ABC transporters and drug resistance in epilepsy: biological plausibility pharmacogenetics and precision medicine

Riquelme-Alcázar J.; González-Vargas R.; Moya P.R.

Abstract

Introduction. A plausible mechanism that may contribute to drug resistance in epilepsy is the failure of drugs to reach the brain tissue, caused by changes in the activity of ABC transporters. The main argument in favour of this hypothesis is that resistance occurs against a wide variety of antiepileptic drugs with different mechanisms of action, suggesting a nonspecific underlying phenomenon that limits the effectiveness of drug treatments. Development. A review of the literature on ABC transporters, their role in the normal physiology of the blood-brain barrier and drug resistance in epilepsy, both in human studies and in animal models, is conducted. Studies of genetic variants in the ABCB1 and ABCC2 genes, which code for these transporters, and recent genomic studies in epilepsy and related pathologies are also reviewed, followed by a discussion of their scope and limitations. Conclusions. To date, the association of genetic variants of ABC transporters with resistance to anticonvulsant drugs remains a matter of debate. The increasingly widespread use and accessibility of modern sequencing technologies is expected to allow the establishment of genetic markers that provide a precision medicine based approach to the treatment of epilepsy.

Más información

Título según WOS: ABC transporters and drug resistance in epilepsy: biological plausibility pharmacogenetics and precision medicine
Título según SCOPUS: ABC transporters and drug resistance in epilepsy: Biological plausibility, pharmacogenetics and precision medicine [Transportadores ABC y resistencia a fármacos en la epilepsia: plausibilidad biológica, farmacogenética y medicina de precisión]
Título de la Revista: REVISTA DE NEUROLOGIA
Volumen: 70
Número: 1
Editorial: REVISTA DE NEUROLOGIA
Fecha de publicación: 2020
Página de inicio: 23
Página final: 32
Idioma: Spanish
DOI:

10.33588/rn.7001.2019188

Notas: ISI, SCOPUS