Marta Olah
Columbia University, NY·Neuroscience
Alzheimer's disease slowly destroys memory, and no treatment yet stops it. Many of the genes that raise a person's risk of the disease are switched on mainly in microglia, the brain's resident immune cells, which help keep brain tissue and nerve-cell wiring healthy.
- Fields
Neuroscience
Microbiology & Immunology
Genetics
- Topics
microglia
Alzheimer's disease
neurodegeneration
- Grants
- 1 known grant, through Jun 2027
What they work on
- Measure how many Cluster 7 microglia, a possibly protective immune-cell subset, are present in brain tissue from many older people with and without Alzheimer's dementia, and relate their numbers to sex, age, pathology, risk genes and cognition.
- Test whether a higher abundance of Cluster 7 microglia goes with cognitive resilience, meaning people who stay mentally sharp despite Alzheimer's-type brain damage.
- Isolate Cluster 7 microglia from human brain tissue and describe their functional and physical characteristics.
- Map the epigenetic landscape of Cluster 7 microglia, the gene-control marks on their DNA, to find which regulatory mechanisms drive cells into this state and what may block it in Alzheimer's.
More about the research
That makes microglia a promising point for treatment. Microglia are not all alike, though. In the aging brain they come in several states, and different states may help or harm.
Why it matters
Late-onset Alzheimer's disease has no cure or disease-modifying therapy. By finding out how a possibly protective group of microglia relates to healthy aging and disease, this work could point to new microglia-based targets. Such targets might be used to monitor the disease or to treat it. Testing for sex differences could also help explain why women and men may be affected differently.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Elizabeth M Bradshaw
Columbia University, NY·Neuroscience
Measure how microglia, the brain's resident immune cells, respond to HSV-1 infection depending on each person's AD-associated genetic background, using transcriptomics and in vitro cell models.
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.
The school
Columbia University: 89 labs on PI Pages, $1.4B a year on research, 625 research doctorates a year.
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