Polymorphism of the brain‐derived neurotrophic factor gene and performance on a cognitive prefrontal test in bipolar patients

Rybakowski, Janusz; Borkowska, Alina; Czerski, Piotr M.; Skibińska, Maria; Hauser, Joanna

doi:10.1046/j.1399-5618.2003.00071.x

Cited by 166 publications

(139 citation statements)

References 21 publications

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“…This study extends and investigates this phenomenon in a within-person, longitudinal framework. Our main result replicates and extends results from a number of between-person cross-sectional studies showing that Met allele carriers have lower episodic memory performance (Dempster et al, 2005;Echeverria et al, 2005;Egan et al, 2003;Hariri et al, 2003;Li et al, 2010;Miyajima et al, 2008;Tan et al, 2005), delayed recall (Miyajima et al, 2008), working memory (Echeverria et al, 2005;Rybakowski et al, 2003;Rybakowski et al, 2006), general intelligence (Tsai et al, 2004), and perceptual speed (Miyajima et al, 2008;Raz et al, 2009) compared with Val/Val homozygotes. In contrast to this earlier work, the present study examined genetic effects on individual differences in withinperson cognitive decline (by analyzing how individuals change across time as they age, rather than analyzing how individuals of different ages are different at a given time point).…”

Section: Discussionsupporting

confidence: 88%

The Val/Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene predicts decline in perceptual speed in older adults.

Ghisletta¹,

Bäckman²,

Bertram³

et al. 2014

Psychology and Aging

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The brain-derived neurotrophic factor (BDNF) promotes activity-dependent synaptic plasticity, and contributes to learning and memory. We investigated whether a common Val66Met missense polymorphism (rs6265) of the BDNF gene is associated with individual differences in cognitive decline (marked by perceptual speed) in old age. A total of 376 participants of the Berlin Aging Study, with a mean age of 83.9 years at first occasion, were assessed longitudinally up to 11 times across more than 13 years on the Digit-Letter task. Met carriers (n ϭ 123, 34%) showed steeper linear decline than Val homozygotes (n ϭ 239, 66%); the corresponding contrast explained 2.20% of the variance in change in the entire sample, and 3.41% after excluding individuals at risk for dementia. These effects were not moderated by sex or socioeconomic status. Results are consistent with the hypothesis that normal aging magnifies the effects of common genetic variation on cognitive functioning. Keywords: cognitive decline, BDNF Val/Met polymorphism, Berlin Aging StudyIn recent years, the field of cognitive aging has enriched its explanatory scope by paying increasing attention to the effects of genetic and epigenetic variation on individual differences in cognitive performance. Two broad approaches can be distinguished

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Section: Discussionsupporting

confidence: 88%

The Val/Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene predicts decline in perceptual speed in older adults.

Ghisletta¹,

Bäckman²,

Bertram³

et al. 2014

Psychology and Aging

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show abstract

“…The difference between BD and healthy subjects is consistent with prior studies (Bearden et al, 2006;Clark et al, 2002;van Gorp et al, 1998), and the results suggesting no difference between the genotypes also support a recent report on CVLT . However, the performance of Val/Met BD patients on the Wisconson Card Sorting Test reportedly is inferior to that of Val/Val BD patients (Rybakowski et al, 2003;Rybakowski et al, 2006). The Wisconsin Card Sorting Test measures working memory and executive functions involving frontal cortex, whereas the CVLT assesses complex cognitive processes and declarative memory involving the hippocampus and frontal regions.…”

Section: Discussionmentioning

confidence: 93%

Neuronal Correlates of Brain-derived Neurotrophic Factor Val66Met Polymorphism and Morphometric Abnormalities in Bipolar Disorder

