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

• Published in: Journal of Alzheimer's disease Vol. 35; no. 4; p. 859
• Main Authors: Burgmans, Saartje, van de Haar, Harm J, Verhey, Frans R J, Backes, Walter H
• Format: Journal Article
• Language: English
• Published: Netherlands 01-01-2013
• Subjects: Amyloid beta-Peptides - physiology; Amyloid beta-Protein Precursor - metabolism; Animals; Blood-Brain Barrier - pathology; Brain - pathology; Cell Adhesion - physiology; Data Interpretation, Statistical; Dementia - pathology; Endothelium - pathology; Humans; Monocytes - pathology
• ISSN: 1875-8908
• DOI: 10.3233/JAD-122155

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.