目的评价脑源性神经营养因子(BDFN)基因Val66Met多态性与注意缺陷多动障碍(ADHD)易感性的关系,以期为ADHD的遗传病因学研究提供线索。方法计算机检索CNKI、WanFang、PubMed、EMbase、Web of Science数据库,搜集公开发表的有关BDNF基因Va...目的评价脑源性神经营养因子(BDFN)基因Val66Met多态性与注意缺陷多动障碍(ADHD)易感性的关系,以期为ADHD的遗传病因学研究提供线索。方法计算机检索CNKI、WanFang、PubMed、EMbase、Web of Science数据库,搜集公开发表的有关BDNF基因Val66Met多态性与ADHD易感性相关的病例对照研究,检索时限为建库至2020年4月。由2名研究者独立筛选文献、提取资料并对纳入研究进行质量评价后,采用RevMan 5.3和Stata11.0软件进行Meta分析。结果共纳入9篇文献,8 458例样本(其中病例4 247例,对照4 211例)。分析结果显示,rs6265多态性与注意缺陷多动障碍易感性无关(显性模型:OR=0.96,95%CI:0.87~1.06,P=0.40;隐性模型:OR=1.01,95%CI:0.88~1.15,P=0.92;加性模型:OR=0.95,95%CI:0.85~1.08,P=0.45)。结论脑源性神经营养因子基因Val66Met多态性与注意缺陷多动障碍易感性无关。展开更多
Brain-derived neurotrophic factor is the most prevalent member of the nerve growth factor family.Since its discovery in 1978,this enigmatic molecule has spawned more than 27,000 publications,most of which are focused ...Brain-derived neurotrophic factor is the most prevalent member of the nerve growth factor family.Since its discovery in 1978,this enigmatic molecule has spawned more than 27,000 publications,most of which are focused on neurological disorders.Brain-derived neurotrophic factor is indispensable during embryogenesis and postnatally for the normal development and function of both the central and peripheral nervous systems.It is becoming increasingly clear,however,that brain-derived neurotrophic factor likewise plays crucial roles in a variety of other biological functions independently of sympathetic or parasympathetic involvement.Brain-derived neurotrophic factor is also increasingly recognized as a sophisticated environmental sensor and master coordinator of whole organismal physiology.To that point,we recently found that a common nonsynonymous(Val66→Met)single nucleotide polymorphism in the brain-derived neurotrophic factor gene(rs6265)not only substantially alters basal cardiac transcriptomics in mice but subtly influences heart gene expression and function differentially in males and females.In addition to a short description of recent results from associative neuropsychiatric studies,this review provides an eclectic assortment of research reports that support a modulatory role for rs6265 including and beyond the central nervous system.展开更多
The val66met polymorphism of the bdnf gene, which is associated with compromised brain-derived neurotrophic factor (BDNF) signaling, impaired synaptic plasticity, and impaired learning, may increase one’s susceptibil...The val66met polymorphism of the bdnf gene, which is associated with compromised brain-derived neurotrophic factor (BDNF) signaling, impaired synaptic plasticity, and impaired learning, may increase one’s susceptibility to stress- and anxiety-related disorders. Indeed, previous work has reported greater anxiety-related behaviors and impairments of fear conditioning and extinction in individuals who carry the met allele that results from this polymorphism. Nevertheless, findings in this area of research have been equivocal. Thus, we examined the influence of the val66met polymorphism on fear conditioning, extinction, and extinction memory testing. One hundred and twenty healthy participants completed differential fear conditioning in a fear-potentiated startle paradigm, followed by extinction and extinction memory testing 24 and 48 hr later, respectively. Participants were genotyped for the val66met polymorphism and divided into met allele carriers and non-carriers. Results revealed that, although both met-carriers and non-carriers developed conditioned fear, met-carriers exhibited significantly weaker fear acquisition than non-carriers. This difference persisted throughout extinction and extinction memory testing and, during these last two days of testing, was primarily evident in females. These results are consistent with previous work demonstrating that this polymorphism is associated with impaired amygdala-dependent fear learning and extend such findings by demonstrating that females may be more sensitive to such effects.展开更多
