The degeneration of pigmented SNc neurons is characterized by chromatolysis (Figure 4A), nuclear condensation (Figure 4B), and severe soma attrition (Figure 4C). The neuronal chromatolysis (Figure 4A) is indicated by the eccentrically placed nucleus, pale cytoplasm, and peripheral margination of the Nissl substance. Glial/macrophage-like cells (Figure 4A, arrows) are laden with phagocytosed cellular debris. The nucleus of SNc neurons undergoes considerable condensation (Figure 4B, arrow) while the Nissl substance dissipates, but before appreciable somal shrinkage. The cell body of SNc neurons then becomes attritional (Figure 4C, arrow), resulting in residual neurons that are ~10–20% their normal size. Cells can be identified as atrophic neurons, rather than a debris-laden macrophage, because of the presence of a condensed nucleus with a single prominent nucleolus (Figure 4C). This degeneration pattern could be indicative of autophagy. The nuclear condensation stage of pigmented SNc neuron degeneration is characterized by the appearance of DNA double-strand breaks (Figure 4D), and in the chromatolytic stage SNc neurons accumulate cleaved caspase-3 immunoreactivity (Figure 4E) prior to their undergoing nuclear condensation and somal attrition. Another neuropathological feature of PD is the formation of eosinophilic proteinaceous intra-neuronal or intra-glial inclusions (Figure 4F, arrow), known as Lewy bodies (LBs), first described by Frederich Lewy in 1912. LBs are comprised of a dense core of filamentous material enshrouded by filaments 10–20 nm in diameter and are usually positive for ubiquitin and α-synuclein (α-Syn) [319]. It is not clear whether LBs are related causally to the disease process.