Puneet Opal on Muck Rack

Puneet Opal

Chicago
As seen in: TIME, USA Today, Wiley Online Library, The Atlantic, U.S. News and World Report, JAMA (The Journal of the American Medical Association), Cell Press, Money, JoVE- Journal of Visualized Experiments, The Journal of Clinical Investigation
Neurologist, Scientist, Writer
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Articles

Beyond neuronal degeneration: oligodendroglial dysfunction as a driver of spinocerebellar ataxia type 1 pathogenesis

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By Puneet Opal, Changwoo Lee, Rosalie M Grijalva
| The Journal of Clinical Investigation
Neurodegenerative diseases have historically been viewed as disorders of neuronal dysfunction and cell loss, with glial alterations often considered secondary or reactive phenomena despite their frequent presence in affected tissue. In spinocerebellar ataxia type 1 (SCA1), disease pathogenesis has similarly centered on degeneration of Purkinje cells, the principal projection neurons of the cerebellar cortex coordinating cerebellar output and motor function.
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The cerebellum in epilepsy

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By Christopher P. Elder, Rebecca Kerestes, Puneet Opal, Maria Raffaella Marchese
| Wiley Online Library Verified
Neurogenetic disorders, antiseizure medications, and seizures can impair cerebellar functions, causing sensorimotor, cognitive and affective disorders. Chronic epilepsy can impair cerebellar functions, with maximal involvement in posterior non-motor lobules, which may contribute to epilepsy progression and treatment resistance. Low grade cerebellar lesions can cause hemifacial motor seizures in early life, which respond to lesion resection, not antiseizure medications.
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Bridging the gap: insights into sensorimotor deficits in NMDA receptor antibody encephalitis

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By Puneet Opal, Geoffrey T. Swanson, Jing Zhou, Michael Wilson
| The Journal of Clinical Investigation
Abstract N-methyl-d-aspartate (NMDA) receptor–mediated autoimmune encephalitis (NMDAR-AE) is the most common cause of autoimmune encephalitis, especially in children and young adults. The disorder is caused by antibodies directed against the GluN1 protein, an obligatory constituent of NMDA receptors, which are key signaling molecules in brain development, learning and memory, and executive function. The manuscript by Zhou et al.
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