TABLE 1.
Feature | Cerebrovascular Amyloid Deposition | Senile Plaque Amyloid Deposition |
---|---|---|
Predominant Aβ type | Aβ40 | Aβ42 (particularly in diffuse plaques) |
Location of Aβ deposition | Relative occipital lobe predominance | Frontal, parietal, temporal lobes |
APOE allele risk factors | APOE ε4 (for amyloid deposition) and APOE ε2 (for vessel breakdown) | APOE ε4 |
Inflammatory subtype with reversible white matter hyperintensities | Occurs spontaneously as CAA-related inflammation | May occur iatrogenically as a result of amyloid immunotherapy or other candidate treatments targeting amyloid |
Cerebral microbleeds | Lobar predominant, particularly occipital | Not associated with senile plaques |
Location of white matter disease | Equal distribution between anterior and posterior subcortical regions (subgroup may have posterior-dominant white matter disease) | Equal distribution between anterior and posterior subcortical regions, but less extensive than advanced CAA |
See text for more details discussion and details.
APOE = apolipoprotein E; CAA = cerebral amyloid angiopathy.