Over the past century, enormous progress has been achieved regarding our
understanding of the dementias. Cognitive decline in the elderly can of
course result from many causes, but the contribution of vascular factors
is becoming more and more widely appreciated.
Vascular dementia is a vague term, encompassing
cognitive impairment resulting from vascular changes. As such, it has
multiple etiologies (frequently co-existing in a given patient), which
operate through different mechanisms. Risk factors for vascular dementia
have been detected and repeatedly confirmed. Very interestingly, many of
the risk factors which were identified for Alzheimer’s disease are also
involved in vascular dementia. These include hypertension, coronary artery
disease and smoking, and possibly also hyperlipidemia and
Other analogies between vascular dementia and
Alzheimer’s disease are depicted in Table 1.
|Risk factors Mechanisms
Primary prevention Secondary prevention
The fact that vascular dementia is a syndrome is
reflected by the multiplicity of causative processes, like hemorrhage or
vascular occlusions, and the site of the lesions, e.g. cortical vs
subcortical, as well as grey matter vs white matter disorders.
The identification of several genetic factors which can
contribute to vascular damage, as well as possible auto-immune damage to
vascular components (for example anticardiolipin antibodies), are
important. It is remarkable that amyloid precursor protein (APP) mutations
can cause the typical pathological changes of Alzheimer’s disease as well
as amyloid deposition around blood vessels. These may lead to deficient
blood perfusion to the brain, changes of the blood-brain barrier, as well
as cerebral hemorrhages.
An unfolding issue relates to the overlap between
Alzheimer’s disease and vascular dementia. The mechanisms underlying this
overlap are only partly understood (amyloid angiopathy, perivascular
amyloid deposits in Alzheimer’s disease), but are probably of even greater
importance as reflected by the Nun study, which demonstrated clearly that
Alzheimer changes alone may be insufficient to cause dementia, but the
addition of vascular brain lesions (usually small, subcortical, clinically
unrecognized) were required for the manifestation of dementia (which was
then diagnosed clinically as Alzheimer’s disease).
In primary prevention of diseases, it is required to
identify risk factors so as to direct attention to those people at higher
risk of developing dementia. Thus, it is not yet clear whether the "risk
factors" which have been identified in vascular dementia are causative or
contributing to the development of cognitive impairment, and which are
coexisting but not directly related (e.g. coronary artery disease). Also,
host factors such as age and education may have a role but this is yet
unproven. Other analogies between vascular dementia and Alzheimer’s
disease are depicted in Table 1.
For many years, treatment of vascular disease was
oriented towards prevention of heart and kidney failure. Later on, the
same classes of drugs were found to help in preventing strokes, and
recently their effect against vascular dementia is being described. It is
quite possible that their efficacy will extend even further. Epidemiologic
and pathological data show that Alzheimer’s disease is associated with
vascular risk factors, such as hypertension and coronary artery disease.
Thus, attention to these risk factors (as well as others such as
hyperlipidemia and smoking) could reduce or delay the incidence of several
types of dementia.
Amos D. Korczyn
The Sieratzki Chair in Neurology
Tel-Aviv University Medical School
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The Efficacy of Chinese Calligraphic Handwriting (CCH) on Stroke
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Feasibility of Vascular Dementia Treatment with Cholinesterase
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Should We Be Studying Cholinergic Drugs for the Treatment of Vascular
Dementia?H. Geerts and C. Grantham
Galantamine Provides Broad Therapeutic Benefits in Patients with
Probable Vascular Dementia or Alzheimer’s Disease with Cerebrovascular
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