Glutamate Neurotoxicity in ALS and Epilepsy 

Glutamate plays a crucial role in brain activity as the primary excitatory neurotransmitter in the mammalian central nervous system. However, it could be a profoundly serious endogenous toxin if any disruption happens in its concentration or function. Glutamate dyshomeostatic effects can range from the induction of neuron death to neural circuit modification. This review will cover the research connecting glutamate neurotransmission, the development of amyotrophic lateral sclerosis (ALS), and epilepsy. It will concentrate on the molecular processes that control glutamate concentration and activity, and how these systems are disrupted in ALS and epilepsy. These molecular processes offer molecular targets that could help to develop novel therapeutic agents.

Abbreviations: ADAR2 – Adenosine deaminase acting on RNA 2; ALS – Amyotrophic lateral sclerosis; AMPAR – Amino-3-Hydroxy-5-Methyl-4-Isoxazolepropionic acid receptors; EATT2 – Excitatory amino acid transporter; FMRP – Fragile X mental retardation protein; mGluR – Metabotropic glutamate receptors; NMDA – N-methyl-D-aspartate; TDP-43 –Tar DNA-binding protein 43; TLE – Temporal lobe epilepsy; VGLUT – Vesicular glutamate transporter.

Keywords: Glutamate excitotoxicity; Amyotrophic lateral sclerosis; Epilepsy

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