Amal Khalil Kaddoumi
Augusta University, GA·Pharmacology
Alzheimer's disease has no treatment that slows its progression. Neither does cerebral amyloid angiopathy (CAA), a condition that often accompanies it.
- Fields
Pharmacology
Neuroscience
Medicine & Clinical Research
- Topics
Alzheimer's disease
cerebral amyloid angiopathy
amyloid-beta
- Grants
- 1 known grant, through Aug 2027
What they work on
- Compare how well racemic etodolac and its R- and S-forms improve a cell-based blood-brain barrier model with amyloid-β pathology, measuring barrier permeability, Aβ clearance and RNA expression changes across doses.
- Determine R-etodolac's pharmacokinetics and brain disposition, meaning how the drug is absorbed and reaches the brain, to support testing in animals.
- Test whether oral R-etodolac restores barrier integrity, improves learning and memory, and reduces amyloid-β deposits in a transgenic mouse model of cerebral amyloid angiopathy and Alzheimer's disease, using cognitive tasks and gadolinium-contrast MRI.
More about the research
In CAA, a sticky protein fragment called amyloid-β (Aβ) builds up in the brain's blood vessels and damages the blood-brain barrier (BBB). The BBB is the tightly sealed vessel lining that controls what enters the brain. Repairing the barrier could be one way to fight the disease.
Why it matters
R-etodolac lacks the COX2-related side effects of standard anti-inflammatory drugs, so it could be safe for long-term use in older adults. If it repairs the blood-brain barrier and reduces amyloid in mice, it may be repurposed to prevent or slow Alzheimer's disease and cerebral amyloid angiopathy, conditions that also greatly raise healthcare costs.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Akihiko Urayama
University of Texas Health Science Center at Houston, TX·Neuroscience
Determine how chimeric versions of aducanumab and lecanemab are cleared from the brain in Alzheimer's model mice, and why clearance slows with age.
Jonathan Kipnis
Washington University in St Louis, MO·Neuroscience
Determine whether failing meningeal lymphatic vessels speed up the aging of nearby meningeal blood vessels, using imaging, surgical and drug-based methods in aged mice and AD mouse models.
Marina Sirota
University of California-San Francisco, CA·Computer Science
Validate repurposed drugs predicted to reverse neuron and glia disease signatures, using iPSC-derived co-cultures and chronic dosing in 5xFAD and hTAU Alzheimer's mice, and measure amyloid, neuroinflammation and synapse loss.
The school
Augusta University: 11 labs on PI Pages, $166M a year on research, 37 research doctorates a year.
Reach out
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