ABSTRACT
Charnoly body (CB) was discovered for the first time in the developing UN rat Purkinje neurons due to nutritional stress-induced free radical overproduction (Sharma et al. 1986; Sharma et al. 1987). CB is a highly unstable, pleomorphic, quasi-crystalline, multi-lamellar, electron-dense membrane stack that is formed due to mitochondrial degeneration in response to nutritional stress and/or toxic exposure (Sharma et al. 1986; Sharma et al. 1987; Sharma et al. 1993). Free radical-induced CMB triggers CB formation in the most vulnerable cell as a primary event in the etiopathogenesis of intra-neuronal inclusions in various NDDs, including AD, PD, major depressive disorders (MDDs), and chronic drug addiction. Free radical-induced mitochondrial ΔΨ collapse triggers oxidation of mtDNA to cause 8-OH, 2dG accumulation, and CB formation, which is the initial step in the etio-pathogenesis of progressive NDDs (Sharma et al. 2003; Sharma et al. 2004). MTs prevent CB formation by serving as potent free radical scavengers to provide neuroprotection by regulating Zn2+-mediated transcriptional activation of genes involved in growth, proliferation, differentiation, and development (Sharma et al. 2013a; Sharma et al. 2013b). Non-specific induction of CB formation causes GIT stress, myelosuppression, and alopecia as noticed in MDR malignancies and major depressive disorders, Parkinsonism, and schizophrenia (Sharma 2014).
