Kim Dore
University of California-San Diego, CA·Neuroscience
In Alzheimer's disease, the earliest change in the brain is the loss of synapses, the junctions where neurons pass signals. If synapses could be made tougher, memory loss might be slowed or prevented.
- Fields
Neuroscience
Pharmacology
- Topics
Alzheimer's disease
synapse loss
palmitoylation
- Grants
- 1 known grant, last ended Oct 2026
What they work on
- Measure PSD-95 palmitoylation, the fatty tag that anchors this scaffold protein in synapses, across brain regions differently affected by Alzheimer's in APP/PS1 model mice and postmortem human brain samples.
- Test whether blocking the PSD-95 depalmitoylating enzyme with the inhibitor Palmostatin B rescues synaptic physiology impairments in APP/PS1 Alzheimer's model mice.
- Test whether increasing synaptic PSD-95 by inhibiting its depalmitoylation improves performance on memory-related behavioral tests in APP/PS1 mice.
- Examine how elevated PSD-95 protects synapses and dendritic spines from amyloid beta-induced synaptic depression, focusing on its interference with NMDA receptor signaling.
More about the research
This project tests whether boosting a single synapse protein can shield synapses from the damage linked to Alzheimer's.
Why it matters
People with Alzheimer's disease lose synapses before other signs appear, and few treatments protect them. If blocking the enzyme that removes PSD-95 from synapses strengthens vulnerable connections, this enzyme could become a new drug target for treating or preventing Alzheimer's. Mapping PSD-95 palmitoylation may also help explain why certain brain regions and people are more vulnerable.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Martin Hruska
West Virginia University, WV·Neuroscience
Test how acute amyloid-beta affects PSD-95 stability in spines with different numbers of nanomodules. Use live-cell STED super-resolution imaging, with CRISPR tags on the neurons' own PSD-95 and AMPA receptors.
Ying Xu
Rutgers University-New Brunswick, NJ·Neuroscience
Test whether removing PDE2A, an enzyme that breaks down the messengers cAMP and cGMP, from the forebrain protects against pathology and memory deficits, by crossing conditional knockout mice with Alzheimer's transgenic mouse models.
Colin Combs
University of North Dakota, ND·Neuroscience
Define oral health across age and disease stage in AppNL-G-F Alzheimer's model mice, including the oral microbiome, enamel thinning and cavities.
The school
University of California-San Diego: 84 labs on PI Pages, $1.9B a year on research, 637 research doctorates a year.
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