Dr. Qi joined the faculty at Case Western Reserve University in 2011 and has built an internationally recognized research program at the intersection of mitochondrial biology, neurodegeneration, and therapeutic discovery. She earned her PhD from Hokkaido University in Japan and completed her postdoctoral training at Stanford University. Dr. Qi’s research investigates how mitochondrial dysfunction, metabolic dysregulation, and neuroimmune signaling contribute to neurodegenerative disease. Her laboratory has identified key mitochondrial proteins and disease-driving pathways in Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis (ALS) and has translated these mechanistic discoveries into innovative therapeutic strategies. These efforts include the development of therapeutic peptides and small molecules designed to restore mitochondrial homeostasis and counter disease-associated mechanisms of neurodegeneration.
Qi Lab
I research altered mitochondrial quality control and metabolic dysregulation in neurodegenerative disease - Huntington's, Parkinson's and Alzheimer's diseases, and develop therapeutics for these diseases.
Research Information
Research Interests
Mitochondrial Biology, Neurodegeneration, and Therapeutic Discovery
Dr. Qi’s research program seeks to understand how mitochondrial dysfunction drives neurodegeneration and to translate fundamental mechanistic discoveries into new therapeutic strategies. Her laboratory focuses on four interconnected areas: mitochondrial dynamics and quality control; mitochondrial proteostasis and organelle homeostasis; metabolism and neuroimmune regulation; and therapeutic discovery. Together, these studies define how alterations in mitochondrial structure, function, metabolism, and signaling contribute to neuronal vulnerability and disease progression.
A major focus of the laboratory is understanding how mitochondrial quality-control pathways and protein homeostasis maintain neuronal health and how their disruption contributes to Alzheimer’s, Parkinson’s, Huntington’s, ALS, and related neurodegenerative disorders. The laboratory investigates mitochondrial dynamics, proteostasis, cristae architecture, organelle communication, cellular metabolism, and mitochondrial stress responses. A complementary area of research examines how mitochondrial dysfunction reshapes cellular metabolism and neuron–glia interactions, thereby linking metabolic dysregulation and neuroimmune responses to disease progression.
The laboratory integrates molecular and cellular biology with functional proteomics, metabolomics, patient-derived iPSC models, and disease-relevant animal models to identify mechanisms that drive neurodegeneration. These multidisciplinary approaches allow the laboratory to move from fundamental mitochondrial biology to disease mechanisms, therapeutic targets, and preclinical intervention.
A central translational goal of the laboratory is the development of “mitochondrial medicine”—therapeutic approaches designed to correct disease-driving mitochondrial abnormalities. Building on mechanistic discoveries, the Qi laboratory develops therapeutic peptides and small molecules that target pathological protein interactions and mitochondrial pathways, restore mitochondrial homeostasis, and protect vulnerable neurons. By bridging fundamental discovery with therapeutic development, the laboratory aims to advance new disease-modifying strategies for neurodegenerative disorders.
Publications
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- Hu D, Sun XY, Shang YT, Lundberg K, Adams D, Qi X. A small-molecule stabilizer of the Calpastatin– Calpain-2 complex restores mitochondrial function and mitigates neurodegeneration. Science Advances. 2026 Mar 27;12(13). PMID: 41894510.
- Baron C, Wang RH, Cooke S, Ng HP, Ferreira RS, Miranda HC, Qi X. TDP-43 impairs glycolysis by sequestering hexokinase 1 in amyotrophic lateral sclerosis. Acta Neuropathologica. 2026 Mar 16;151(1):26. PMID: 41838122.
- Hu D, Sun XY, Qi X. Disrupting α-synuclein–ClpP interaction restores mitochondrial function and attenuates neuropathology in Parkinson’s disease models. Molecular Neurodegeneration. 2025 Dec 22;20(1):126. PMID: 41430713.
- Zhao YY, Hu D, Wang RH, Sun XY, Ropelewski P, Hubler Z, Lundberg K, Wang QQ, Adams D, Xu R, Qi X. ATAD3A oligomerization promotes neuropathology and cognitive deficits in Alzheimer's disease models by impairing brain cholesterol turnover. Nature Communications. 2022 Mar 2;13(1):1121. PMID: 35236834.
- Zhang XW, Wang RH, Hu D, Sun XY, Fujioka H, Lundberg K, Chan ER, Wang QQ, Xu R, Flanagan ME, Pieper AA, Qi X. Oligodendroglial glycolytic stress triggers inflammasome activation and neuropathology in Alzheimer’s disease. Science Advances. 2020 Dec 4;6(49). PMID: 33277246.
- 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. PMID: 30914652.