Cerebral amyloid angiopathy and its relationship to Alzheimer’s disease
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- Thal, D.R., Griffin, W.S.T., de Vos, R.A.I. et al. Acta Neuropathol (2008) 115: 599. doi:10.1007/s00401-008-0366-2
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Cerebral amyloid angiopathy (CAA) is characterized by the deposition of the amyloid β-protein (Aβ) within cerebral vessels. The involvement of different brain areas in CAA follows a hierarchical sequence similar to that of Alzheimer-related senile plaques. Alzheimer’s disease patients frequently exhibit CAA. The expansion of CAA in AD often shows the pattern of full-blown CAA. The deposition of Aβ within capillaries distinguishes two types of CAA. One with capillary Aβ-deposition is characterized by a strong association with the apolipoprotein E (APOE) ε4 allele and by its frequent occurrence in Alzheimer’s disease cases whereas the other one lacking capillary Aβ-deposits is not associated with APOE ε4. Capillary CAA can be seen in every stage of CAA or AD-related Aβ-deposition. AD cases with capillary CAA show more widespread capillary Aβ-deposition than non-demented cases as well as capillary occlusion. In a mouse model of CAA, capillary CAA was associated with capillary occlusion and cerebral blood flow disturbances. Thus, blood flow alterations with subsequent hypoperfusion induced by CAA-related capillary occlusion presumably point to a second mechanism in which Aβ adversely affects the brain in AD in addition to its direct neurotoxic effects.