Association between BDNF Val66Met polymorphism and optic neuritis damage in neuromyelitis optica spectrum disorder

Research output: Contribution to journalArticleResearchpeer-review

Abstract

Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system (CNS). The purpose of the study was to examine the association between the brain-derived neurotrophic factor (BDNF) Val66Met genotype and structural and functional optic nerve damage in the eyes of NMOSD patients. A total of 17 NMOSD subjects (34 eyes) were included in the study and were divided into subgroups based on optic neuritis (ON) history and BDNF Val66Met polymorphisms. The mean (range) age was 47.8 (23–78) years, and the mean (SD) disease duration was 7.4 (2–39) years. All participants had undergone optical coherence tomography (OCT) scans for global retinal nerve fiber layer (gRNFL) and ganglion cell-inner plexiform layer (GCIPL) thickness and multifocal visual evoked potential (mfVEP) test for amplitude and latency. BDNF Val66Met polymorphisms were genotyped in all participants. OCT and mfVEP changes were compared between two genotype groups (Met carriers vs. Val homozygotes) by using the generalised estimating equation (GEE) models. The BDNF Val66Met polymorphism was significantly associated with more severe nerve fiber layer damage and axonal loss in ON eyes of NMOSD subjects. Met carriers had more significantly reduced GCIPL (P = 0.002) and gRNFL (P < 0.001) thickness as well as more delayed mfVEP latency (P = 0.008) in ON eyes. No association was found between Val66Met variants and non-ON (NON)-eye of the participants. These findings suggest that the BDNF Val66Met polymorphism may be associated with optic nerve damage caused by acute ON attacks in NMOSD patients.

LanguageEnglish
Article number1236
Pages1-6
Number of pages6
JournalFrontiers in Neuroscience
Volume13
DOIs
Publication statusPublished - 19 Nov 2019

Fingerprint

Neuromyelitis Optica
Optic Neuritis
Brain-Derived Neurotrophic Factor
Visual Evoked Potentials
Nerve Fibers
Optical Coherence Tomography
Optic Nerve
Ganglia
Genotype
Neuritis
Homozygote
Autoimmune Diseases
Central Nervous System

Bibliographical note

Copyright the Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • BDNF
  • NMOSD
  • optic nerve damage
  • optic neuritis
  • Val66Met

Cite this

@article{658cf2ac7554470f9c50c040351e991c,
title = "Association between BDNF Val66Met polymorphism and optic neuritis damage in neuromyelitis optica spectrum disorder",
abstract = "Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system (CNS). The purpose of the study was to examine the association between the brain-derived neurotrophic factor (BDNF) Val66Met genotype and structural and functional optic nerve damage in the eyes of NMOSD patients. A total of 17 NMOSD subjects (34 eyes) were included in the study and were divided into subgroups based on optic neuritis (ON) history and BDNF Val66Met polymorphisms. The mean (range) age was 47.8 (23–78) years, and the mean (SD) disease duration was 7.4 (2–39) years. All participants had undergone optical coherence tomography (OCT) scans for global retinal nerve fiber layer (gRNFL) and ganglion cell-inner plexiform layer (GCIPL) thickness and multifocal visual evoked potential (mfVEP) test for amplitude and latency. BDNF Val66Met polymorphisms were genotyped in all participants. OCT and mfVEP changes were compared between two genotype groups (Met carriers vs. Val homozygotes) by using the generalised estimating equation (GEE) models. The BDNF Val66Met polymorphism was significantly associated with more severe nerve fiber layer damage and axonal loss in ON eyes of NMOSD subjects. Met carriers had more significantly reduced GCIPL (P = 0.002) and gRNFL (P < 0.001) thickness as well as more delayed mfVEP latency (P = 0.008) in ON eyes. No association was found between Val66Met variants and non-ON (NON)-eye of the participants. These findings suggest that the BDNF Val66Met polymorphism may be associated with optic nerve damage caused by acute ON attacks in NMOSD patients.",
keywords = "BDNF, NMOSD, optic nerve damage, optic neuritis, Val66Met",
author = "Ting Shen and Vivek Gupta and Con Yiannikas and Alexander Klistorner and Graham, {Stuart L.} and Yuyi You",
note = "Copyright the Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.",
year = "2019",
month = "11",
day = "19",
doi = "10.3389/fnins.2019.01236",
language = "English",
volume = "13",
pages = "1--6",
journal = "Frontiers in Neuroscience",
issn = "1662-4548",
publisher = "Frontiers Media S.A.",

}

Association between BDNF Val66Met polymorphism and optic neuritis damage in neuromyelitis optica spectrum disorder. / Shen, Ting; Gupta, Vivek; Yiannikas, Con; Klistorner, Alexander; Graham, Stuart L.; You, Yuyi.

