Chronic Diseases

By Marvin Stein; Andrew Baum | Go to book overview

1 Neuropathology and Molecular Biology of Alzheimer's Disease

Miguel A. Pappolla University of Texas Medical School

Nikolaos K. Robakis Mount Sinai School of Medicine

Alzheimer's disease (AD) is the most frequent form of intellectual impairment in older people. Heightened awareness of the disorder and of its marked social and financial consequences have spurred unparalleled interest and a rapid accumulation of scientific literature on the pathology and molecular biology of AD. Yet, the cause of this disease remains elusive.

Senile dementia of Alzheimer's type includes presenile dementia that develops before age 65 and senile dementia of a later appearance. The neuropathological substratum is identical in both forms. Most cases are sporadic, although smaller subgroups are dominantly inherited. This latter AD form is known as familial AD (FAD).

Macroscopic Pathology . The cases of earlier onset show the most severe changes. These are characterized by symmetrical and diffuse atrophy of cerebral gyri. Less frequently, the atrophy can be relatively circumscribed, resembling Pick's disease and affect the temporal (most often), frontal, parietal, or occipital lobes. Sections through the cerebral hemispheres reveal thinning of the cortical ribbon and symmetrical enlargement of the ventricular system (hydrocephalus ex-vacuo). The basal ganglia, diencephalon, mesencephalon and brain stem show no gross abnormalities.

Microscopic Pathology . Senile plaques, neurofibrillary tangles, and vascular deposition of amyloid are among the most conspicuous abnormalities long ago recognized with conventional silver and amyloid stains. The hippocampal formation, subiculum, amygdala, and neocortical association areas bear the brunt of the pathology. The nucleus basalis of Meynert, a poorly defined area below the

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