Despite the fact that DS patients have early the Alzheimer
type lesions in their brains, these patients do not systematically develop
an Alzheimer-type dementia.
The genetic heterogenity of these patients should push researchers to use
this pathology with care, because of possible pittfalls in their interpretation.
APP on chromosome 21 is likely to explain the amyloid plaques, since this protein is overexpressed in DS.
Tau pathology is similar to the Alzheimer one, with a characteristic triplet of pathological tau proteins.