Balaji Krishnan
University of Texas Medical Branch at Galveston, TX·Neuroscience
Alzheimer's disease (AD) is a leading cause of death that cannot yet be prevented, cured or even slowed. Memory loss in AD and related dementias (ADRD) begins with early damage at synapses, the junctions where neurons communicate.
- Fields
Neuroscience
Pharmacology
Biochemistry
- Topics
Alzheimer's disease
dementia
phospholipase D1
- Grants
- 1 known grant, through Mar 2027
What they work on
- Test how elevated levels and signaling of phospholipase D1 (PLD1), a lipid-cleaving enzyme, at synapses contribute to synaptic dysfunction and memory deficits in Alzheimer's disease and related dementias.
- Evaluate the contribution of elevated PLD1 to synaptic dysfunction and memory loss in preclinical mouse models, and identify the signaling partners involved.
- Explore whether a well-tolerated small-molecule PLD1 inhibitor can prevent memory deficits associated with dementia progression.
More about the research
What triggers this early synaptic failure remains unclear, and this gap has held back treatment.
Why it matters
Stopping synaptic damage early could keep memory problems from progressing in Alzheimer's disease and related dementias. By establishing PLD1 and its partners as drivers of synaptic vulnerability, this work could point to a new drug target. Small-molecule PLD1 inhibitors could eventually lead to therapies that preserve memory and quality of life for patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Glenn Smith
University of Florida, FL·Medicine & Clinical Research
Complete 230 planned longitudinal follow-up visits with harmonized assessments across 1Florida ADRC sites and provide the data to the National Alzheimer's Coordinating Center (NACC).
David Weinshenker
Emory University, GA·Neuroscience
Determine how neuromelanin, a pigment in norepinephrine neurons, affects locus coeruleus survival in mice, using a viral vector expressing human tyrosinase (hTyr) to make these neurons produce neuromelanin.
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.
The school
University of Texas Medical Branch at Galveston: 14 labs on PI Pages, $241M a year on research, 141 research doctorates a year.
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