Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2015 Apr 1;128(7):1259-67.
doi: 10.1242/jcs.161216.

Autophagosome dynamics in neurodegeneration at a glance

Affiliations
Review

Autophagosome dynamics in neurodegeneration at a glance

Yvette C Wong et al. J Cell Sci. .

Abstract

Autophagy is an essential homeostatic process for degrading cellular cargo. Aging organelles and protein aggregates are degraded by the autophagosome-lysosome pathway, which is particularly crucial in neurons. There is increasing evidence implicating defective autophagy in neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), Alzheimer's disease, Parkinson's disease and Huntington's disease. Recent work using live-cell imaging has identified autophagy as a predominantly polarized process in neuronal axons; autophagosomes preferentially form at the axon tip and undergo retrograde transport back towards the cell body. Autophagosomes engulf cargo including damaged mitochondria (mitophagy) and protein aggregates, and subsequently fuse with lysosomes during axonal transport to effectively degrade their internalized cargo. In this Cell Science at a Glance article and the accompanying poster, we review recent progress on the dynamics of the autophagy pathway in neurons and highlight the defects observed at each step of this pathway during neurodegeneration.

Keywords: Alzheimer's disease; Amyotrophic lateral sclerosis; Autophagy; Axonal transport; Huntington’s disease; Parkinson’s disease.

PubMed Disclaimer

Similar articles

Cited by

References

    1. Alegre-Abarrategui J., Christian H., Lufino M. M. P., Mutihac R., Venda L. L., Ansorge O., Wade-Martins R. (2009). LRRK2 regulates autophagic activity and localizes to specific membrane microdomains in a novel human genomic reporter cellular model. Hum. Mol. Genet. 18, 4022–4034 10.1093/hmg/ddp346 - DOI - PMC - PubMed
    1. Allen G. F. G., Toth R., James J., Ganley I. G. (2013). Loss of iron triggers PINK1/Parkin-independent mitophagy. EMBO Rep. 14, 1127–1135 10.1038/embor.2013.168 - DOI - PMC - PubMed
    1. Ashrafi G., Schlehe J. S., LaVoie M. J., Schwarz T. L. (2014). Mitophagy of damaged mitochondria occurs locally in distal neuronal axons and requires PINK1 and Parkin. J. Cell Biol. 206, 655–670 10.1083/jcb.201401070 - DOI - PMC - PubMed
    1. Atwal R. S., Xia J., Pinchev D., Taylor J., Epand R. M., Truant R. (2007). Huntingtin has a membrane association signal that can modulate huntingtin aggregation, nuclear entry and toxicity. Hum. Mol. Genet. 16, 2600–2615 10.1093/hmg/ddm217 - DOI - PubMed
    1. Baldo B., Soylu R., Petersén A. (2013). Maintenance of basal levels of autophagy in Huntington's disease mouse models displaying metabolic dysfunction. PLoS ONE 8, e83050 10.1371/journal.pone.0083050 - DOI - PMC - PubMed

Publication types