Disturbances in selective information processing associated with the BDNF Val66Met polymorphism: Evidence from cognition, the P300 and fronto-hippocampal systems

Schofield, Peter R.; Williams, Leanne M.; Paul, Robert; Gatt, Justine M.; Brown, Kerri J.; Luty, Agnes A.; Cooper, Nicholas; Grieve, Stuart M.; Dobson‐Stone, Carol; Morris, Charlotte; Kuan, S; Gordon, Evian

doi:10.1016/j.biopsycho.2008.09.001

Cited by 117 publications

(137 citation statements)

References 64 publications

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“…The smaller hippocampal volumes in the Val66Met BDNF polymorphism detected in this meta-analysis have been also found in some (Pezawas et al 2004;Matsuo et al 2009;Schofield et al 2009), but not other (Ho et al 2006;Nemoto et al 2006;Joffe et al 2009;Montag et al 2009) studies using voxel-based morphometry. Converging lines of evidence from basic science as well as clinical studies further corroborate the effects of Val66Met BDNF polymorphism on hippocampal volumes.…”

Section: Discussionsupporting

confidence: 69%

Reduced hippocampal volumes in healthy carriers of brain-derived neurotrophic factor Val66Met polymorphism: Meta-analysis

Hájek

Kopeček

Höschl

2011

The World Journal of Biological Psychiatry

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Objectives-Converging evidence suggests that the brain-derived neurotrophic factor (BDNF) gene Val66Met polymorphism affects brain structure. Yet the majority of studies have shown no effect of this polymorphism on hippocampal volumes, perhaps due to small effect size.Methods-We performed a meta-analysis of studies investigating the association between Val66Met BDNF polymorphism and hippocampal volumes in healthy subjects by combining standardized differences between means (SDM) from individual studies using random effect models. Conclusions-Healthy carriers of BDNF gene Val66Met polymorphism show bilateral hippocampal volume reduction. The effect size was small, but the same direction of effect was seen in all meta-analyzed studies. The association with the BDNF gene Val66Met polymorphism makes hippocampal volume a potential candidate for an endophenotype of disorders presenting with reduced hippocampal volumes. Results-Data

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Section: Discussionsupporting

confidence: 69%

Reduced hippocampal volumes in healthy carriers of brain-derived neurotrophic factor Val66Met polymorphism: Meta-analysis

Hájek

Kopeček

Höschl

2011

The World Journal of Biological Psychiatry

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“…52 Met allele carriers show comparatively lower hippocampal gray matter 53,54 and poorer cognitive performance. 2,3,52,54 It has also been shown that, in otherwise healthy individuals with the BDNF Met variant, low emotional stability (higher neuroticism) with higher syndromal depression is associated with lower hippocampal volume. 55 Animal evidence indicates that stress exacerbates the effects of reduced BDNF on both hippocampal networks and autonomic arousal.…”

Section: -51mentioning

confidence: 96%

Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety

et al. 2009

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The Brain Resource International Database and Brain Resource, Sydney, NSW, Australia and San Francisco, CA, USA Individual risk markers for depression and anxiety disorders have been identified but the explicit pathways that link genes and environment to these markers remain unknown. Here we examined the explicit interactions between the brain-derived neurotrophic factor (BDNF) Val66Met gene and early life stress (ELS) exposure in brain (amygdala-hippocampalprefrontal gray matter volume), body (heart rate), temperament and cognition in 374 healthy European volunteers assessed for depression and anxiety symptoms. Brain imaging data were based on a subset of 89 participants. Multiple regression analysis revealed main effects of ELS for body arousal (resting heart rate, P = 0.005) and symptoms (depression and anxiety, P < 0.001) in the absence of main effects for BDNF. In addition, significant BDNF-ELS interactions indicated that BDNF Met carriers exposed to greater ELS have smaller hippocampal and amygdala volumes (P = 0.013), heart rate elevations (P = 0.0002) and a decline in working memory (P = 0.022). Structural equation path modeling was used to determine if this interaction predicts anxiety and depression by mediating effects on the brain, body and cognitive measures. The combination of Met carrier status and exposure to ELS predicted reduced gray matter in hippocampus (P < 0.001), and associated lateral prefrontal cortex (P < 0.001) and, in turn, higher depression (P = 0.005). Higher depression was associated with poorer working memory (P = 0.005), and slowed response speed. The BDNF Met-ELS interaction also predicted elevated neuroticism and higher depression and anxiety by elevations in body arousal (P < 0.001). In contrast, the combination of BDNF V/V genotype and ELS predicted increases in gray matter of the amygdala (P = 0.003) and associated medial prefrontal cortex (P < 0.001), which in turn predicted startle-elicited heart rate variability (P = 0.026) and higher anxiety (P = 0.026). Higher anxiety was linked to verbal memory, and to impulsivity. These effects were specific to the BDNF gene and were not evident for the related 5HTT-LPR polymorphism. Overall, these findings are consistent with the correlation of depression and anxiety, yet suggest that partially differentiated gene-brain cognition pathways to these syndromes can be identified, even in a nonclinical sample. Such findings may aid establishing an evidence base for more tailored intervention strategies.

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“…Further evidence for a genetic basis for abnormal emotional processing in AN is the strong association of AN with the Met allele of the Val66Met (Met66) Brain Derived Neurtrophic Factor (BDNF) polymorphism (Ribases et al, 2003(Ribases et al, , 2005. The variant has been associated with abnormalities in emotionrelated functioning including neuroticism and depressed mood (Gatt et al, 2008;Joffe et al, 2009) and selective processing of emotion or significant stimuli (Schofield et al, 2009). …”

Section: Genesmentioning

confidence: 97%

Anorexia nervosa: Towards an integrative neuroscience model

Hatch

Madden

Kohn

et al. 2010

Euro Eating Disorders Rev

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We reviewed the evidence for emotion-related disturbances in anorexia nervosa (AN) from behavioural, cognitive, biological and genetic domains of study. These domains were brought together within the framework of an integrative neuroscience model that emphasizes the role of emotion and feeling and their regulation, in brain organization. PsychInfo and Medline searches were performed to identify published peer-reviewed papers on AN within each domain. This review revealed evidence for 'Emotion', 'Thinking and Feeling' and 'Self-regulation' disturbances in AN that span non-conscious to conscious processes. An integrative neuroscience framework was then applied to develop a model of AN, from which hypotheses for empirical investigation are generated. We propose that AN reflects a core disturbance in emotion at the earliest time stage of information processing with subsequent effects on the later stages of thinking, feeling and self-regulation.

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Disturbances in selective information processing associated with the BDNF Val66Met polymorphism: Evidence from cognition, the P300 and fronto-hippocampal systems

Cited by 117 publications

References 64 publications

Reduced hippocampal volumes in healthy carriers of brain-derived neurotrophic factor Val66Met polymorphism: Meta-analysis

Reduced hippocampal volumes in healthy carriers of brain-derived neurotrophic factor Val66Met polymorphism: Meta-analysis

Interactions between BDNF Val66Met polymorphism and early life stress predict brain and arousal pathways to syndromal depression and anxiety

Anorexia nervosa: Towards an integrative neuroscience model

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