Wenzhang Wang
Case Western Reserve University, OH·Neuroscience
Alzheimer's disease is one of the most common brain-wasting disorders of old age. The biggest genetic risk factor for the common late-onset form is the ε4 version of APOE (apolipoprotein E), a protein that carries fats and influences how amyloid beta (Aβ), the sticky protein fragment that forms plaques, builds up.
- Fields
Neuroscience
Biology
Biochemistry
- Topics
Alzheimer's disease
neurodegeneration
APOE ε4
- Grants
- 1 known grant, through Jun 2027
What they work on
- 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.
- Define how the risk gene APOE ε4 and its cargo amyloid beta (Aβ) drive these contacts and Aβ build-up inside mitochondria through enhanced interaction with STARD3, a protein at organelle contact sites.
- Test whether interfering with the APOE ε4–STARD3 contact mechanism protects mitochondria and neurons, to assess its potential as a therapeutic target for late-onset Alzheimer's disease.
More about the research
Damaged mitochondria, the cell's energy factories, are also a hallmark of the disease. This project asks how these pieces connect. It focuses on direct physical contacts between mitochondria and the endolysosomal system, the cell's network for sorting and breaking down material.
Why it matters
Most Alzheimer's patients have the common late-onset form, and many carry the APOE ε4 risk gene. By linking APOE ε4 and amyloid beta to abnormal contacts between mitochondria and the cell's recycling system, this work could reveal a new mechanism of nerve cell damage. It could also identify STARD3-mediated contacts as an uncharacterized drug target for this broad patient population.
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.
Fei Yin
University of Arizona, AZ·Neuroscience
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.
Bernard G. Schreurs
West Virginia University, WV·Neuroscience
Test whether removing or restoring estrogen changes memory, neural function and Alzheimer's-like pathology in intact and castrated male and intact and ovariectomized female cholesterol-fed rabbits.
The school
Case Western Reserve University: 34 labs on PI Pages, $643M a year on research, 213 research doctorates a year.
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