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BMC Biol. 2012; 10: 78.
Published online Sep 21, 2012. doi:  10.1186/1741-7007-10-78
PMCID: PMC3448508
Autophagy impairment: a crossroad between neurodegeneration and tauopathies
Melissa Nassif1,2 and Claudio Hetzcorresponding author1,2,3,4
1Biomedical Neuroscience Institute, Faculty of Medicine, University of Chile, Santiago, Chile
2Center for Molecular Studies of the Cell, Institute of Biomedical Sciences, University of Chile, Santiago, Chile
3Neurounion Biomedical Foundation, Santiago, Chile
4Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115, USA
corresponding authorCorresponding author.
Melissa Nassif: melnassif/at/gmail.com; Claudio Hetz: chetz/at/hsph.harvard.edu
Received September 11, 2012; Accepted September 14, 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.
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