Maria Galazo
Tulane University of Louisiana, LA·Neuroscience
No treatment currently restores brain circuits once their neurons are lost. When disease or injury kills neurons, the connections they carried are gone, and the resulting motor and cognitive problems are permanent.
- Fields
Neuroscience
Genetics
Biology
- Topics
direct reprogramming
neuronal identity
cerebral cortex
- Grants
- 1 known grant, through Jun 2027
What they work on
- Test whether manipulating identity-maintenance mechanisms can reprogram corticothalamic neurons, which project to the thalamus, into functional subcerebral projection neurons that send axons to the brainstem and spinal cord in the living mouse brain.
- Determine whether these identity-maintenance mechanisms can be inactivated in already-mature corticothalamic neurons, removing the barriers that normally prevent their conversion into subcerebral projection neurons.
- Elucidate the downstream molecular signals that block conversion of corticothalamic neurons into subcerebral projection neurons in vivo, defining the barriers to functional conversion between neuron subtypes.
- Assess whether reprogrammed neurons acquire the connectivity of their target subtype, including the long-range projections typical of subcerebral neurons that degenerate in amyotrophic lateral sclerosis.
More about the research
One promising strategy is direct reprogramming: converting another cell into a replacement neuron inside the living brain. The catch is precision. A repaired circuit needs neurons that match the ones it lost, including the long axons they sent to specific distant targets. In the mouse cerebral cortex, such precise conversion has been achieved between cortical output neurons, which send signals out of the cortex, but only when reprogramming is started in embryos or in immature neurons. In mature, fully differentiated neurons it fails. Why mature neurons lock in their identity, and what that lock is made of, is not understood. This project investigates the mechanisms that maintain neuron subtype identity throughout life and asks how they shut the door on reprogramming over time.
Why it matters
Patients with amyotrophic lateral sclerosis lose the cortical neurons that drive movement, and spinal cord injury severs their axons; in both cases the circuitry cannot currently be rebuilt. Identifying what locks a mature neuron into its identity could show how to lift that lock deliberately and generate replacement neurons with the right connections inside the brain, a prerequisite for any reprogramming-based repair strategy. More immediately, the work would explain how neurons keep a stable identity for a lifetime.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Anna La Torre
University of California-Davis, CA·Neuroscience
Map how microRNA expression and the messenger RNAs they target change over time in cortical radial glial progenitors, using miR-eCLIP to capture miRNA–target pairs.
Karunesh Ganguly
University of California-San Francisco, CA·Neuroscience
Compare two neural decoding methods for their ability to give paralyzed patients stable, plug-and-play control of a robotic arm and hand with ECoG for at least 8 weeks without recalibration.
Zuoshang Xu
University of Massachusetts Chan Medical School, MA·Neuroscience
Map which spinal cord proteins are citrullinated and how this changes across disease stages, using proteomics in SOD1 G93A and PFN1 C71G ALS mouse models.
The school
Tulane University of Louisiana: 17 labs on PI Pages, $276M a year on research, 187 research doctorates a year.
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