Autophagy impairment: a crossroad between neurodegeneration and tauopathiesReport as inadecuate

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BMC Biology

, 10:78

First Online: 21 September 2012Received: 11 September 2012Accepted: 14 September 2012DOI: 10.1186-1741-7007-10-78

Cite this article as: Nassif, M. & Hetz, C. BMC Biol 2012 10: 78. doi:10.1186-1741-7007-10-78


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 3 GSK3 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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Electronic supplementary materialThe online version of this article doi:10.1186-1741-7007-10-78 contains supplementary material, which is available to authorized users.

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Author: MelissaNassif - ClaudioHetz


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