Joseph Wider
University of Michigan, MI·Neuroscience
After a blow to the head, much of the brain damage happens in the hours and days that follow, as injured cells keep dying. Traumatic brain injury (TBI) affects up to 1.7 million Americans each year, and no treatment is approved for patients.
- Fields
Neuroscience
Physiology
Medicine & Clinical Research
- Topics
traumatic brain injury
neuroprotection
mitochondria
- Grants
- 1 known grant, through Apr 2030
What they work on
- Determine how brain trauma and therapeutic near-infrared light affect mitochondrial dynamics and turnover, the processes by which mitochondria reshape themselves and are replaced, after TBI.
- Identify the cell-specific effects of NIR therapy on neurons, support cells, and blood vessels in the brain's neurovascular unit after traumatic brain injury.
- Test alternative ways of applying therapeutic near-infrared light after TBI to broaden how the treatment that partly inhibits cytochrome c oxidase can be delivered.
More about the research
Mitochondria, the cell's energy factories, are a common driver of this ongoing damage. After injury, their energy-producing machinery, the electron transport chain, becomes overactive and releases reactive oxygen species (ROS), harmful molecules that injure cells.
Why it matters
There is currently no approved treatment for traumatic brain injury, a leading cause of death and lasting disability. A non-invasive near-infrared light therapy that calms overactive mitochondria could become a treatment that limits secondary brain damage after injury. The project's mechanistic and delivery studies are intended to support progress toward FDA approval.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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Produce isogenic human induced pluripotent stem cell lines with and without the Piezo1 E756del variant, which keeps this stretch-activated calcium channel open longer.
Dmitry A Terentyev
Ohio State University, OH·Physiology
Test whether overactive RyR2, the heart's calcium-release channel, activates calpain, a calcium-activated enzyme inside mitochondria, which then breaks down OPA1, a protein that shapes mitochondrial inner folds, using a rat model of CPVT the lab created.
Shuchi Gulati
University of California-Davis, CA·Medicine & Clinical Research·Early-career
Test whether a gene-activity signature built from electron transport chain, mitochondrial ribosomal protein and MHC class II genes separates localized clear cell renal cell carcinoma into tumors at risk of early relapse versus not.
The school
University of Michigan: 124 labs on PI Pages, $2.1B a year on research, 963 research doctorates a year.
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