NH2-truncated human tau induces deregulated mitophagy in neurons by aberrant recruitment of Parkin and UCHL-1: implications in Alzheimer's disease

• Published in: Human molecular genetics Vol. 24; no. 11; pp. 3058 - 3081
• Main Authors: Corsetti, V., Florenzano, F., Atlante, A., Bobba, A., Ciotti, M.T., Natale, F., Della Valle, F., Borreca, A., Manca, A., Meli, G., Ferraina, C., Feligioni, M., D'Aguanno, S., Bussani, R., Ammassari-Teule, M., Nicolin, V., Calissano, P., Amadoro, G.
• Format: Journal Article
• Language: English
• Published: England 01.06.2015
• Subjects: Alzheimer Disease - genetics; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Animals; HeLa Cells; Humans; Mice, Inbred C57BL; Mice, Transgenic; Mitochondrial Degradation; Mitochondrial Proteins - metabolism; Neurons - metabolism; Neurons - physiology; Protein Transport; Rats, Wistar; tau Proteins - genetics; tau Proteins - physiology; Ubiquitin Thiolesterase - metabolism; Ubiquitin-Protein Ligases - metabolism

Disarrangement in functions and quality control of mitochondria at synapses are early events in Alzheimer's disease (AD) pathobiology. We reported that a 20-22 kDa NH2-tau fragment mapping between 26 and 230 amino acids of the longest human tau isoform (aka NH2htau): (i) is detectable in cellul...