Sustained inflammation in AD brains, originally thought to be reactive to the neuronal loss associated with the disorder, facilitates and exacerbates both Aβ and tau pathologies and may even provide a link between the initial Aβ pathology and the later development of tangles, and as such, has been suggested as a mechanism potentially central to the accumulation and progression of AD neuropathology.52 This evidence concerns the gene MAPT and Alzheimer disease.