目的:探讨脑源性神经营养因子(BDNF)Val66Met多态性与脑卒中腿部功能障碍患者经颅直流电刺激(transcranial direct current stimulation,t DCS)治疗效果的联系。方法:研究受试者为2021年2月至2023年3月期间因卒中后偏瘫康复治疗而入住...目的:探讨脑源性神经营养因子(BDNF)Val66Met多态性与脑卒中腿部功能障碍患者经颅直流电刺激(transcranial direct current stimulation,t DCS)治疗效果的联系。方法:研究受试者为2021年2月至2023年3月期间因卒中后偏瘫康复治疗而入住本院的住院患者。所有患者接受相同疗程的tDCS治疗。在三个不同阶段采用腿部Fugl-Meyer量表(Fugl-Meyer Assessment,FMA)、改良Barthel指数(modified Barthel index,MBI)对患者的腿部运动功能进行评估:治疗前、治疗后4周和治疗后8周。收集血样用于分析BDNF多态性和检测BDNF、proBDNF水平。结果:在纳入分析的47例患者中,16例具有met等位基因的患者,纳入Val66Met组,其余31例患者纳入Val66Val组。在治疗4周和8周后,Val66Val组的FMA、MBI评分明显高于Val66Met组(P<0.05)。2组FMA、MBI评分在治疗4周后显著高于治疗前(P<0.05),并且在治疗8周后高于治疗4周后(P<0.05)。2组的血清成熟BDNF水平和成熟BDNF水平与总BDNF水平比率显示显著的组-时间交互作用(F(组x时间)=4.62、7.43,P=0.037、0.009)。此外,Val66Val组在tDCS治疗后的血清成熟BDNF水平和成熟BDNF水平与总BDNF水平比率显著高于Val66Met组(P<0.05)。在Val66Val组中,观察到t DCS治疗前后患者血清成熟BDNF水平变化与MBI、FMA评分呈显著正相关(r=0.539、0.585,均P<0.001)。结论:tDCS可显著促进卒中后偏瘫患者腿部运动功能的恢复,且在卒中恢复阶段tDCS对纯合Val66Val携带者的治疗效果优于Val66Met多态性携带者。展开更多
基金supported by a Kentucky INBRE IDeA grant (P20GM103436)(to CLG)a New Investigator Start-up Grant from Ogden College of Science (to CLG)the WKU Ogden College of Science (to CLG)
文摘Brain-derived neurotrophic factor is the most prevalent member of the nerve growth factor family.Since its discovery in 1978,this enigmatic molecule has spawned more than 27,000 publications,most of which are focused on neurological disorders.Brain-derived neurotrophic factor is indispensable during embryogenesis and postnatally for the normal development and function of both the central and peripheral nervous systems.It is becoming increasingly clear,however,that brain-derived neurotrophic factor likewise plays crucial roles in a variety of other biological functions independently of sympathetic or parasympathetic involvement.Brain-derived neurotrophic factor is also increasingly recognized as a sophisticated environmental sensor and master coordinator of whole organismal physiology.To that point,we recently found that a common nonsynonymous(Val66→Met)single nucleotide polymorphism in the brain-derived neurotrophic factor gene(rs6265)not only substantially alters basal cardiac transcriptomics in mice but subtly influences heart gene expression and function differentially in males and females.In addition to a short description of recent results from associative neuropsychiatric studies,this review provides an eclectic assortment of research reports that support a modulatory role for rs6265 including and beyond the central nervous system.
文摘The val66met polymorphism of the bdnf gene, which is associated with compromised brain-derived neurotrophic factor (BDNF) signaling, impaired synaptic plasticity, and impaired learning, may increase one’s susceptibility to stress- and anxiety-related disorders. Indeed, previous work has reported greater anxiety-related behaviors and impairments of fear conditioning and extinction in individuals who carry the met allele that results from this polymorphism. Nevertheless, findings in this area of research have been equivocal. Thus, we examined the influence of the val66met polymorphism on fear conditioning, extinction, and extinction memory testing. One hundred and twenty healthy participants completed differential fear conditioning in a fear-potentiated startle paradigm, followed by extinction and extinction memory testing 24 and 48 hr later, respectively. Participants were genotyped for the val66met polymorphism and divided into met allele carriers and non-carriers. Results revealed that, although both met-carriers and non-carriers developed conditioned fear, met-carriers exhibited significantly weaker fear acquisition than non-carriers. This difference persisted throughout extinction and extinction memory testing and, during these last two days of testing, was primarily evident in females. These results are consistent with previous work demonstrating that this polymorphism is associated with impaired amygdala-dependent fear learning and extend such findings by demonstrating that females may be more sensitive to such effects.
文摘目的:探讨脑源性神经营养因子(BDNF)Val66Met多态性与脑卒中腿部功能障碍患者经颅直流电刺激(transcranial direct current stimulation,t DCS)治疗效果的联系。方法:研究受试者为2021年2月至2023年3月期间因卒中后偏瘫康复治疗而入住本院的住院患者。所有患者接受相同疗程的tDCS治疗。在三个不同阶段采用腿部Fugl-Meyer量表(Fugl-Meyer Assessment,FMA)、改良Barthel指数(modified Barthel index,MBI)对患者的腿部运动功能进行评估:治疗前、治疗后4周和治疗后8周。收集血样用于分析BDNF多态性和检测BDNF、proBDNF水平。结果:在纳入分析的47例患者中,16例具有met等位基因的患者,纳入Val66Met组,其余31例患者纳入Val66Val组。在治疗4周和8周后,Val66Val组的FMA、MBI评分明显高于Val66Met组(P<0.05)。2组FMA、MBI评分在治疗4周后显著高于治疗前(P<0.05),并且在治疗8周后高于治疗4周后(P<0.05)。2组的血清成熟BDNF水平和成熟BDNF水平与总BDNF水平比率显示显著的组-时间交互作用(F(组x时间)=4.62、7.43,P=0.037、0.009)。此外,Val66Val组在tDCS治疗后的血清成熟BDNF水平和成熟BDNF水平与总BDNF水平比率显著高于Val66Met组(P<0.05)。在Val66Val组中,观察到t DCS治疗前后患者血清成熟BDNF水平变化与MBI、FMA评分呈显著正相关(r=0.539、0.585,均P<0.001)。结论:tDCS可显著促进卒中后偏瘫患者腿部运动功能的恢复,且在卒中恢复阶段tDCS对纯合Val66Val携带者的治疗效果优于Val66Met多态性携带者。
