A pilot study of the role of the BDNF Val66Met polymorphism in response to exercise-augmented exposure therapy for posttraumatic stress disorder.

BDNF Exercise Genetic Posttraumatic stress disorder Psychotherapy

Journal

Psychoneuroendocrinology
ISSN: 1873-3360
Titre abrégé: Psychoneuroendocrinology
Pays: England
ID NLM: 7612148

Informations de publication

Date de publication:
21 Jun 2024
Historique:
received: 03 01 2024
revised: 16 06 2024
accepted: 17 06 2024
medline: 30 6 2024
pubmed: 30 6 2024
entrez: 29 6 2024
Statut: aheadofprint

Résumé

Brain-Derived Neurotrophic Factor (BDNF) is implicated in extinction learning, which is a primary mechanism of exposure therapy for posttraumatic stress disorder (PTSD). Brief aerobic exercise has been shown to promote BDNF release and augment extinction learning. On the premise that the Val allele of the BDNF Val66Met polymorphism facilitates greater release of BDNF, this study examined the extent to which the Val allele of the BDNF polymorphism predicted treatment response in PTSD patients who underwent exposure therapy combined with aerobic exercise or passive stretching. PTSD patients (N = 85) provided saliva samples in order to extract genomic DNA to identify Val/Val and Met carriers of the BDNF Val66Met genotype, and were assessed for PTSD severity prior to and following a 9-week course of exposure therapy combined with aerobic exercise or stretching. The sample comprised 52 Val/Val carriers and 33 Met carriers. Patients with the BDNF high-expression Val allele display greater reduction of PTSD symptoms at posttreatment than Met carriers. Hierarchical regression analysis indicated that greater PTSD reduction was specifically observed in Val/Val carriers who received exposure therapy in combination with the aerobic exercise. This finding accords with animal and human evidence that the BDNF Val allele promotes greater extinction learning, and that these individuals may benefit more from exercise-augmented extinction. Although preliminary, this result represents a possible avenue for augmented exposure therapy in patients with the BDNF Val allele.

Identifiants

pubmed: 38943720
pii: S0306-4530(24)00150-1
doi: 10.1016/j.psyneuen.2024.107106
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

107106

Informations de copyright

Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest No conflict

Auteurs

Richard A Bryant (RA)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia; Brain Dynamics Centre, Westmead Institute for Medical Research, Sydney, New South Wales, Australia. Electronic address: r.bryant@unsw.edu.au.

Katie S Dawson (KS)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Suzanna Azevedo (S)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Srishti Yadav (S)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Catherine Cahill (C)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Lucy Kenny (L)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Fiona Maccallum (F)

School of Psychology, University of Queensland, Brisbane, Queensland, Australia.

Jenny Tran (J)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Natasha Rawson (N)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Julia Tockar (J)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Benjamin Garber (B)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Dharani Keyan (D)

School of Psychology, University of New South Wales, Sydney, New South Wales, Australia.

Classifications MeSH