Fei Yin, Ph.D.

Associate Professor, Pharmacology

Assistant Director for Translational Neuroscience, Center for Innovation in Brain Science

Associate Professor, GIDP in Neuroscience

Associate Professor, Clinical Translational Science

BSRL 471

(520) 626-4102

feiyin@arizona.edu

Links

Lab Website

Brain’s self-cleaning machinery may be key to Alzheimer’s

New study links impaired lipid clearance in brain to Alzheimer’s disease

Researchers focus on building a resilient brain to prevent Alzheimer’s disease

Fei Yin, PhD, is an Associate Professor in the Department of Pharmacology at the University of Arizona. His work focuses on translational neuroscience, brain aging, Alzheimer’s disease, metabolism, mitochondrial function, neuroinflammation, and mechanisms that support brain resilience.

Dr. Yin also serves as Assistant Director for Translational Neuroscience at the Center for Innovation in Brain Science and is affiliated with the GIDP in Neuroscience and Clinical Translational Science.

Degrees

2018 - MS, University of Southern California (Computer Science)
2012 - Ph.D., University of Southern California (Pharmaceutical Sciences)
2010 - MS, University of Southern California (Regulatory Science)
2005 - BS, Nanjing University (Biochemistry)

Awards

2024 - Fellow, Research Leadership Institute, University of Arizona
2019 - The Bio5 Institute Team Scholars Award, University of Arizona
2017 - Research Endowment, Packer Wentz Endowment
2014 - Linus Pauling Institute young Investigator Award, Oxygen Club of California

Research Interests

Laboratory of Neurometabolism and Neuroinflammation

The Yin Laboratory is dedicated to advancing the understanding of the molecular and cellular mechanisms of neurodegeneration and the development of novel therapeutics against neurodegenerative diseases. A major focus of our research is on the role of lipid metabolism in Alzheimer’s disease (AD) and its mechanistic interactions with mitochondrial dysfunction, neuroinflammation and major AD risk factors such as the APOE4 gene and the female sex. Built upon our recent findings, we propose a lipid-centric AD cascade that bridges the amyloid hypothesis, the mitochondrial hypothesis, and the APOE4 hypothesis of AD by their convergence at lipid metabolism. We are now actively developing novel disease-modifying AD therapeutics by restoring the lipid homeostasis in the degenerating brain. In addition, we are also interested in the role of the maternally inherited mitochondrial genome (mtDNA) in metabolically reprogramming the brain and modifying AD risks.

Publications

Wang, Tian, et al. “APOE4 Accelerates Menopause-Associated Brain Metabolic Shift and Disrupts Bioenergetic Adaptation”. Frontiers in Aging Neuroscience, vol. 18, June 2026, p. 1796680, https://doi.org/10.64898/2026.03.11.710133.

Pan, Huajun, and Yin, Fei. “Mitochondrial ROS Sources Steer Neuroinflammation”. Nature Metabolism, vol. 7, no. 11, Nov. 2025, pp. 2192-4, https://doi.org/10.1038/s42255-025-01391-x.

Garcia-Macia, Marina, and Yin, Fei. “Career Pathways, Part 15”. Nature Metabolism, vol. 6, no. 10, Oct. 2024, pp. 1842-5, https://doi.org/10.1038/s42255-024-01122-8.

Schultheis, Nicholas, et al. “Altering Heparan Sulfate Suppresses Cell Abnormalities and Neuron Loss in Drosophila Presenilin Model of Alzheimer Disease”. IScience, vol. 27, no. 7, July 2024, p. 110256, https://doi.org/10.1016/j.isci.2024.110256.

Yin, Fei. “Lipid Metabolism and Alzheimer’s Disease: Clinical Evidence, Mechanistic Link and Therapeutic Promise.”. FEBS J, vol. 290, no. 6, Mar. 2023, pp. 1420-53, https://doi.org/10.1111/febs.16344.

Mi, Yashi, et al. “Loss of Fatty Acid Degradation by Astrocytic Mitochondria Triggers Neuroinflammation and Neurodegeneration.”. Nat Metab, vol. 5, no. 3, Mar. 2023, pp. 445-6, https://doi.org/10.1038/s42255-023-00756-4.

Mishra, Aarti, et al. “A Tale of Two Systems: Lessons Learned from Female Mid-Life Aging With Implications for Alzheimer’s Prevention & Treatment.”. Ageing Res Rev, vol. 74, Feb. 2022, p. 101542, https://doi.org/10.1016/j.arr.2021.101542.

