Journal
CELLS
Volume 7, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/cells7050037
Keywords
ageing; Alzheimer's disease; amyotrophic lateral sclerosis; autophagy; Huntington's disease; mitophagy; neurodegeneration; Parkinson's sisease; protein aggregation; treatment
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Funding
- standard Marie Curie intra-European individual fellowship
- General Secretariat for Research and Technology (GSRT)
- Hellenic Foundation for Research and Innovation (HFRI) [1324]
- European Research Council [ERC-GA695190-MANNA, ERC-GA737599-NeuronAgeScreen]
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The elimination of abnormal and dysfunctional cellular constituents is an essential prerequisite for nerve cells to maintain their homeostasis and proper function. This is mainly achieved through autophagy, a process that eliminates abnormal and dysfunctional cellular components, including misfolded proteins and damaged organelles. Several studies suggest that age-related decline of autophagy impedes neuronal homeostasis and, subsequently, leads to the progression of neurodegenerative disorders due to the accumulation of toxic protein aggregates in neurons. Here, we discuss the involvement of autophagy perturbation in neurodegeneration and present evidence indicating that upregulation of autophagy holds potential for the development of therapeutic interventions towards confronting neurodegenerative diseases in humans.
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