Ghanim Ullah
University of South Florida, FL·Neuroscience
The brain runs on rapid, finely balanced exchanges of ions, chemical messengers and energy between neurons and their support cells, the astrocytes. When this balance shifts, during a stroke or just during ordinary signaling, it can change how brain cells communicate and may push the brain toward disease.
- Fields
Neuroscience
Biophysics
- Topics
Alzheimer's disease
amyloid beta
Aβ42
- Grants
- 3 known grants, through Jun 2029
What they work on
- Test whether recurrent metabolic stress and spreading depolarization, a wave of electrical silencing in the brain, promote amyloid β40 and β42 clumping in the space between cells and in endosomes/lysosomes.
- Determine how potassium chloride, sodium chloride, pH and Aβ concentration shape different Aβ40 and Aβ42 aggregate types, using high-resolution imaging, optical spectroscopy and shape-specific antibodies.
- Simulate Aβ aggregation from nanoseconds to months using Markov chain models and kinetic Monte Carlo algorithms, linked to biophysical models of ions, pH, oxygen and neurovascular coupling in neurons and astrocytes.
- Test model predictions in the C. elegans strain JKM7, which expresses human Aβ42, by measuring paralysis and using antibody staining and microscopy.
- Test whether astrocytes control glutamate spillover between synapses by tracking their sodium gradients, which drive glutamate uptake, through quantitative fluorescence imaging, astrocyte manipulations and computer modeling.
More about the research
The lab combines computer models built across many scales of time and space with experiments to understand these dynamics. One project asks how brief chemical crises in the brain could trigger the protein clumping seen in Alzheimer's disease. A second asks how astrocytes control how far a signaling chemical spreads between synapses.
Why it matters
Finding which brain conditions trigger toxic amyloid β clumping could help explain why stroke, traumatic brain injury and migraine raise the risk of Alzheimer's disease. It may point to new therapeutic targets. Models of how astrocytes shape signaling between neurons add basic understanding of brain communication and could support wider computational neuroscience.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Investigating the aggregation of amyloid β during metabolic stress using multiscale modeling
NIH · Sep 2024 – Jun 2029
CRCNS US-German Research Proposal: Quantitative and Computational Dissection of Glutamatergic Crosstalk at Tripartite Synapses
NIH · Feb 2023 – Jan 2027
Investigating the aggregation of amyloid β during metabolic stress using multiscale modeling
NIH · Sep 2024 – Dec 2026
Closest labs
Claude Shuttleworth
University of New Mexico, NM·Neuroscience
Test whether spreading depolarization, a wave of mass electrical silencing in brain tissue, activates protective mechanisms over seconds to minutes, examining diffusible protective factors and metabolic substrate support in brain slices.
Maciej Stawikowski
Florida Atlantic University, FL·Chemistry
Design and synthesize environment-sensitive fluorescent cholesterol probes (CNDs) built on a 1,8-naphthalimide dye, using computational chemistry to tune their properties for different imaging uses.
Jeffrey Nicholas Savas
Northwestern University, IL·Neuroscience
Build a dynamic map of how amyloid beta (Aβ) plaques form and change in the brains of aging Alzheimer's model mice, tracking distinct plaque classes and Aβ forms such as Aβ42 and Aβ38.
The school
University of South Florida: 20 labs on PI Pages, $522M a year on research, 305 research doctorates a year.
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