The 196G/A (val66met) polymorphism of the BDNF gene is significantly associated with binge eating behavior in women with bulimia nervosa or binge eating disorder

Monteleone, Palmiero; Zanardini, Roberta; Tortorella, Alfonso; Gennarelli, Massimo; Castaldo, Eloisa; Canestrelli, Benedetta; Maj, Mario

doi:10.1016/j.neulet.2006.07.040

Cited by 59 publications

(44 citation statements)

References 17 publications

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“…BDNF polymorphisms have been linked to eating disorders in humans (Koizumi et al, 2004;Monteleone et al, 2006;Mercader et al, 2007) and the human phenotype of FASD is remarkably similar to that described for BDNF haplodeficient mice. Therefore, BDNF is involved in neuronal systems that regulate multiple aspects of alcoholism and alcohol use disorders.…”

Section: Bdnf-trkb Polymorphisms In Humans: Depression Anxiety and Amentioning

confidence: 52%

Ethanol–BDNF interactions: Still more questions than answers

Davis

2008

Pharmacology & Therapeutics

127

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Brain Derived Neurotrophic Factor (BDNF) has emerged as a regulator of development, plasticity and, recently, addiction. Decreased neurotrophic activity may be involved in ethanol-induced neurodegeneration in the adult brain and in the etiology of alcohol-related neurodevelopmental disorders. This can occur through decreased expression of BDNF or through inability of the receptor to transduce signals in the presence of ethanol. In contrast, recent studies implicate region-specific up-regulation of BDNF and associated signaling pathways in anxiety, addiction and homeostasis after ethanol exposure. Anxiety and depression are precipitating factors for substance abuse and these disorders also involve region-specific changes in BDNF in both pathogenesis and response to pharmacotherapy. Polymorphisms in the genes coding for BDNF and its receptor TrkB are linked to affective, substance abuse and appetitive disorders and therefore may play a role in the development of alcoholism. This review summarizes historical and pre-clinical data on BDNF and TrkB as it relates to ethanol toxicity and addiction. Many unresolved questions about region-specific changes in BDNF expression and the precise role of BDNF in neuropsychiatric disorders and addiction remain to be elucidated. Resolution of these questions will require significant integration of the literature on addiction and comorbid psychiatric disorders that contribute to the development of alcoholism.

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Section: Bdnf-trkb Polymorphisms In Humans: Depression Anxiety and Amentioning

confidence: 52%

Ethanol–BDNF interactions: Still more questions than answers

Davis

2008

Pharmacology & Therapeutics

127

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“…Entire screening of the NTRK2 gene in eating disorder patients has revealed a strong association between certain haplotypes and ANB but failed to support the participation of epistatic effects between BDNF and NTRK2 in the risk to develop eating disorders (Ribases et al, 2005a). A recent study suggested that, while the 196G/A SNP of the human BDNF gene did not contribute to the genetic susceptibility to bulimia nervosa and binge eating disorder in their population, it may predispose these patients to a more severe binge eating behavior (Monteleone et al, 2006b). Implication of the Val66Met substitution in the pathophysiology of eating disorders remains unclear but this polymorphism has been shown to alter the intracellular trafficking and the regulated secretion of the mature BDNF (Lu, 2003).…”

Section: Discussionmentioning

confidence: 98%

Family trios analysis of common polymorphisms in the obestatin/ghrelin, BDNF and AGRP genes in patients with Anorexia nervosa: Association with subtype, body-mass index, severity and age of onset

Dardennes

Zizzari

Tolle

et al. 2007

Psychoneuroendocrinology

111

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“…BDNF levels were determined by ELISA method using the BDNF Emax Immunoassay System kit (Promega) according to manufacturer's instructions (Monteleone et al 2004(Monteleone et al , 2006. The lower detection limit was 7 .…”

Section: Bdnf Levelsmentioning

confidence: 99%

Enhanced brain performance in mice following postnatal stress

Loizzo

Spampinato

Campana

et al. 2012

Journal of Endocrinology

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The double postnatal stress model (brief maternal separation plus sham injection daily applied from birth to weaning) induces metabolic alterations similar to type 2 diabetes in young-adult male mice. We verify whether 1) the stress also induces brain metabolic-functional alterations connected to diabetes and 2) different alterations are modulated selectively by two stress-damaged endogenous systems (opioid-and/or ACTH-corticosteroid-linked). Here, diabetes-like metabolic plus neurophysiologicneurometabolic parameters are studied in adult mice following postnatal stress and drug treatment. Surprisingly, together with 'classic' diabetes-like alterations, the stress model induces in young-adult mice significantly enhanced brain neurometabolic-neurophysiologic performances, consisting of decreased latency to flash-visual evoked potentials (Kw8%); increased level (Cw40%) and reduced latency (Kw30%) of NAD(P)H autofluorescence postsynaptic signals following electric stimuli; enhanced passive avoidance learning (Cw135% latency); and enhanced brain-derived neurotrophic factor level (Cw70%). Postnatal treatment with the opioid receptor antagonist naloxone prevents some alterations, moreover the treatment with antisense (AS; AS vs proopiomelanocortin mRNA) draws all parameters to control levels, thus showing that some alterations are bound to endogenous opioid-system hyper-functioning, while others depend on ACTHcorticosterone system hyper-functioning. Our stress model induces diabetes-like metabolic alterations coupled to enhanced brain neurometabolic-neurophysiologic performances. Taken all together, these findings are compatible with an 'enduring acute-stress' reaction, which puts mice in favorable survival situations vs controls. However, prolonged hormonal-metabolic imbalances are expected to also produce diabetes-like complications at later ages in stressed mice.

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The 196G/A (val66met) polymorphism of the BDNF gene is significantly associated with binge eating behavior in women with bulimia nervosa or binge eating disorder

Cited by 59 publications

References 17 publications

Ethanol–BDNF interactions: Still more questions than answers

Ethanol–BDNF interactions: Still more questions than answers

Family trios analysis of common polymorphisms in the obestatin/ghrelin, BDNF and AGRP genes in patients with Anorexia nervosa: Association with subtype, body-mass index, severity and age of onset

Enhanced brain performance in mice following postnatal stress

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