Table 1.

Extracellular cerebral amyloid deposits commonly present in familial and sporadic Aβ-CAA and AD patients and transgenic mouse models.

CAA	Cerebral amyloid angiopathy; pathological changes occurring in cerebral blood vessels caused by deposition of amyloid protein of different origins, but here due to Aβ.
Dense-core plaques	Also referred to as “neuritic”, “senile”, “classic”, or “mature” plaques. The central compact dense-core is surrounded by a corona of diffuse plaque. The corona contains predominantly Aβ42 and is ThS-negative. The core is ThS-positive. Almost always associated with proximate phospho-tau pathology.
Dense plaques	ThS-positive compact amyloid without the corona of diffuse plaques. Major compact plaque type in transgenic mouse models. Biochemically resembles cores of the dense-core plaques. In this review, also sometimes used to include dense-core plaques.
Diffuse plaques	Loosely arranged fibrils that are usually ThS-negative. Best recognized with immunohistochemistry and are constituted predominantly of Aβ42. Are not commonly associated with proximate phospho-tau pathology.