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FIGURE 4–2. Normal brain: lateral view (left). Alzheimer's disease brain: lateral view (right).In the Alzheimer's brain, moderate diffuse cortical atrophy is apparent. The gyri are narrowed, and the sulci are widened.

FIGURE 4–3. Normal brain: coronal section through the basal ganglia (left). Alzheimer's disease brain: coronal section through the basal ganglia (right).In the normal brain, the lateral ventricles are small and there is no atrophy. In the Alzheimer's brain, the lateral ventricles are enlarged and dilated from neuronal loss and atrophy of the cortex.

FIGURE 4–4. Alzheimer's disease brain.The neocortex is filled with senile neuritic plaques and neurofibrillary tangles. (King's silver impregnation stain; original magnification x400.)

FIGURE 4–5. Alzheimer's disease brain: hippocampus, neurofibrillary tangle.Note the fibrillary nature of this intraneuronal inclusion. The tangle is shaped like the neuron and fills the cell body. Tangle formation is due to abnormal assembly of phosphorylated microtubule-associated protein into paired helical filaments. (King's silver impregnation stain; original magnification x1,000.)

FIGURE 4–6. Alzheimer's disease brain: hippocampus.This neuron has undergone granulovacuolar degeneration (small arrows). Granulovacuolar degenerations are seen almost exclusively in the hippocampal formation. The frequency of granulovacuolar degeneration increases as neurofibrillary change increases elsewhere in the neocortex. Also seen here is a Hirano body (large arrow). Hirano bodies are eosinophilic aggregates of actin protein. Hirano bodies are usually closely associated with granulovacuolar degeneration. (Hematoxylin-eosin stain; original magnification x1,000.)

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