Alzheimer’s disease is by far the most common of the neurodegenerative dementias. Patients with AD initially show memory loss, and as the disease progresses they develop impaired executive function, confusion and personality changes. A corresponding progression of pathological involvement is evident, with tau-bearing lesions appearing initially in the entorhinal cortex and hippocampus, then progressing to neocortex of the frontal and temporal poles, and finally involving much of the temporal, frontal, and parietal cortices. Interestingly, primary sensory and motor cortex is spared, except in extremely advanced cases. Histopathologically, AD is characterized by amyloid plaques, comprised of the amyloid A-beta peptides, and by aggregates of tau appearing as neurofibrillary tangles, neuritic plaques, and neuronal threads. Although neuritic plaques surround amyloid cores, not all amyloid plaques are associated with neuritic plaques, and amyloid plaque distribution does not correspond to the functional progression of the disease noted above.

Reference: Braak & Braak, 1991