Melissa Borgen
Florida Institute of Technology, FL·Neuroscience
Diseases like Alzheimer's slowly destroy nerve cells, and by the time symptoms appear, much of the damage cannot be undone. Current drugs do not stop this decline.
- Fields
Neuroscience
Genetics
Biology
- Topics
tauopathy
ptl-1
PHR proteins
- Grants
- 1 known grant, through Aug 2027
What they work on
- Map the genetic network linking Tau (ptl-1) and the RPM-1 signaling pathway in neurodegeneration, using genetic analysis in a C. elegans tauopathy model.
- Build a time course of changes in synapses, mitochondria and microtubule dynamics from development through late-stage degeneration in living tauopathy worms.
- Test how the Tau–RPM-1 network alters synaptic, mitochondrial and microtubule changes at key stages of degeneration in C. elegans neurons.
More about the research
One hallmark of several of these diseases is the clumping of Tau, a protein that normally helps keep microtubules (the cell's internal scaffolding tracks) stable. Clumped Tau tracks closely with symptoms. What happens downstream of Tau inside neurons is still poorly understood, and knowing it could reveal early warning signs (biomarkers) and new drug targets.
Why it matters
Dementia affects an estimated 6 million Americans, and existing treatments cannot halt its progression. By identifying the genetic pathway that works downstream of Tau, this work could point to new drug targets and biomarkers for earlier diagnosis of Tau-related neurodegenerative diseases.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Alexandra Byrne
University of Massachusetts Chan Medical School, MA·Neuroscience
Determine how TIR-1/SARM1, a conserved protein that usually drives axon degeneration, instead protects C. elegans neurons from damage caused by excess acetylcholine receptor activity or paraquat-induced oxidative stress.
Francesca Bartolini
Columbia University, NY·Neuroscience
Test whether unrelated CIPN-causing chemotherapy drugs share a mechanism of altering tubulin post-translational modifications early, before neuropathy symptoms appear, using cellular and preclinical models.
Ju Gao
University of Arizona, AZ·Neuroscience
Test whether raising TMEM106B levels, a gene variant linked to dementia risk, impairs mitochondrial shape, membrane potential and respiration and causes damage in cultured cortical neurons.
The school
Florida Institute of Technology: 2 labs on PI Pages, $18M a year on research, 49 research doctorates a year.
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