Axonal autophagy: Mini-review for autophagy in the CNS.

Axonal autophagy: Mini-review for autophagy in the CNS.
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DOI:
10.1016/j.neulet.2018.03.025
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发表时间:
2019-04-01
影响因子:
2.5
通讯作者:
Holzbaur ELF
Holzbaur ELF
中科院分区:
医学4区
文献类型:
--
作者:
Stavoe AKH;Holzbaur ELF

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Neurons are long-lived and highly polarized cells that depend on autophagy to maintain cellular homeostasis. The robust, constitutive biogenesis of autophagosomes in the distal axon occurs via a conserved pathway that is required to maintain functional synapses and prevent axon degeneration. Autophagosomes are formed de novo at the axon terminal in a stepwise assembly process, engulfing mitochondrial fragments, aggregated proteins, and bulk cytosol in what appears to be a nonselective uptake mechanism. Following formation, autophagosomes fuse with late endosomes/lysosomes and then are rapidly and efficiently transported along the axon toward the soma, driven by the microtubule motor cytoplasmic dynein. Motile autophagosomes mature to autolysosomes in transit by fusing with additional late endosomes/lysosomes, arriving at the soma as fully competent degradative organelles. Misregulation of neuronal autophagy leads to axonal degeneration and synaptic destabilization, and has been implicated in neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and ALS.
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