Our laboratory focuses on understanding the roles of mitochondrial quality control and metabolism in neurodegenerative diseases. We use unbiased proteomics and genomics, cellular and molecular biology, patient iPS cells-derived cell culture and diseased animals to investigate the fundamental mechanisms by which mitochondrial impairment contributes to cellular metabolism disturbance and neurodegeneration.

We also utilize rationally designed peptide inhibitors of protein-protein interactions and the high throughput screening approach to developing “mitochondrial medicine” as therapeutic strategies for treating neurodegenerative diseases.

Publication

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• ​Sep 2022- Yutong's paper "A CHCHD6-APP axis connects amyloid and mitochondrial dysfunction in Alzheimer's disease" was accepted by Acta Neuropathologica! Congratulations, Awesome work! 

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• August 2022- Qi lab is awarded Vinney Award for Alzheimer's disease. 

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• June 2022- Dr. Rui Zhang joins our lab as a postdoc scholar. Welcome, Rui! 

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• June 2022- Qi lab is awarded an NIH R01 grant to study MICOS complex dysregulation in Alzheimer's disease.

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• June 2022- Shuai's review paper is accepted for publication! Congratulations! 

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• March 2022- Aya's review paper is accepted. Congratulations! 

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• February 2022- Our paper "ATAD3A oligomerization promotes neuropathology and cognitive deficits in Alzheimer's disease models" is accepted by Nature Communications. Congratulations to Yuanyuan, Di and Rihua, and other co-authors! 

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• January 2022- Qi lab is awarded an NIH R01 grant to study oligodendroglial metabolism and white matter degeneration in Alzheimer's disease. 

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• Shang YT, Sun XY, Chen XQ, Wang QQ, Wang EJ, Miller M, Xu R, Pieper AA and Qi X,  A CHCHD6-APP axis connects amyloid and mitochondrial dysfunction in Alzheimer's disease. Acta Neuropathologica, 2022 Sep 14. doi: 10.1007/s00401-022-02499-0

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• Zhao YY, Hu D, Wang RH, Sun XY, Ropelewski P, Hubler Z, Lundberg K, Wang QQ, Adams D, Xu R and Qi X, ATAD3A oligomerization promotes neuropathology and cognitive deficits in Alzheimer's disease models by impairing brain cholesterol turnover. Nature Communications, 2022.  https://doi.org/10.1038/s41467-022-28769-9

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• Hu D, Sun SY, Magpusao A, Fedorov Y, Thompson M, Wang BL, Lundberg K, Adams D and Qi X, Small-molecule suppression of calpastatin degradation reduces neuropathology in models of Huntington’s disease. Nature Communications, 2021 12, 5305. https://doi.org/10.1038/s41467-021-25651-y

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• Zhang XW, Wang RH, Hu D, Sun XY, Fujioka H, Lundberg K, Chan ER, Wang QQ, Xu R, Flanagan ME, Pieper AA, and Qi X, Oligodendroglial glycolytic stress triggers inflammasome activation and neuropathology in Alzheimer’s disease. Science Advances.  2020 Dec 4;6(49):eabb8680.

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• Zhao YY, Sun XY, Hu D, Prosdoci D, Jain M, Hoppel C, Ramachandran R, Qi X, ATAD3A oligomerization causes neurodegeneration by coupling mitochondrial fragmentation with bioenergetics defects. Nature Communications, 2019, Mar 26;10(1):1371. 

• ​Hu D, Sun XY, Zarabi S, Hong YN, Schimmer A, Liao XD, Ford CP, Luo Y, Qi X, Alpha-synuclein suppresses mitochondrial protease ClpP to trigger mitochondrial oxidative damage and neurotoxicity. Acta Neuropathologica, 2019 Mar 15. doi: 10.1007/s00401-019-01993-2.

• Guo X, Sun XY, Di H, Wang YJ, Fujioka H, Vyas R, Chakrapani S, Joshi UA, Luo Y, Mochly-Rosen D and Qi X, VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease. Nature Communications, 2016 Aug 26;7: 12646.  

• Guo X, Disatnik MH, Monbureau M, Shamloo M, Mochly-Rosen D and Qi X, Inhibition of mitochondrial fragmentation diminishes Huntington’s disease-associated neurodegeneration. J Clin Invest., 2013 Dec;123(12):5371-88.

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