Ren, Bo, et al. “Methionine Restriction Alleviates Age-Associated Cognitive Decline via Fibroblast Growth Factor 21.”. Redox Biol, vol. 41, May 2021, p. 101940, https://doi.org/10.1016/j.redox.2021.101940.

Qi, Guoyuan, et al. “ApoE4 Impairs Neuron-Astrocyte Coupling of Fatty Acid Metabolism.”. Cell Rep, vol. 34, no. 1, Jan. 2021, p. 108572, https://doi.org/10.1016/j.celrep.2020.108572.

Qi, Guoyuan, et al. “Characterizing Brain Metabolic Function Ex vivo With Acute Mouse Slice Punches.”. STAR Protoc, vol. 2, no. 2, Jan. 2021, p. 100559, https://doi.org/10.1016/j.xpro.2021.100559.

Liu, Xiaoning, et al. “High-Fiber Diet Mitigates Maternal Obesity-Induced Cognitive and Social Dysfunction in the Offspring via Gut-Brain Axis.”. Cell Metab, vol. 33, no. 5, Jan. 2021, pp. 923-938.e6, https://doi.org/10.1016/j.cmet.2021.02.002.

Mi, Yashi, et al. “Mitochondria-Targeted Therapeutics for Alzheimer’s Disease: The Good, the Bad, the Potential.”. Antioxid Redox Signal, vol. 34, no. 8, Jan. 2021, pp. 611-30, https://doi.org/10.1089/ars.2020.8070.

Mishra, Aarti, et al. “Dynamic Neuroimmune Profile During Mid-Life Aging in the Female Brain and Implications for Alzheimer Risk.”. IScience, vol. 23, no. 12, Jan. 2020, p. 101829, https://doi.org/10.1016/j.isci.2020.101829.

Liu, Zhigang, et al. “Gut Microbiota Mediates Intermittent-Fasting Alleviation of Diabetes-Induced Cognitive Impairment.”. Nat Commun, vol. 11, no. 1, Jan. 2020, p. 855, https://doi.org/10.1038/s41467-020-14676-4.

Wang, Yiwei, et al. “Retrospective Analysis of PhytoSERM for Management of Menopause-Associated Vasomotor Symptoms and Cognitive Decline: A Pilot Study on Pharmacogenomic Effects of Mitochondrial Haplogroup and APOE Genotype on Therapeutic Efficacy.”. Menopause, vol. 27, no. 1, Jan. 2020, pp. 57-65, https://doi.org/10.1097/GME.0000000000001418.

Bacon, Eliza R, et al. “Neuroendocrine Aging Precedes Perimenopause and Is Regulated by DNA Methylation.”. Neurobiol Aging, vol. 74, Feb. 2019, pp. 213-24, https://doi.org/10.1016/j.neurobiolaging.2018.09.029.

Qi, Guoyuan, et al. “Cellular Specificity and Inter-Cellular Coordination in the Brain Bioenergetic System: Implications for Aging and Neurodegeneration.”. Front Physiol, vol. 10, Jan. 2019, p. 1531, https://doi.org/10.3389/fphys.2019.01531.

Yin, Fei, et al. “Editorial: The Metabolic-Inflammatory Axis in Brain Aging and Neurodegeneration”. Front Aging Neurosci, vol. 9, Jan. 2017, p. 209, https://doi.org/10.3389/fnagi.2017.00209.

Klosinski, Lauren P, et al. “White Matter Lipids As a Ketogenic Fuel Supply in Aging Female Brain: Implications for Alzheimer’s Disease.”. EBioMedicine, vol. 2, no. 12, Dec. 2015, pp. 1888-904, https://doi.org/10.1016/j.ebiom.2015.11.002.

Brinton, Roberta D, et al. “Perimenopause As a Neurological Transition State.”. Nat Rev Endocrinol, vol. 11, no. 7, July 2015, pp. 393-05, https://doi.org/10.1038/nrendo.2015.82.

Yin, Fei, et al. “The Perimenopausal Aging Transition in the Female Rat Brain: Decline in Bioenergetic Systems and Synaptic Plasticity.”. Neurobiol Aging, vol. 36, no. 7, July 2015, pp. 2282-95, https://doi.org/10.1016/j.neurobiolaging.2015.03.013.

Jiang, Tianyi, et al. “Lipoic Acid Restores Age-Associated Impairment of Brain Energy Metabolism through the Modulation of Akt JNK Signaling and PGC1α Transcriptional Pathway.”. Aging Cell, vol. 12, no. 6, Dec. 2013, pp. 1021-31, https://doi.org/10.1111/acel.12127.

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