Abstract

Neural plasticity is a consequence of a delicate balance between the processes of neurodegeneration and neurogenesis. When neurodegeneration overcomes neurogenesis, neurodegenerative diseases occur, which affect cognitive functions such as memory, language, and executive functions. Neurodegeneration, the process of neuronal cell death, presents several aspects that were categorized according to their macroscopic and/or morphological characteristics. The concept of apoptosis, autophagy, and necrosis is still widely used today. On the other hand, more in-depth forms emerge in the clinical and academia, describing the cascade of cell death events through biochemical approaches, and the essential (causal) and accessory (correlative) aspects of the cell death process. New concepts were introduced, addressed in the modules of signal translation involving issues such as the initiation, execution, and propagation of cell death, as well as the pathophysiological relevance of each of the main types. Currently, twelve types of cell death are already defined, not only apoptosis, necrosis, and autophagy. In this review, we will address the main mechanisms of cell death, with special emphasis on the participation of caspases and other proteins in these mechanisms. We will discuss some types of cell death such as extrinsic and intrinsic apoptosis, necrosis, necroptosis, and autophagy-dependent cell death. We hope to elucidate key points in molecular systems, including the receptors involved in cell death and their role in neurodegeneration, and showing that neurodegeneration has characteristics beyond morphological (apoptosis and necrosis).

Full Text
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