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Visualizing subcellular vesicles to quantitate autophagy in neuronal cells

Jayne Hesley, Molecular Devices, Sunnyvale, CA

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Autophagy is an intracellular catabolic process that sequesters and degrades proteins and organelles that have either been recognized as faulty or simply no longer needed by the cell. Autophagy supports normal cellular processes by carrying out the “housekeeping” function of removing invasive microorganisms, misfolded proteins, and degraded organelles. Autophagy is essential to the maintenance of cell homeostasis and, in addition to its role as a mechanism of cell material turnover, supports the response of an organism to challenges such as starvation by adjusting rates of energy consumption and material reutilization.

Both beneficial and harmful roles for autophagy have been discovered in cancer, infectious disease, diabetes, neurodegenerative disease, and other conditions. The role of autophagy is of particular interest in the study of neuronal cells, where it helps to maintain protein structure and function over long axonal distances. Unlike the cells of other tissues, the cytosolic contents of neurons are not routinely diluted by mitosis. Altered autophagy and accumulation of cellular toxins are seen in Alzheimer’s disease, Parkinson’s disease, and other neurological disorders. These observations have led to the consideration of the various mechanisms of autophagy as potential areas of therapeutic interventions. Quantitation of the effects of experimental variables on this process is an essential element of research that may lead to the development of safe and effective treatments targeting autophagy.

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