The incidence of
dementia is increasing at an alarming rate, and has become a major public health concern.
Alzheimer disease (AD) is the most common form of
dementia and is characterized by progressive
cognitive impairment. In addition to classical neuropathological features such as
amyloid plaques and neurofibrillary tangles (NFT), accumulation of activated immune cells has been documented in the AD brain, suggesting a contribution of
neuroinflammation in the pathogenesis of AD. Besides cognitive deterioration, non-
cognitive symptoms, such as agitation, aggression, depression and
psychosis, are often observed in demented patients, including those with AD, and these neuropsychological symptoms place a heavy burden on caregivers. These symptoms often exhibit sudden onset and tend to fluctuate over time, and in many cases, they are triggered by an
infection in peripheral organs, suggesting that
inflammation plays an important role in the pathogenesis of these non-
cognitive symptoms. However, there is no mechanistic explanation for the relationship between
inflammation and neuropsychiatric symptoms. Observations from experimental mouse models indicate that alteration of brain blood vessels, especially blood-brain barrier (BBB) dysfunction, may contribute to the relationship. The current review summarizes the results from recent studies on the relationship between
inflammation and AD, while focusing on cerebrovascular alterations, which might provide an insight into the pathogenesis of cognitive/non-
cognitive symptoms in AD patients and suggest a basis for the development of new therapeutic treatments for these conditions.