ABSTRACT
It is now well-established that CB is formed as a universal biomarker of cell injury in response to intrauterine malnutrition, nicotine, ethanol, and/or ZIKV infection in the NPCs, EPCs, and CPCs, derived from iPPCs (Sharma and Ebadi 2014; Sharma et al. 2014; Sharma 2017a,b). Environmental neurotoxins such as KA and DOM also induce CB formation in the hippocampal CA-3 and dentate gyrus regions of the developing mice to induce dementia as noticed in AD due to CMB (Sharma et al. 1993; Sharma 2014; Sharma 2017c). We reported CB as a novel biomarker in drug addiction (Sharma 2015) and highlighted its clinical significance to evaluate the theranostic potential and toxicity of nanomedicines (Sharma et al. 2013). We also highlighted that MTs prevent CB formation by serving as potent free radical scavengers (Sharma and Ebadi 2014). Recently, we proposed that CB can be used as a novel biomarker of nutritional stress and CMB in AD and in the clinical evaluation of vascular dementia (Sharma et al. 2016; Jagtap et al. 2015). Various parkinsonian neurotoxins such as salsolinol, rotenone, MPTP, MPP+, and 1 benzyl-TIQs induce CB formation in the cultured human DAergic (SK-N-SH and SH-S-Y5Y) neurons and genetic mouse models, whereas antioxidants such as glutathione and MTs prevent CB formation by scavenging free radicals involved in lipid peroxidation and mtDNA oxidation in progressive NDDs.
