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Review
. 2021 Jan 7:13:604158.
doi: 10.3389/fnmol.2020.604158. eCollection 2020.

Neuroproteomics in Epilepsy: What Do We Know so Far?

Amanda M do Canto  1   2 , Amanda Donatti  1   2 , Jaqueline C Geraldis  1   2 , Alexandre B Godoi  1   2 , Douglas C da Rosa  1   2 , Iscia Lopes-Cendes  1   2
Affiliations
Review

Neuroproteomics in Epilepsy: What Do We Know so Far?

Amanda M do Canto et al. Front Mol Neurosci. .

Abstract

Epilepsies are chronic neurological diseases that affect approximately 2% of the world population. In addition to being one of the most frequent neurological disorders, treatment for patients with epilepsy remains a challenge, because a proportion of patients do not respond to the antiseizure medications that are currently available. This results in a severe economic and social burden for patients, families, and the healthcare system. A characteristic common to all forms of epilepsy is the occurrence of epileptic seizures that are caused by abnormal neuronal discharges, leading to a clinical manifestation that is dependent on the affected brain region. It is generally accepted that an imbalance between neuronal excitation and inhibition generates the synchronic electrical activity leading to seizures. However, it is still unclear how a normal neural circuit becomes susceptible to the generation of seizures or how epileptogenesis is induced. Herein, we review the results of recent proteomic studies applied to investigate the underlying mechanisms leading to epilepsies and how these findings may impact research and treatment for these disorders.

Keywords: epileptogenesis; hippocampal sclerosis; malformations of cortical development; mesial temporal lobe epilepsy; proteomics; seizures.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
A schematic of the main epilepsy studies and their divisions, highlighting the complexity of the disease. TLE, temporal lobe epilepsy; MCD, malformations of cortical development; FCD, focal cortical dysplasia; TS, tuberous sclerosis; PILO, pilocarpine model; KA, kainic acid model; PTZ, pentylenetetrazol model; ES, electrical stimulation models; GAERS, genetic absence epilepsy rats from Strasbourg; WAG/Rjj, Wistar Albino Glaxo/Rijswijk rat; BS/Orl and BR/Orl, mouse strains.
Figure 2
Figure 2
(A) The main biological processes associated with epilepsy in human tissue and in tissues from rodent models of the disease. (B) The biological processes present in two types of human epilepsy, namely temporal lobe epilepsy (TLE) and malformations of cortical development. (C) The main biological processes present in studies with different animal models of epilepsy. Pilo, pilocarpine model; KA, kainic acid model; PTZ, pentylenetetrazol model.
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