Affiliations: [a] Department of Psychiatry and Neuropsychology/Alzheimer Center Limburg, Maastricht University Medical Center, Maastricht, The Netherlands | [b] Department of Radiology, Maastricht University Medical Center, Maastricht, The Netherlands
Correspondence:
[*]
Correspondence to: Saartje Burgmans, Department of Psychiatry and Neuropsychology/Alzheimer Center Limburg, Maastricht University Medical Center, PO Box 616, 6200 MD Maastricht, The Netherlands. Tel.: +31 43 3881942; Fax: +31 43 3884092; E-mail: s.burgmans@maastrichtuniversity.nl.
Abstract: To 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.
