Tae-Wan Kim
Columbia University, NY·Neuroscience
Alzheimer's disease (AD), the leading cause of dementia in older adults, involves more than amyloid plaques, tangles and the loss of neurons. The brain also becomes strongly inflamed.
- Fields
Neuroscience
Microbiology & Immunology
Biology
- Topics
Alzheimer's disease
dementia
neurodegeneration
- Grants
- 2 known grants, through Dec 2027
What they work on
- 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.
- Define the mechanism linking SEMA3A signaling to microglial activation and its functional role in Alzheimer's disease biology.
- Test the role of microglial FOXO3, a longevity-linked transcription factor, in AD-associated features using a transgenic mouse model of Alzheimer's disease.
- Investigate how FOXO3 controls microglial functions, including lipid droplet buildup and type-I interferon signaling downstream of TREM2, in human iMGLs.
More about the research
Microglia are the brain's resident immune cells, and many genes linked to AD risk are active mainly in them. Both projects ask which signals push microglia into the activated states seen in AD, focusing on a nerve-derived signal and on a transcription factor tied to aging.
Why it matters
Alzheimer's disease is the leading cause of dementia in the elderly, and microglial activity is closely tied to its progression. Identifying SEMA3A and FOXO3 as controllers of microglial activation could point to new molecular targets for therapies that restore normal microglial function and modulate brain inflammation in people with AD.
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.
Riqiang Yan
University of Connecticut, CT·Neuroscience
Identify potent short peptides from the CX3CL1 C-terminal domain (CX3CL1-ICD), a neuron-protecting protein region, that reduce Alzheimer's pathology and cell death in neurons and AD mouse models.
Izumi Maezawa
University of California-Davis, CA·Neuroscience
Map lipid and metabolite changes in single microglia near amyloid plaques, blood vessels and lipid droplet-rich ACSL1-positive cells across human Alzheimer's progression using MALDI mass spectrometry imaging with multiplexed immunofluorescence.
The school
Columbia University: 89 labs on PI Pages, $1.4B a year on research, 625 research doctorates a year.
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