D-serine mitigates cell loss associated with temporal lobe epilepsy

Stephen Beesley, Thomas Sullenberger, Kathryn Crotty, Roshan Ailani, Cameron D’Orio, Kimberly Evans, Emmanuel O. Ogunkunle, Michael G. Roper and Sanjay S. Kumar ()
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Stephen Beesley: Florida State University
Thomas Sullenberger: Florida State University
Kathryn Crotty: Florida State University
Roshan Ailani: Florida State University
Cameron D’Orio: Florida State University
Kimberly Evans: Florida State University
Emmanuel O. Ogunkunle: Florida State University
Michael G. Roper: Florida State University
Sanjay S. Kumar: Florida State University

Nature Communications, 2020, vol. 11, issue 1, 1-13

Abstract: Abstract Temporal lobe epilepsy (TLE) is the most common type of drug-resistant epilepsy in adults, with an unknown etiology. A hallmark of TLE is the characteristic loss of layer 3 neurons in the medial entorhinal area (MEA) that underlies seizure development. One approach to intervention is preventing loss of these neurons through better understanding of underlying pathophysiological mechanisms. Here, we show that both neurons and glia together give rise to the pathology that is mitigated by the amino acid D-serine whose levels are potentially diminished under epileptic conditions. Focal administration of D-serine to the MEA attenuates neuronal loss in this region thereby preventing epileptogenesis in an animal model of TLE. Additionally, treatment with D-serine reduces astrocyte counts in the MEA, alters their reactive status, and attenuates proliferation and/or infiltration of microglia to the region thereby curtailing the deleterious consequences of neuroinflammation. Given the paucity of compounds that reduce hyperexcitability and neuron loss, have anti-inflammatory properties, and are well tolerated by the brain, D-serine, an endogenous amino acid, offers new hope as a therapeutic agent for refractory TLE.

Date: 2020
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DOI: 10.1038/s41467-020-18757-2

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