Email updates

Keep up to date with the latest news and content from BMC Biology and BioMed Central.

Journal App

google play app store
Open Access Highly Accessed Commentary

Autophagy impairment: a crossroad between neurodegeneration and tauopathies

Melissa Nassif12 and Claudio Hetz1234*

Author affiliations

1 Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile

2 Center for Molecular Studies of the Cell, Institute of Biomedical Sciences, University of Chile, Santiago, Chile

3 Neurounion Biomedical Foundation, Santiago, Chile

4 Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA

For all author emails, please log on.

Citation and License

BMC Biology 2012, 10:78  doi:10.1186/1741-7007-10-78

Published: 21 September 2012

Abstract

Most neurodegenerative diseases involve the accumulation of misfolded proteins in the nervous system. Impairment of protein degradation pathways such as autophagy is emerging as a consistent and transversal pathological phenomenon in neurodegenerative diseases, including Alzheimer's, Huntington's, and Parkinson's disease. Genetic inactivation of autophagy in mice has demonstrated a key role of the pathway in maintaining protein homeostasis in the brain, triggering massive neuronal loss and the accumulation of abnormal protein inclusions. However, the mechanism underlying neurodegeneration due to autophagy impairment remains elusive. A paper in Molecular Neurodegeneration from Abeliovich's group now suggests a role for phosphorylation of Tau and the activation of glycogen synthase kinase 3β (GSK3β) in driving neurodegeneration in autophagy-deficient neurons. We discuss the implications of this study for understanding the factors driving neurofibrillary tangle formation in Alzheimer's disease and tauopathies.

See research article http://www.molecularneurodegeneration.com/content/7/1/48 webcite