There is overwhelming evidence to suggest that the neuropathology of Alzhei
mer disease (AD) extends beyond amyloid plaques and neurofibrillary tangles
. Review of various consortium data shows that more than 30% of AD cases ex
hibit cerebrovascular pathology. However, certain vascular lesions such as
cerebral amyloid angiopathy, microvascular degeneration, and periventricula
r white matter lesions are evident in almost all cases of AD. Whether these
vascular lesions are coincidental or causal in the pathogenetic processes
of AD remains to be defined. Although systemic vascular influences such as
hypertension, coronary artery disease, and other cardiovascular disturbance
s may be responsible for such pathology in AD, it is equally intriguing tha
t about one third of patients diagnosed with vascular dementia (VaD) will h
ave AD-type pathology at autopsy. Moreover, previous studies have revealed
that deficits in cholinergic indices related to the basal forebrain neurone
s are apparent in multi-infarct dementia. In this short review we evaluate
cerebrovascular pathology of AD in light of peripheral vascular pathophysio
logy implicated in the etiopathogenesis of the dementia. We also consider p
athological findings in relation to genetic influences such as apolipoprote
in E that may shed light on the link between AD and VaD. In view of these c
ommonalties, it is reasonable to consider the same treatment strategies for
both AD and VaD.