Acta Neuropathologica

, Volume 115, Issue 6, pp 599-609

First online:

Cerebral amyloid angiopathy and its relationship to Alzheimer’s disease

  • Dietmar Rudolf ThalAffiliated withLaboratory of Neuropathology, Institute of Pathology, University of Ulm Email author 
  • , W. Sue T. GriffinAffiliated withDonald W. Reynolds Center on Aging, UAMS, Geriatric Research Education and Clinical Center, Veterans’ Affairs Medical Center
  • , Rob A. I. de VosAffiliated withLaboratorium Pathologie Oost Nederland
  • , Estifanos GhebremedhinAffiliated withInstitute for Clinical Neuroanatomy, J. W. Goethe University

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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.


Alzheimer’s disease Cerebral amyloid angiopathy Amyloid β-protein Cerebral blood flow Drainage