Lipid peroxidation is one of the primary events of the cell injury process. In pathophysiological condition, it is undergoing the initiation of organ damage. Various free radicals are playing a key role in this lipid peroxidation process. Free radical associated organ damage involves the three major phases, that is, initiation, propagation and termination. The primary source of various free radical formations is mediated through the pathophysiological function of mitochondria. Lipid peroxidation is contributed to the multiple neurodegenerative disorders. Thus, the various endogenous cellular anti-oxidant systems are regulated lipid peroxidation process and control the neurodegenerative action. Some of the molecules are targeted to attenuate the lipid peroxidation and their mediators for the prevention of neurodegeneration.
Part of the book: Lipid Peroxidation Research
The basic understanding of vascular dementia (VaD) and their molecular mechanisms are a too complex phenomenon. VaD associated neurodegeneration and cognitive impairment are due to multiple complications of the neurovascular system. The progress of VaD is due to the central and/or peripheral pathophysiological process of the neurovascular system. There are limited nootropic agents are employed for the treatment of VaD. Moreover, the explored nootropic agents act on multiple targets such as receptors, enzymes, ion channel, free radicals, cytokines, chemokines, and apoptotic proteins. However, the enzyme targets, especially acetylcholinesterase inhibitors played a crucial role in the management of cognitive disorders. The pathogenesis of VaD is involved in the vascular complication and neurodegenerative process. Hence, the enzymatic regulation of neurovascular complication is expected to prevent the VaD. The present chapter attempts to explore the recent advancement of enzyme targets for the management of VaD.
Part of the book: Advances in Dementia Research