Hesong Liu
Upstate Medical University, NY·Neuroscience·Early-career
Drugs that clear amyloid β, the sticky protein that forms plaques in Alzheimer's disease (AD), can shrink those plaques. Yet they do little to restore memory.
- Fields
Neuroscience
Pharmacology
- Topics
Alzheimer's disease
serotonin
dorsal raphe nucleus
- Grants
- 1 known grant, through Jun 2028
What they work on
- Record the real-time activity of vCA1-projecting dorsal raphe serotonin neurons, and serotonin release in ventral CA1, during memory learning and recall in mice, using fiber photometry.
- Test whether silencing vCA1-projecting serotonin neurons impairs memory, and whether activating them rescues memory, in APPNL-G-F Alzheimer's model mice and aged mice, using intersectional retrograde chemogenetics.
- Determine how vCA1 neurons carrying the 5-HT2C serotonin receptor contribute to spatial memory, using fiber photometry and chemogenetic control of these neurons.
- Test whether combining aducanumab, which lowers amyloid β, with lorcaserin, a 5-HT2C receptor activator, improves memory in APPNL-G-F mice and aged mice.
More about the research
One reason may be that the brain circuits that support memory are themselves damaged as the disease progresses. Repairing those circuits could work together with plaque removal. This project asks whether a pathway that carries serotonin (5-HT), a chemical messenger, into the hippocampus, the brain's memory hub, is one such circuit and a treatable target.
Why it matters
Patients with Alzheimer's disease and older adults with age-related memory loss currently lack treatments that restore memory. Plaque-clearing drugs such as aducanumab lower amyloid β but bring little cognitive benefit. This work could show whether activating the serotonin 2C receptor, together with amyloid-lowering therapy, offers a new way to treat memory symptoms.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Xiaoting Wu
Icahn School of Medicine at Mount Sinai, NY·Neuroscience
Identify neuromodulatory inputs to ventral CA1 (vCA1), a hippocampal region, that drive positive social memories, using optogenetics in Cre-driver mice, fiber photometry during social interactions, and conditional deletion of neuromodulators.
Jonathan Hommel
University of Texas Medical Branch at Galveston, TX·Neuroscience
Test whether a GABA pathway running from the dorsal raphe nucleus to the nucleus accumbens converges on the ventral pallidum, a reward and motivation center, to control cocaine taking, using transsynaptic tracing to map connections between neurons.
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
Upstate Medical University: 7 labs on PI Pages, $59M a year on research, 23 research doctorates a year.
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