Sharan Srinivasan
University of Michigan, MI·Neuroscience·Early-career
Spinocerebellar ataxias (SCAs) are inherited brain diseases. Over time they rob people of coordination, clear speech and steady walking, and they lead to early death.
- Fields
Neuroscience
Medicine & Clinical Research
Physiology
- Topics
spinocerebellar ataxia
neurodegeneration
neurodegenerative disease
- Grants
- 1 known grant, through Nov 2029
What they work on
- Test whether exercise improves motor behavior in spinocerebellar ataxia mouse models by correcting abnormal Purkinje neuron firing or through other pathways, using electrophysiology and motor testing.
- Determine how abnormal Purkinje cell firing leads to changes in dendrites, the branches that receive signals, and to eventual neuron degeneration, in mouse models of SCA.
- Use genetic manipulation of disease models, transcriptomics and bioinformatics to define the pathways linking circuit correction to the cells' survival.
More about the research
No approved drug exists for any SCA. Doctors mainly recommend vigorous aerobic exercise, which helps, though no one knows exactly why. A central problem in several common SCAs is that Purkinje cells, the main output neurons of the cerebellum, fire electrical signals abnormally and later die. This project asks whether fixing that faulty firing explains the benefits of exercise, and whether faulty firing drives the cells' decline.
Why it matters
People with spinocerebellar ataxias have no approved treatments. Clarifying how exercise and corrected Purkinje cell firing protect the cerebellum could reveal new therapy targets for these fatal disorders. It could also show whether restoring normal brain-circuit activity is a useful treatment strategy.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Vikram Shakkottai
University of Texas Southwestern Medical Center, TX·Neuroscience
Define how membrane excitability, meaning how easily a neuron fires, relates to inferior olive degeneration in SCA1 knockin mice. Test whether restoring normal excitability prevents the degeneration.
Indira M Raman
Northwestern University, IL·Neuroscience
Determine how the synchrony of inhibitory input from many Purkinje neurons shapes the firing of cerebellar nuclei neurons, using in vitro synaptic studies in mice and larval zebrafish.
Adam Avery
Oakland University, MI·Neuroscience
Define the neuronal interactomes, the full sets of binding partners, of normal and SCA5-mutant L253P β-III-spectrin in Drosophila neurons, using immunoprecipitation coupled to mass spectrometry.
The school
University of Michigan: 124 labs on PI Pages, $2.1B a year on research, 963 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.