BDNF Gene Polymorphism, Cognition and Symptom Severity in a Brazilian Population-Based Sample of First-Episode Psychosis Subjects

Martinho, Eduardo; Michelon, Leandro; Ayres, Adriana M.; Scazufca, Márcia; Menezes, Paulo Rossi; Schaufelberger, Maristela S.; Murray, Robin M.; Rushe, Teresa; Vallada, Homero; Busatto, Geraldo F.

doi:10.1016/j.rbp.2012.06.004

Cited by 7 publications

(1 citation statement)

References 34 publications

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“…The obvious additional candidates for sources of such between-study heterogeneity are demographic characteristics such as gender, age and phase of illness, ethnicity, physical exercise, cardio-vascular health status and diagnosis (Verhagen et al, 2010; Lu et al, 2012; Martinho et al, 2012; Nagata et al, 2012; Smith et al, 2012). Furthermore, it is possible that the genetic variant may be associated with some intermediate phenotypes, which, in turn, could be related to some but not all of the cognitive phenotypes examined.…”

Section: Clinical Aspects Of Val66metmentioning

confidence: 99%

Toward a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking

et al. 2013

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Brain-derived neurotrophic factor (BDNF) represents promotesa key molecule for the survival and differentiation of specific populations of neurons in the central nervous system. BDNF also regulates plasticity-related processes underlying memory and learning. A common single nucleotide polymorphism (SNP) rs6265 has been identified on the coding sequence of human BDNF located at 11p13. The SNP rs6265 is a single base mutation with an adenine instead of a guanine at position 196 (G196A), resulting in the amino acid substitution Val66Met. This polymorphism only exists in humans and has been associated with a plethora of effects ranging from molecular, cellular and brain structural modifications in association with deficits in social and cognitive functions. To date, the literature on Val66Met polymorphism describes a complex and often conflicting pattern of effects. In this review, we attempt to provide a unifying model of the Val66Met effects. We discuss the clinical evidence of the association between Val66Met and memory deficits, as well as the molecular mechanisms involved including the reduced transport of BDNF mRNA to the dendrites as well as the reduced processing and secretion of BDNF protein through the regulated secretory pathway.

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Section: Clinical Aspects Of Val66metmentioning

confidence: 99%

Toward a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking

et al. 2013

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Impact of brain‐derived neurotrophic factor genetic polymorphism on cognition: A systematic review

Toh

Tan

et al. 2018

Brain and Behavior

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IntroductionBrain‐derived neurotrophic factor (BDNF) has an important role in the neurogenesis and neuroplasticity of the brain. This systematic review was designed to examine the association between BDNF Val66Met (rs6265) polymorphism and four cognitive domains—attention and concentration, executive function, verbal fluency, and memory, respectively.MethodologyPrimary literature search was performed using search engines such as PubMed and Scopus. Observational studies that evaluated the neurocognitive performances in relation to BDNF polymorphism within human subjects were included in this review, while animal studies, overlapping studies, and meta‐analysis were excluded.ResultsForty of 82 reviewed studies (48.8%) reported an association between Val66Met polymorphism and neurocognitive domains. The proportion of the studies showing positive findings in cognitive performances between Val/Val homozygotes and Met carriers was comparable, at 30.5% and 18.3%, respectively. The highest percentage of positive association between Val66Met polymorphism and neurocognition was reported under the memory domain, with 26 of 63 studies (41.3%), followed by 18 of 47 studies (38.3%) under the executive function domain and four of 23 studies (17.4%) under the attention and concentration domain. There were no studies showing an association between Val66Met polymorphism and verbal fluency. In particular, Val/Val homozygotes performed better in tasks related to the memory domain, while Met carriers performed better in terms of executive function, in both healthy individuals and clinical populations.ConclusionWhile numerous studies report an association between Val66Met polymorphism and neurocognitive changes in executive function and memory domains, the effect of Met allele has not been clearly established.

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The role of BDNF and NGF plasma levels in first-episode schizophrenia: A longitudinal study

Martínez-Pinteño

Mezquida

Bioque

et al. 2022

European Neuropsychopharmacology

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BDNF Gene Polymorphism, Cognition and Symptom Severity in a Brazilian Population-Based Sample of First-Episode Psychosis Subjects

Cited by 7 publications

References 34 publications

Toward a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking

Toward a unified biological hypothesis for the BDNF Val66Met-associated memory deficits in humans: a model of impaired dendritic mRNA trafficking

Impact of brain‐derived neurotrophic factor genetic polymorphism on cognition: A systematic review

The role of BDNF and NGF plasma levels in first-episode schizophrenia: A longitudinal study

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