Chapters authored
The Apoptosis Regulation Mechanisms in Hypothalamic Neurons in Physiological and Pathological (Overexpression of Oncogene HER-2/Neu) Aging
This study reveals the molecular regulation mechanisms of neurosecretory cell apoptosis in physiological and pathological (oncogene human epidermal growth factor receptor (HER)-2/Neu overexpression) aging. As we have shown previously, apoptosis level in hypothalamic neurosecretory centers increases in aging, and a low level of apoptosis in aged HER-2/Neu transgenic mice is associated with p53-dependent cascade suppression. In this chapter, we consider the participation of p53-regulating genes and p53 target genes in activation of this cascade during physiological aging, as well as suppression under HER-2/Neu overexpression. However, cell resistance to apoptosis may also be due to the activity of cytokine-dependent STAT-signaling pathway, including the high expression of survivin belonging to the family of inhibitors of apoptosis proteins (IAP). Also, another cytokine-dependent signaling, an extrinsic apoptosis pathway associated with the family of tumor necrosis factor (TNF) receptors, has been investigated. Thus, in the present work, three signaling cascades are considered: p53-dependent (the expression and interaction of apoptosis-associated proteins p53, WRN, pin1, p21, and caspase-3), STAT-mediated (STAT1, 3, 5, 6, and survivin), and TNF-dependent (CD95 (FAS), Fas-associated death domain (FADD), TNF receptor–associated death domain (TRADD), and caspase-8). These cascades are involved in both the activation of apoptosis and its suppression. This will reveal the general trends of regulation of neurosecretory cell apoptosis during aging.
Part of the book: Hypothalamus in Health and Diseases
Epileptic Focus in Drug-Resistant Epilepsy: Structure, Organization, and Pathophysiology
The chapter focuses on how different cutting-edge techniques can be used to study electrophysiological, pathomorphological, and biochemical changes in the “epileptic focus” area of the cerebral cortex and white matter to see how epileptic seizures become drug-resistant and how it affects the other regions of the brain. The authors highlight the significance of neuroinflammation and apoptosis in the epilepsy pathogenesis providing EEG characteristics and describing structural changes in the cortex and white matter under such conditions as focal cortical dysplasia and epileptic leukoencephalopathy. Particular focus is given to structural and functional changes in the hippocampus and the role of hippocampal sclerosis in epilepsy. Key conceptions regarding the epileptic focus formation are outlined.
Part of the book: Epilepsy