Krishnan Dhandapani
Augusta University, GA·Neuroscience
Two out of three Americans living with Alzheimer's disease are women, and the risk is higher in women after menopause who have lower blood levels of the hormone 17β-estradiol. Patients treated with drugs that block estrogen production or its receptor, as in some cancer therapies, often report cognitive decline as well.
- Fields
Neuroscience
Pharmacology
Physiology
- Topics
Alzheimer's disease
aromatase
17beta-estradiol
- Grants
- 1 known grant, through Aug 2030
What they work on
- Test whether reducing or inhibiting aromatase, the brain enzyme that makes 17β-estradiol locally, worsens cognitive decline, and whether pulsed photobiomodulation or estradiol prevents both the enzyme's decline and memory deficits in a rat model of Alzheimer's disease.
- Determine whether brain aromatase is required for the benefits of pulsed laser therapy, using forebrain neuron-specific aromatase knockout mice crossed with Alzheimer's disease models to see if light still raises local estradiol and improves cognition.
- Ask whether pulsed photobiomodulation increases synapse and dendritic spine formation through an aromatase/estradiol–irisin–BDNF signaling chain, testing this in TgF344-AD and 3xTg-AD animals and in cultured rat primary neurons exposed to light.
- Examine why aromatase loss affects females more severely, comparing disease progression and cognitive outcomes between sexes in transgenic Alzheimer's models with systemic aromatase inhibition or brain-specific aromatase knockdown.
More about the research
These clues point toward estrogen made locally in the brain. The enzyme that makes it there is aromatase, which converts other hormones into estradiol inside brain cells. This project asks whether losing brain aromatase helps cause Alzheimer's disease, why the effect differs between the sexes, and whether the enzyme can be coaxed back into action with light.
Why it matters
Alzheimer's disease has no proven prevention and falls disproportionately on women, and patients taking aromatase or estrogen-receptor inhibitors frequently experience added cognitive decline. If brain aromatase proves to be a target that pulsed laser light can engage, non-invasive photobiomodulation could be developed as a preventive or add-on treatment for cognitive loss, and the work would help explain why Alzheimer's risk differs between women and men.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
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University of Minnesota, MN·Neuroscience
Test whether spinal estrogen receptor signaling is necessary for respiratory neuroplasticity in female and male rats, using nerve recordings of breathing output with estrogen receptor drugs and siRNA gene knockdown.
Charleen T Chu
University of Pittsburgh, PA·Neuroscience
Test whether loss of PINK1, a mitochondrial enzyme, impairs the transport of mitochondria into dendrites, using molecular genetic manipulations in Pink1-knockout mouse neurons and patient iPSC-derived cortical neurons.
Kim Dore
University of California-San Diego, CA·Neuroscience
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.
The school
Augusta University: 11 labs on PI Pages, $166M a year on research, 37 research doctorates a year.
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