| Literature DB >> 28279350 |
Fiona M Menzies1, Angeleen Fleming1, Andrea Caricasole2, Carla F Bento1, Stephen P Andrews2, Avraham Ashkenazi1, Jens Füllgrabe1, Anne Jackson1, Maria Jimenez Sanchez1, Cansu Karabiyik1, Floriana Licitra1, Ana Lopez Ramirez1, Mariana Pavel1, Claudia Puri1, Maurizio Renna1, Thomas Ricketts1, Lars Schlotawa1, Mariella Vicinanza1, Hyeran Won1, Ye Zhu1, John Skidmore2, David C Rubinsztein3.
Abstract
Autophagy is a conserved pathway that delivers cytoplasmic contents to the lysosome for degradation. Here we consider its roles in neuronal health and disease. We review evidence from mouse knockout studies demonstrating the normal functions of autophagy as a protective factor against neurodegeneration associated with intracytoplasmic aggregate-prone protein accumulation as well as other roles, including in neuronal stem cell differentiation. We then describe how autophagy may be affected in a range of neurodegenerative diseases. Finally, we describe how autophagy upregulation may be a therapeutic strategy in a wide range of neurodegenerative conditions and consider possible pathways and druggable targets that may be suitable for this objective.Entities:
Keywords: Alzheimer’s disease; Huntington’s disease; Parkinson’s disease; autophagy; dementia; lysosome; motor neuron disease; neurodegeneration; tau
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Year: 2017 PMID： 28279350 DOI： 10.1016/j.neuron.2017.01.022
Source DB: PubMed Journal: Neuron ISSN： 0896-6273 Impact factor: 17.173