The concept of mild cognitive impairment (MCI) was first introduced for the purpose of
identifying individuals in an intermediate state between no cognitive impairment and Alzheimer’s disease
(AD). Recently, the heterogeneity of MCI has attracted attention as it has become clear that other
diseases, such as cerebrovascular disease and Parkinson disease can also cause mild cognitive deficits,
prompting a redefinition of MCI. Heterogeneity of MCI has been confirmed by neuropathological examinations.
Most MCI patients not only possess amyloid plaques and neurofibrillary tau tangles, but
also cerebral vascular pathology such as arteriosclerosis and cerebral amyloid angiopathy (CAA). CAA induces cerebral
infarcts or hemorrhage of varying size and type, attributing to further cognitive impairment. Sporadic AD and CAA has
been suggested to be the consequence of Aβ elimination failure, mainly caused by disturbance of the perivascular drainage
system. Since severe CAA is an independent risk factor for dementia, facilitation of Aβ clearance has been suggested
as a potential treatment of AD and MCI. Many epidemiological studies have shown that vascular risk factors increase incidence
of MCI and its progression to AD. Accordingly, control of such factors has been shown to reduce risk of conversion
to AD and ameliorate cognitive impairment in AD patients. Neurovascular approaches may therefore hold promise
for the treatment of dementia in an era of preventive neurology.
Keywords: Alzheimer’s disease, cerebral amyloid angiopathy, cerebrovascular disease, cilostazol, diagnosis, microinfarcts,
mild cognitive impairment, neurocognitive disorder.
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