• J. Alzheimers Dis. · Jan 2013

    Review

    Amyloid-β interacts with blood-brain barrier function in dementia: a systematic review.

    • Saartje Burgmans, Harm J van de Haar, Frans R J Verhey, and Walter H Backes.
    • Department of Psychiatry and Neuropsychology/Alzheimer Center Limburg, Maastricht University Medical Center, Maastricht, The Netherlands. s.burgmans@maastrichtuniversity.nl
    • J. Alzheimers Dis. 2013 Jan 1; 35 (4): 859-73.

    AbstractTo date, the exact pathogenesis of dementia is still unknown. The most frequently hypothesized initiating factor is an accumulation of the protein amyloid-β in the brain, which has been associated with dementia of the Alzheimer type. Another potentially important initiating factor is a disrupted blood-brain barrier. This can initiate cerebral microangiopathy, which has frequently been associated with vascular dementia. Although amyloid-β and blood-brain barrier dysfunction have both been associated with one particular type of dementia (Alzheimer's disease and vascular dementia, respectively), they co-exist in most demented patients. In fact, increasing evidence indicates that amyloid-β and blood-brain barrier disruption may interact and facilitate each other in their effect on neurodegeneration. The present systematic analysis describes the available evidence for a significant interplay between amyloid-β and blood-brain barrier function in dementia.

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