Marina Sirota
University of California-San Francisco, CA·Computer Science
Alzheimer's disease (AD) is a common brain disease with few effective treatments, and it can look very different from one patient to the next. Brain cells such as neurons, support cells and blood-vessel cells each go wrong in their own ways.
- Fields
Computer Science
Neuroscience
Pharmacology
- Topics
Alzheimer's disease
drug repurposing
drug repositioning
- Grants
- 2 known grants, through May 2031
What they work on
- 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.
- Use VINE-seq single-cell signatures of brain blood-vessel cells to find and test drugs that reverse vascular and immune dysfunction in TgAPP23 mice. Endpoints include cerebral amyloid angiopathy, amyloid buildup in vessel walls, and blood-brain barrier integrity.
- Predict drug candidates for Alzheimer's disease with Connectivity Map and LINCS, databases of drug-induced gene expression changes, by matching drugs that reverse cell-type-specific disease patterns.
- Develop software and pipelines to integrate single-cell sequencing, CyTOF and electronic health record data for rheumatic disease studies, and share the data through ImmPort.
More about the research
One faster route to new treatments is drug repurposing, which means finding existing approved or tested drugs that could work against a new disease. Matching drugs to the specific cell types that are failing is one way to do this. More broadly, the lab applies computational analysis of large genomic and clinical datasets to precision medicine, the idea of tailoring prevention and treatment to individual patients. Its work spans Alzheimer's disease and rheumatic diseases, which are autoimmune and inflammatory disorders such as lupus and arthritis.
Why it matters
Patients with Alzheimer's disease have few treatment options. Finding existing drugs that reverse disease-linked gene activity in specific brain cell types could yield therapies that move quickly into clinical trials. Combinations aimed at both nerve-cell damage and blood-vessel damage are also being explored. Separately, shared computational tools could help researchers studying rheumatic diseases apply precision medicine to diagnosis and treatment.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Amal Khalil Kaddoumi
Augusta University, GA·Pharmacology
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.
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.
Ethan Lippmann
Vanderbilt University, TN·Biomedical Engineering
Measure how dose affects gene and protein silencing by siRNA-EG18, an siRNA linked to an albumin-binding fatty acid carrier, in brain myeloid cells after injection into cerebrospinal fluid, targeting the Alzheimer's risk gene Cd33.
The school
University of California-San Francisco: 89 labs on PI Pages, $2.1B a year on research, 164 research doctorates a year.
Reach out
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