Matsuo

Walss‐Bass

Nery

et al. 2009

Neuropsychopharmacol

112

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The brain-derived neurotrophic factor (BDNF) Val66Met polymorphism has been proposed as a possible candidate for involvement in the pathophysiology of bipolar disorder (BD). To determine whether an association exists between the BDNF Val66Met genotype and morphometric abnormalities of the brain regions involved in memory and learning in BD and healthy subjects. Forty-two BD patients and 42 healthy subjects were studied. Interactions between BDNF Val66Met genotype and diagnosis in gray (GM) volumes were analyzed using an optimized voxel-based morphometry technique. Declarative memory function was assessed with the California Verbal Learning Test II. Left and right anterior cingulate GM volumes showed a significant interaction between genotype and diagnosis such that anterior cingulate GM volumes were significantly smaller in the Val/Met BD patients compared with the Val/Val BD patients (left P ¼ 0.01, right P ¼ 0.01). Within-group comparisons revealed that the Val/Met carriers showed smaller GM volumes of the dorsolateral prefrontal cortex compared with the Val/Val subjects within the BD patient (P ¼ 0.01) and healthy groups (left P ¼ 0.03, right P ¼ 0.03). The Val/ Met healthy subjects had smaller GM volumes of the left hippocampus compared with the Val/Val healthy subjects (Po0.01). There was a significant main effect of diagnosis on memory function (P ¼ 0.04), but no interaction between diagnosis and genotype was found (P ¼ 0.48). The findings support an association between the BDNF Val66Met genotype and differential gray matter content in brain structures, and suggest that the variation in this gene may play a more prominent role in brain structure differences in subjects affected with BD.

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“…Additionally, the BDNF Met66 substitution has been associated with lower hippocampal NAA in healthy subjects (Egan et al, 2003) and a therapeutic response to atypical antipsychotics in patients with schizophrenia (Hong et al, 2003). In another study, cognitive functioning was significantly better in subjects with Val/Val BDNF genotype compared with Val/Met genotype (Rybakowski et al, 2003). Future studies examining whether the association between olanzapine-induced remission and increases in prefrontal NAA is specific to bipolar youth and whether bipolar youth with the Val66 or Met66 BDNF gene are more likely to respond to olanzapine, might clarify the meaning of these associations.…”

Section: Discussionmentioning

confidence: 96%

Neurochemical Effects of Olanzapine in First-Hospitalization Manic Adolescents: A Proton Magnetic Resonance Spectroscopy Study

DelBello

Cecil

Adler

et al. 2005

Neuropsychopharmacol

115

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We used proton magnetic resonance spectroscopy ( 1 H MRS) to compare the in vivo effects of olanzapine on prefrontal N-acetylaspartate (NAA) levels in treatment remitters and nonremitters. Secondary aims of this study were to identify neurochemical predictors of successful olanzapine treatment and other neurochemical effects of olanzapine. In all, 20 adolescents admitted for their first hospitalization for bipolar disorder, type I, manic or mixed and 10 demographically matched healthy subjects were recruited. Manic adolescents were treated with olanzapine monotherapy and scanned at three time points (N ¼ 19). Medial and left and right lateral ventral prefrontal NAA, choline, creatine/phosphocreatine, myo-inositol, and glutamate/glutamine were measured at baseline, prior to receiving medication, and on days 7 and 28 of treatment. Healthy subjects did not receive medication but underwent 1 H MRS scans at the same time points to assess for normal variability in metabolites over time. Although there was no overall increase in NAA in manic adolescents following 28 days of treatment with olanzapine, olanzapine remitters (N ¼ 11, 58%) exhibited a greater increase in medial ventral prefrontal NAA compared with nonremitters (N ¼ 8, 42%, p ¼ 0.006). Specifically, from baseline to end point, NAA levels decreased in nonremitters (p ¼ 0.03) and increased in remitters (p ¼ 0.05). Manic adolescents treated with olanzapine had an increase from baseline to day 7 in medial (p ¼ 0.002) and right lateral (p ¼ 0.02) ventral prefrontal choline. Baseline medial ventral prefrontal choline was greater in olanzapine remitters than in nonremitters (p ¼ 0.001). Successful treatment of mania with olanzapine may lead to increased ventral prefrontal neuronal viability and/or function as compared to unsuccessful treatment with olanzapine. Additionally, olanzapine-induced increases in choline may lead to alteration of abnormalities in cell membrane metabolism or second messenger pathways that are thought to be involved in the pathophysiology of bipolar disorder.

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Polymorphism of the brain‐derived neurotrophic factor gene and performance on a cognitive prefrontal test in bipolar patients

Abstract: The results suggest a role of BDNF in prefrontal cognitive function in bipolar illness. The tests of prefrontal cognition may be considered as endophenotypic markers in bipolar illness.

Cited by 166 publications

References 21 publications

The Val/Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene predicts decline in perceptual speed in older adults.

The Val/Met polymorphism of the brain-derived neurotrophic factor (BDNF) gene predicts decline in perceptual speed in older adults.

Neuronal Correlates of Brain-derived Neurotrophic Factor Val66Met Polymorphism and Morphometric Abnormalities in Bipolar Disorder

Neurochemical Effects of Olanzapine in First-Hospitalization Manic Adolescents: A Proton Magnetic Resonance Spectroscopy Study

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