Chiara Scopa
Thomas Jefferson University, PA·Neuroscience
Alzheimer's disease (AD) slowly destroys memory and brain function. Two features drive much of the damage: inflammation in the brain and the death of nerve cells.
- Fields
Neuroscience
Medicine & Clinical Research
Biochemistry
- Topics
Alzheimer's disease
neuroinflammation
neurodegeneration
- Grants
- 1 known grant, through Nov 2026
What they work on
- Generate intrabodies, small antibodies that work inside cells, that bind and neutralize the RNA::DNA hybrids previously found in cerebral organoid models of sporadic and familial Alzheimer's disease.
- Deliver the intrabodies with an AAV vector, a harmless virus that carries genes into cells, and test whether they block cGAS-STING alarm signaling in Alzheimer's brain organoids, using immunofluorescence and western blots.
- Test whether removing RNA::DNA hybrids lowers cleaved caspase-3, a marker of programmed cell death, in organoids, and so interrupts the c-Jun, retrotransposon and STING chain that drives nerve-cell death.
More about the research
A key question is what sets off this harmful inflammation and whether it can be switched off at its source. The team recently found one such trigger. A protein called c-Jun, part of a gene-control complex named AP-1, becomes more abundant. This loosens tightly packed stretches of DNA that hold retrotransposable elements (RTEs), which are 'jumping gene' sequences that can copy themselves. These regions then build up RNA::DNA hybrids, paired strands of RNA and DNA. The hybrids activate cGAS-STING, a cellular alarm system that normally detects stray genetic material. The alarm ends in programmed cell death, marked by cleaved caspase-3, an enzyme that carries out cell suicide. The team reported this chain of events in several AD cell models, including cerebral organoids, which are small lab-grown clusters of human brain tissue.
Why it matters
People with Alzheimer's disease could eventually benefit from treatments that calm brain inflammation and slow nerve-cell loss. If intrabodies that clear RNA::DNA hybrids prove able to quiet the cGAS-STING pathway in human brain organoids, they could serve as a starting point for precision therapies. Such therapies would act on one defined cause of harmful inflammation and may have fewer side effects than broad anti-inflammatory approaches.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Hyejung Won
University of North Carolina at Chapel Hill, NC·Genetics
Develop single-cell massively parallel reporter assays (scMPRA), which combine DNA barcoding with single-cell RNA sequencing, to measure thousands of Alzheimer's-linked regulatory elements in different brain cell types at once.
Christina Pacak
University of Minnesota, MN·Genetics
Optimize the capsid, or virus shell, and the promoter, the DNA switch controlling gene activity, of an AAV vector that delivers the ERCC5 (XPG) gene to improve treatment in Xpg-/- mice.
Mohanish Deshmukh
University of North Carolina at Chapel Hill, NC·Neuroscience
Identify which brain cell types are most affected when miR-29, a microRNA that rises during brain maturation, is reduced in the adult mouse brain, using single-cell RNA sequencing and analysis of dendritic spines and neuron branching.
The school
Thomas Jefferson University: 12 labs on PI Pages, $271M a year on research, 33 research doctorates a year.
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