| Popis: |
Like senile plaques, cerebral amyloid angiopathy (CAA) does not result from accumulation of the amyloid β(Aβ) protein alone, but also contains a number of other components, referred to as amyloid β-associated proteins. In this review we will discuss which proteins can be found in the cerebral vessel walls that are affected by CAA, what the possible source of these proteins is, and to what extent they might contribute to the pathogenesis of CAA. The data generated in our laboratory are in agreement with a pathogenesis of CAA that is different from that of the amyloidosis in senile plaques, although part of the amyloid-associated proteins in both these lesions may have the same parenchymal source. Since vascular malfunction is an independent risk factor for developing Alzheimer’s disease (AD), and CAA formation may depend on the interactions of Aβ with Aβ-associated proteins, pharmacological interference with these interactions may provide a new approach for treatment of AD and related cerebral vasculopathies. |
