Fei Yin
University of Arizona, AZ·Neuroscience
The brain uses a huge share of the body's energy, and most of it is made by mitochondria, the cell's power plants. In late-onset Alzheimer's disease (LOAD), brain sugar use and mitochondrial function decline early, yet treatments that simply boost mitochondria in every brain cell have not worked.
- Fields
Neuroscience
Biochemistry
Pharmacology
- Topics
Alzheimer's disease
apolipoprotein E
astrocytes
- Grants
- 1 known grant, through Apr 2027
What they work on
- Determine how APOE variants, including APOE4, shift energy metabolism differently in neurons and astrocytes, using single-cell transcriptomics (gene-activity profiles of single cells) and functional tests in cultured cells.
- Test how APOE version and its source (made by neurons or by astrocytes) change fatty acid handoff and breakdown between the two cell types, using a neuron–astrocyte co-culture system.
- Test whether APOE4-driven disruption of neuron–astrocyte metabolic coupling produces Alzheimer's-risk features during aging in vivo, including fat imbalance, neuroinflammation and cognitive decline.
More about the research
The brain is a mix of cell types with very different energy habits. This project asks how they share the metabolic workload, and how a common risk gene disrupts that teamwork.
Why it matters
About APOE4 carriers, who face the highest genetic risk of Alzheimer's disease, the work could explain why energy failure appears early in their brains and why some cell types are especially vulnerable. It may point to drug targets tailored to a person's APOE genotype and to specific brain cells. Such targets could help restore brain energy and fat balance, and potentially prevent or delay memory decline.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Giuseppina Tesco
Tufts University, MA·Neuroscience
Test whether the ABCA7 p.Ala1527Gly variant lowers ABCA7 protein levels and causes loss of function in iPSC-derived human excitatory neurons, measuring Aβ42/40 ratios, a readout of harmful amyloid-β.
Wenzhang Wang
Case Western Reserve University, OH·Neuroscience
Determine whether and how abnormally increased contacts between mitochondria and the endolysosomal system cause mitochondrial defects in Alzheimer's disease neurons, using in vivo and in vitro disease models.
Roberta Eileen Brinton
University of Arizona, AZ·Neuroscience
Test in a Phase 2 double-blind, placebo-controlled trial whether PhytoSERM, a plant-derived estrogen receptor beta (ERβ) modulator, preserves brain glucose metabolism in women with menopausal symptoms, measured by FDG-PET brain scans.
The school
University of Arizona: 36 labs on PI Pages, $1.0B a year on research, 487 research doctorates a year.
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