medicine, Tel Aviv University, Tel Aviv, Israel
(Shlomo Noy, Michael Davidson,
Ramit Ravona-Springer)Address for correspondence: Michael
Davidson, MD, Chaim Sheba Medical Center, Beitan 39A,
Tel-Hashomer 52621, Israel
(e-mail: davidso@netvision.net.il)BAdvances in epidemiological, clinical,
imaging, and neuro-pathological studies have undermined
the clear distinc-tion between vascular and Alzheimer-type
dementia,which has characterized the last
two decades of researchin dementia. A significant degree
of overlap between thetwo entities was demonstrated in
terms of clinical expres-sion, risk factors, and postmortem
brain autopsy. In thisarticle, we propose mechanisms by
which cardiovascularrisk factors might affect the manifestation
of Alzheimersdisease, suggest possible explanations
for the overlap withvascular dementia, and discuss the
implications this mighthave on future differential diagnosis and treatmentstrategies.Dialogues Clin Neurosci.
2003;5:7-15.