Attention-deficit hyperactivity disorder may be associated with decreased central brain-derived neurotrophic factor activity: Clinical, and therapeutic implications

被引:57
作者
Tsai, Shih-Jen [1 ]
机构
[1] Vet Gen Hosp, Dept Psychiat, Taipei 11217, Taiwan
关键词
D O I
10.1016/j.mehy.2006.06.025
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Attention-deficit hyperactivity disorder (ADHD) is a common childhood psychiatric disorder. Despite intensive research efforts, the aetiology of ADHD remains unknown. Current evidence suggests that the aetiology of ADHD is heterogeneous, comprising of multiple factors. Recently, it has been proposed that brain-derived neurotrophic factor (BDNF), a member of the neurotrophic factor family, may be implicated in the pathogenesis of ADHD. This hypothesis is supported by recent genetic studies in ADHD. Drawing on findings from studies into the drugs for ADHD relating to central BDNF expression, hyperactivity in BDNF knockout mice, BDNF effects in midbrain dopaminergic function and the close association between BDNF and the dopamine transporter (an important molecule for ADHD pathogenesis), it is proposed here that decreased central BDNF, particularly in the midbrain region, may play an important role in the pathogenesis ADHD. This hypothesis may have some implications for clinical findings in ADHD (for example, the co-morbidity between ADHD and major depression), and provide a new direction for the development of medication for ADHD treatment. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:896 / 899
页数:4
相关论文
共 38 条
[1]   Zinc in attention-deficit/hyperactivity disorder [J].
Arnold, LE ;
DiSilvestro, RA .
JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY, 2005, 15 (04) :619-627
[2]   Attention-deficit hyperactivity disorder [J].
Biederman, J ;
Faraone, SV .
LANCET, 2005, 366 (9481) :237-248
[3]  
Blochl A, 1996, J BIOL CHEM, V271, P21100
[4]  
Bobb AJ, 2005, AM J MED GENET B, V132B, P109
[5]   Cystamine and cysteamine increase brain levels of BDNF in Huntington disease via HSJ1b and transglutaminase [J].
Borrell-Pagès, M ;
Canals, JM ;
Cordelières, FP ;
Parker, JA ;
Pineda, JR ;
Grange, G ;
Bryson, EA ;
Guillermier, M ;
Hirsch, E ;
Hantraye, P ;
Cheetham, ME ;
Néri, C ;
Alberch, J ;
Brouillet, E ;
Saudou, F ;
Humbert, S .
JOURNAL OF CLINICAL INVESTIGATION, 2006, 116 (05) :1410-1424
[6]  
Duman RS, 1997, ARCH GEN PSYCHIAT, V54, P597
[7]   The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function [J].
Egan, MF ;
Kojima, M ;
Callicott, JH ;
Goldberg, TE ;
Kolachana, BS ;
Bertolino, A ;
Zaitsev, E ;
Gold, B ;
Goldman, D ;
Dean, M ;
Lu, B ;
Weinberger, DR .
CELL, 2003, 112 (02) :257-269
[8]   Corticostriatal brain-derived neurotrophic factor dysregulation in adult rats following prenatal stress [J].
Fumagalli, F ;
Bedogni, F ;
Perez, J ;
Racagni, G ;
Riva, MA .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2004, 20 (05) :1348-1354
[9]   BDNF gene expression is reduced in the frontal cortex of dopamine transporter knockout mice [J].
Fumagalli, F ;
Racagni, G ;
Colombo, E ;
Riva, MA .
MOLECULAR PSYCHIATRY, 2003, 8 (11) :898-899
[10]   Role of serotonin in the paradoxical calming effect of psychostimulants on hyperactivity [J].
Gainetdinov, RR ;
Wetsel, WC ;
Jones, SR ;
Levin, ED ;
Jaber, M ;
Caron, MG .
SCIENCE, 1999, 283 (5400) :397-401