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TitleDysregulation of autophagosome-mitochondria contacts contributes to autophagy dysfunction and neurodegeneration in tauopathy.
Journal, issue, pagesProc Natl Acad Sci U S A, Vol. 123, Issue 24, Page e2520331123, Year 2026
Publish dateJun 16, 2026
AuthorsNuo Jia / Hongyuan Guan / Yantao Zuo / Yu Young Jeong / Niharika Amireddy / Gavesh Rajapaksha / Cuauhtemoc Ulises Gonzalez / Nora Jaber / Yun-Kyung Lee / Marialaina Nissenbaum / David J Margolis / Wei Dai / Alexander W Kusnecov / Qian Cai /
PubMed AbstractMitochondria (Mito) engage in extensive communication with other organelles through membrane contacts. Perturbed mitochondria-organelle interactions are indicated in a variety of neurodegenerative ...Mitochondria (Mito) engage in extensive communication with other organelles through membrane contacts. Perturbed mitochondria-organelle interactions are indicated in a variety of neurodegenerative diseases, but the underlying mechanisms remain poorly understood. Here, we report a class of mitochondria-organelle communication: autophagosome/autophagic vacuole (AV)-Mito contact, which exhibits hypertethering in tauopathy neurons, consequently hampering AV retrograde transport. Such defects are attributed to accelerated turnover of the contact release factor TBC1D15, triggered by mitochondrial bioenergetic deficit-induced hyperactivity of the adenosine monophosphate-activated protein kinase (AMPK). Increasing TBC1D15 levels or repressing AMPK activity normalizes AV-Mito contact release and restores retrograde transport of AVs, thereby increasing autophagic cargo clearance and reducing tau burden in tauopathy axons. Furthermore, overexpression of TBC1D15 enhances autophagic clearance and attenuates tau pathology, alleviating neurodegeneration and cognitive dysfunction in tauopathy mice. Taken together, our study provides mechanistic insights into AV-Mito contact dysregulation in tauopathy-related autophagy failure, laying the groundwork for the development of potential therapeutics to combat tauopathy diseases.
External linksProc Natl Acad Sci U S A / PubMed:42258714 / PubMed Central
MethodsEM (tomography)
Structure data

EMDB-75946: In situ cryo-ET analysis of mitochondria and autophagosome contact in tauP301S Tg mouse cortical neurons
Method: EM (tomography)

EMDB-75947: In situ cryo-ET analysis of mitochondria and autophagosome contact in tauP301S Tg mouse cortical neurons Supplementary 1
Method: EM (tomography)

EMDB-75949: In situ cryo-ET analysis of mitochondria and autophagosome contact in tauP301S Tg mouse cortical neurons Supplementary 2
Method: EM (tomography)

Source
  • Mus musculus (house mouse)

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