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Acta Neuropathol. 2008 Jun;115(6):599-609. doi: 10.1007/s00401-008-0366-2. Epub 2008 Mar 28.

Cerebral amyloid angiopathy and its relationship to Alzheimer's disease.

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Laboratory of Neuropathology, Institute of Pathology, University of Ulm, Albert-Einstein-Allee 7, 89081 Ulm, Germany.


Cerebral amyloid angiopathy (CAA) is characterized by the deposition of the amyloid beta-protein (A beta) 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 A beta within capillaries distinguishes two types of CAA. One with capillary A beta-deposition is characterized by a strong association with the apolipoprotein E (APOE) epsilon 4 allele and by its frequent occurrence in Alzheimer's disease cases whereas the other one lacking capillary A beta-deposits is not associated with APOE epsilon 4. Capillary CAA can be seen in every stage of CAA or AD-related A beta-deposition. AD cases with capillary CAA show more widespread capillary A beta-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 A beta adversely affects the brain in AD in addition to its direct neurotoxic effects.

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