In: Frontiers in Neuroscience, Vol. 13, 1236, 19.11.2019, p. 1-6.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Association between BDNF Val66Met polymorphism and optic neuritis damage in neuromyelitis optica spectrum disorder

AU - Shen, Ting

AU - Gupta, Vivek

AU - Yiannikas, Con

AU - Klistorner, Alexander

AU - Graham, Stuart L.

AU - You, Yuyi

N1 - Copyright the Author(s) 2019. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

PY - 2019/11/19

Y1 - 2019/11/19

N2 - Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system (CNS). The purpose of the study was to examine the association between the brain-derived neurotrophic factor (BDNF) Val66Met genotype and structural and functional optic nerve damage in the eyes of NMOSD patients. A total of 17 NMOSD subjects (34 eyes) were included in the study and were divided into subgroups based on optic neuritis (ON) history and BDNF Val66Met polymorphisms. The mean (range) age was 47.8 (23–78) years, and the mean (SD) disease duration was 7.4 (2–39) years. All participants had undergone optical coherence tomography (OCT) scans for global retinal nerve fiber layer (gRNFL) and ganglion cell-inner plexiform layer (GCIPL) thickness and multifocal visual evoked potential (mfVEP) test for amplitude and latency. BDNF Val66Met polymorphisms were genotyped in all participants. OCT and mfVEP changes were compared between two genotype groups (Met carriers vs. Val homozygotes) by using the generalised estimating equation (GEE) models. The BDNF Val66Met polymorphism was significantly associated with more severe nerve fiber layer damage and axonal loss in ON eyes of NMOSD subjects. Met carriers had more significantly reduced GCIPL (P = 0.002) and gRNFL (P < 0.001) thickness as well as more delayed mfVEP latency (P = 0.008) in ON eyes. No association was found between Val66Met variants and non-ON (NON)-eye of the participants. These findings suggest that the BDNF Val66Met polymorphism may be associated with optic nerve damage caused by acute ON attacks in NMOSD patients.

AB - Neuromyelitis optica spectrum disorder (NMOSD) is an autoimmune inflammatory disease of the central nervous system (CNS). The purpose of the study was to examine the association between the brain-derived neurotrophic factor (BDNF) Val66Met genotype and structural and functional optic nerve damage in the eyes of NMOSD patients. A total of 17 NMOSD subjects (34 eyes) were included in the study and were divided into subgroups based on optic neuritis (ON) history and BDNF Val66Met polymorphisms. The mean (range) age was 47.8 (23–78) years, and the mean (SD) disease duration was 7.4 (2–39) years. All participants had undergone optical coherence tomography (OCT) scans for global retinal nerve fiber layer (gRNFL) and ganglion cell-inner plexiform layer (GCIPL) thickness and multifocal visual evoked potential (mfVEP) test for amplitude and latency. BDNF Val66Met polymorphisms were genotyped in all participants. OCT and mfVEP changes were compared between two genotype groups (Met carriers vs. Val homozygotes) by using the generalised estimating equation (GEE) models. The BDNF Val66Met polymorphism was significantly associated with more severe nerve fiber layer damage and axonal loss in ON eyes of NMOSD subjects. Met carriers had more significantly reduced GCIPL (P = 0.002) and gRNFL (P < 0.001) thickness as well as more delayed mfVEP latency (P = 0.008) in ON eyes. No association was found between Val66Met variants and non-ON (NON)-eye of the participants. These findings suggest that the BDNF Val66Met polymorphism may be associated with optic nerve damage caused by acute ON attacks in NMOSD patients.

KW - BDNF

KW - NMOSD

KW - optic nerve damage

KW - optic neuritis

KW - Val66Met

UR - http://www.scopus.com/inward/record.url?scp=85076689144&partnerID=8YFLogxK

U2 - 10.3389/fnins.2019.01236

DO - 10.3389/fnins.2019.01236

M3 - Article

VL - 13

SP - 1

EP - 6

JO - Frontiers in Neuroscience

T2 - Frontiers in Neuroscience

JF - Frontiers in Neuroscience

SN - 1662-4548

M1 - 1236

ER -