Giuseppina Tesco
Tufts University, MA·Neuroscience
Most cases of Alzheimer's disease (AD), the leading cause of dementia, are not caused by a single faulty gene. Instead, risk builds up from many common genetic variants, and none of them alone is enough to cause the disease.
- Fields
Neuroscience
Genetics
Medicine & Clinical Research
- Topics
Alzheimer's disease
apolipoprotein E
amyloid-β
- Grants
- 1 known grant, through Jan 2028
What they work on
- 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.
- Determine how APOE genotype changes the effect of the ABCA7 variant, comparing APOE3/3 and APOE4/4 human neurons and microglia that carry one or both risk variants.
- Examine the ABCA7 variant's effects in microglia, the brain's immune cells, which express ABCA7 at high levels, using 2D and 3D human brain cell culture models.
More about the research
Working out how these variants act, and how they act on each other, could explain why some carriers develop AD and others do not.
Why it matters
Most people with Alzheimer's disease carry several modest genetic risk variants rather than one causal mutation. Showing how the ABCA7 variant and APOE genotype combine to drive amyloid buildup could help doctors sort patients into groups by genetic risk. It could also point to treatments matched to a person's specific combination of variants, an approach to personalized medicine for late-onset AD.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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.
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.
Tae-Wan Kim
Columbia University, NY·Neuroscience
Determine how the neuronal signal SEMA3A promotes β-amyloid uptake and a disease-associated microglia gene profile in human iPSC-derived microglia (iMGLs), independently of the TREM2 receptor.
The school
Tufts University: 19 labs on PI Pages, $278M a year on research, 144 research doctorates a year.
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