Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy
Abstract Mesial temporal lobe epilepsy (MTLE) is the most common type of focal epilepsy in adults, and hippocampal sclerosis (HS) is a frequent histopathological feature in patients with MTLE. Pharmacoresistance is present in at least one‐third of patients with MTLE with HS (MTLE+HS). Several hypoth...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
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Wiley
2022-08-01
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| Series: | Epilepsia Open |
| Subjects: | |
| Online Access: | https://doi.org/10.1002/epi4.12536 |
| _version_ | 1818018282396975104 |
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| author | Estela M. Bruxel Amanda M. doCanto Danielle C. F. Bruno Jaqueline C. Geraldis Iscia Lopes‐Cendes |
| author_facet | Estela M. Bruxel Amanda M. doCanto Danielle C. F. Bruno Jaqueline C. Geraldis Iscia Lopes‐Cendes |
| author_sort | Estela M. Bruxel |
| collection | DOAJ |
| description | Abstract Mesial temporal lobe epilepsy (MTLE) is the most common type of focal epilepsy in adults, and hippocampal sclerosis (HS) is a frequent histopathological feature in patients with MTLE. Pharmacoresistance is present in at least one‐third of patients with MTLE with HS (MTLE+HS). Several hypotheses have been proposed to explain the mechanisms of pharmacoresistance in epilepsy, including the effect of genetic and molecular factors. In recent years, the increased knowledge generated by high‐throughput omic technologies has significantly improved the power of molecular genetic studies to discover new mechanisms leading to disease and response to treatment. In this review, we present and discuss the contribution of different omic modalities to understand the basic mechanisms determining pharmacoresistance in patients with MTLE+HS. We provide an overview and a critical discussion of the findings, limitations, new approaches, and future directions of these studies to improve the understanding of pharmacoresistance in MTLE+HS. However, it is important to point out that, as with other complex traits, pharmacoresistance to anti‐seizure medications is likely a multifactorial condition in which gene‐gene and gene‐environment interactions play an important role. Thus, studies using multidimensional approaches are more likely to unravel these intricate biological processes. |
| first_indexed | 2024-04-14T07:37:03Z |
| format | Article |
| id | doaj.art-adb60feb56b54acc842acc7e829ebdb4 |
| institution | Directory Open Access Journal |
| issn | 2470-9239 |
| language | English |
| last_indexed | 2024-04-14T07:37:03Z |
| publishDate | 2022-08-01 |
| publisher | Wiley |
| record_format | Article |
| series | Epilepsia Open |
| spelling | doaj.art-adb60feb56b54acc842acc7e829ebdb42022-12-22T02:05:39ZengWileyEpilepsia Open2470-92392022-08-017S1S94S12010.1002/epi4.12536Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsyEstela M. Bruxel0Amanda M. doCanto1Danielle C. F. Bruno2Jaqueline C. Geraldis3Iscia Lopes‐Cendes4Departments of Translational Medicine School of Medical Sciences University of Campinas (UNICAMP) Campinas BrazilDepartments of Translational Medicine School of Medical Sciences University of Campinas (UNICAMP) Campinas BrazilDepartments of Translational Medicine School of Medical Sciences University of Campinas (UNICAMP) Campinas BrazilDepartments of Translational Medicine School of Medical Sciences University of Campinas (UNICAMP) Campinas BrazilDepartments of Translational Medicine School of Medical Sciences University of Campinas (UNICAMP) Campinas BrazilAbstract Mesial temporal lobe epilepsy (MTLE) is the most common type of focal epilepsy in adults, and hippocampal sclerosis (HS) is a frequent histopathological feature in patients with MTLE. Pharmacoresistance is present in at least one‐third of patients with MTLE with HS (MTLE+HS). Several hypotheses have been proposed to explain the mechanisms of pharmacoresistance in epilepsy, including the effect of genetic and molecular factors. In recent years, the increased knowledge generated by high‐throughput omic technologies has significantly improved the power of molecular genetic studies to discover new mechanisms leading to disease and response to treatment. In this review, we present and discuss the contribution of different omic modalities to understand the basic mechanisms determining pharmacoresistance in patients with MTLE+HS. We provide an overview and a critical discussion of the findings, limitations, new approaches, and future directions of these studies to improve the understanding of pharmacoresistance in MTLE+HS. However, it is important to point out that, as with other complex traits, pharmacoresistance to anti‐seizure medications is likely a multifactorial condition in which gene‐gene and gene‐environment interactions play an important role. Thus, studies using multidimensional approaches are more likely to unravel these intricate biological processes.https://doi.org/10.1002/epi4.12536complex inheritanceepigenomicsmetabolomicsmultifactorial inheritancepharmacogenomicsproteomics |
| spellingShingle | Estela M. Bruxel Amanda M. doCanto Danielle C. F. Bruno Jaqueline C. Geraldis Iscia Lopes‐Cendes Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy Epilepsia Open complex inheritance epigenomics metabolomics multifactorial inheritance pharmacogenomics proteomics |
| title | Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy |
| title_full | Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy |
| title_fullStr | Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy |
| title_full_unstemmed | Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy |
| title_short | Multi‐omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy |
| title_sort | multi omic strategies applied to the study of pharmacoresistance in mesial temporal lobe epilepsy |
| topic | complex inheritance epigenomics metabolomics multifactorial inheritance pharmacogenomics proteomics |
| url | https://doi.org/10.1002/epi4.12536 |
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