Lysosomes have a unique and specialized structure, as well as having the second largest intracellular Ca2+ store. Lysosomal Ca2+ channels are mainly involved in endocytic membrane trafficking, lysosomal exocytosis, phagocytosis of large particles, lysosomal pH control, and autophagy. Lysosomal dysfunction may therefore underlie several neurodegenerative disorders that are determined by organellar Ca2+ dyshomeostasis. It was recently postulated that channelopathy-like mechanisms could contribute to the progression of Parkinson's disease, Amyotrophic Lateral Sclerosis, Alzheimer's disease and Huntington's disease via pathological alterations of neuronal biophysical properties. This may occur by modulation of the autophagic flux. The boosting of lysosomal exocytosis and autophagy has been shown to have neuroprotective effects in some neurodegenerative diseases, whereas in others the reduction of autophagy may produce better results. The clarification of these mechanisms is critical for the identification of new druggable targets in neurodegeneration.
Prof. Dr. Agnese Secondo
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