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
. 2017 Apr;54(3):1797-1807.
doi: 10.1007/s12035-016-9778-5. Epub 2016 Feb 18.

Adoptive Autophagy Activation: a Much-Needed Remedy Against Chemical Induced Neurotoxicity/Developmental Neurotoxicity

Affiliations
Review

Adoptive Autophagy Activation: a Much-Needed Remedy Against Chemical Induced Neurotoxicity/Developmental Neurotoxicity

A Srivastava et al. Mol Neurobiol. 2017 Apr.

Abstract

The profound significance of autophagy as a cell survival mechanism under conditions of metabolic stress is a well-proven fact. Nearly a decade-long research in this area has led scientists to unearth various roles played by autophagy other than just being an auto cell death mechanism. It is implicated as a vital cell survival pathway for clearance of all the aberrant cellular materials in case of cellular injury, metastasis, disease states, cellular stress, neurodegeneration and so on. In this review, we emphasise the critical role of autophagy in the environmental stressors-induced neurotoxicity and its therapeutic implications for the same. We also attempt to shed some light on the possible protective role of autophagy in developmental neurotoxicity (DNT) which is a rapidly growing health issue of the human population at large and hence a point of rising concern amongst researchers. The intimate association between DNT and neurodegenerative disorders strongly indicates towards adopting autophagy activation as a much-needed remedy for DNT.

Keywords: Autophagy; Developmental neurotoxicity (DNT); Neurodegeneration; Neuroprotection; Neurotoxicity.

PubMed Disclaimer

References

    1. Neuron. 2014 Sep 3;83(5):1131-43 - PubMed
    1. Cell Mol Life Sci. 2016 Feb;73(3):475-96 - PubMed
    1. Environ Health Perspect. 1998 Feb;106 Suppl 1:131-58 - PubMed
    1. PLoS One. 2014 Jun 04;9(6):e98892 - PubMed
    1. Cell Res. 2012 Jan;22(1):43-61 - PubMed

Publication types

MeSH terms

LinkOut - more resources