Death of the Neurons

Neurons die in one of two ways: through apoptosis or necrosis. Apoptosis, or programmed cell death, is genetically regulated and commonly occurs in degenerative diseases. During brain development, the apoptosis of excess neurons is physiologic. In apoptotic cell death, the nuclear chromatin condenses into masses of various sizes and shapes, the nuclear membrane buds and fragments. These nuclear buds, along with cytoplasmic buds, form the apoptotic bodies, which then are phago-cytosed by macrophages or neighboring cells. An apop-totic cell in HE-stained section appears as a round, dense, strongly eosinophilic mass. Apoptosis occurs rapidly, usually affects individual neurons, and elicits no inflammatory response.

Necrosis is initiated by a variety of exogenous factors: toxins, infectious pathogens, metabolic disorders and, chiefly, by hypoxia and ischemia. The nucleus undergoes pyknosis, fragmentation, and lysis. The cytoplasm loses its organelles, becomes strongly eosinophilic and, ultimately, by enzymatic digestion, dissolves.

Torpedo Purkinje Cell

FIGURE 2.4

Axonal degeneration. (A) Fusiform swelling and (B) disintegration of axon into small argyrophilic fragments (Holmes stain). C. Beta-amyloid precursor protein (P-APP) immunoreaction of injured axons (immunostain). D. Axonal spheroids in traumatic injury (Holmes stain) E. Fusiform enlargement of the axon (torpedo) of a degenerated Purkinje cell (Bodian stain).

FIGURE 2.4

Axonal degeneration. (A) Fusiform swelling and (B) disintegration of axon into small argyrophilic fragments (Holmes stain). C. Beta-amyloid precursor protein (P-APP) immunoreaction of injured axons (immunostain). D. Axonal spheroids in traumatic injury (Holmes stain) E. Fusiform enlargement of the axon (torpedo) of a degenerated Purkinje cell (Bodian stain).

Necrosis usually affects a group of neurons and is accompanied by an inflammatory response.

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