Cerebral hypoperfusion induces cortical watershed microinfarcts which may further aggravate cognitive decline in Alzheimer's disease.

Increasing number of data, including the existence of common risk factors, indicate an association between cerebrovascular disease and Alzheimer's disease (AD). AD is known to be often associated with cerebral hypoperfusion. Recent histopathological evidence showed a significant association between watershed cortical microinfarcts and AD indicating that cerebral hypoperfusion induces not only white matter damage, known as leuko-araiosis, but cortical border zone infarcts as well, further aggravating the degenerative process and worsening dementia. In late stages of Alzheimer's disease--in cases with neuropathologically confirmed definite AD--the occurrence of watershed cortical microinfarcts was ten times higher than in aged matched control cases. Congophilic angiopathy and perturbed hemodynamic factors were found to be important factors in the genesis of watershed microinfarcts. To consider the vulnerability of the cerebral blood flow and the perturbed cortical vascular network in AD is important. Neuroleptic and sedative treatments frequently employed in AD may further accentuate cerebral hypoperfusion by decreasing blood pressure. Therefore, to treat and prevent arterial hypotension and maintain cerebral perfusion at an appropriate level in AD is essential.