Association between the BDNF gene and schizophrenia

Muglia, Pierandrea; Vicente, Astrid M.; Verga, M.; King, Nicole; Macciardi, Fabìo; Kennedy, James L.

doi:10.1038/sj.mp.4001221

Cited by 77 publications

(38 citation statements)

References 12 publications

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“…Genetic association studies between polymorphisms of the BDNF gene and schizophrenia are inconclusive, with negative 55-58 and positive 59,60 studies. BDNF polymorphisms have been associated with treatment responsivity 61 and negative symptom severity.…”

Section: Expanding the 'Central Dogma' Do Perkins Et Almentioning

confidence: 99%

Expanding the ‘central dogma’: the regulatory role of nonprotein coding genes and implications for the genetic liability to schizophrenia

2004

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Section: Expanding the 'Central Dogma' Do Perkins Et Almentioning

confidence: 99%

Expanding the ‘central dogma’: the regulatory role of nonprotein coding genes and implications for the genetic liability to schizophrenia

2004

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“…The risk increases with the closeness of the relative but only reaches ϳ50% concordance in monozygotic twins (4), suggesting that environmental risk factors play an important role. Patterns of inheritance are not straightforward or fully understood, and no individual schizophrenia-associated gene has been identified, although there are several well documented susceptibility genes (5)(6)(7)(8). Diagnosis is based purely on subjective clinical symptoms and an interview with diagnosis being confirmed against diagnostic criteria set out in the Diagnostic and Statistical Manual of Mental Disorders, 4th Ed.…”

Section: Molecular and Cellular Proteomics 7: 1204 -1213 2008mentioning

confidence: 99%

Increased α-Defensins as a Blood Marker for Schizophrenia Susceptibility

Craddock

Huang

Jackson

et al. 2008

Molecular & Cellular Proteomics

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Schizophrenia is a severe psychotic illness affecting 1% of the general population. There are no consistent pathological features, and the disorder is defined by a complex symptomatology, which overlaps with other psychiatric illnesses. Diagnosis is based on a clinical interview, relying on the patient meeting criteria according to diagnosis manuals, including Diagnostic and Statistical Manual of Mental Disorders, 4th Ed. and International Statistical Classification of Diseases, 10th Revision. Because of the ambiguous symptoms, the diagnostic process can take many months and often years. Rapid and effective treatment has been shown to impact positively on disease progression and outcome, and it is therefore important to identify disease-associated biomarkers allowing early diagnosis. Reliable biomarkers can be used for the development of diagnostic tests and may also help us understand the underlying pathology of this disorder. In the present study, proteins from anti-CD3 stimulated and unstimulated peripheral blood T cell lysates from 15 minimally medicated and unmedicated patients and 15 age-, sex-, race-, and smoking-matched controls were profiled on cation exchange (CM10) chips using SELDI-TOF. Partial least squares discriminate analysis was used to separate patient and control groups according to the expression of 108 detected peaks, and two peaks of 3,374 and 3,450 Da, corresponding to ␣-defensins based on masses and cationic properties, were found to contribute significantly to the separation of patient and control groups. Reduction of T cell lysates with DTT resulted in a 6-Da shift in the mass of these peaks consistent with the presence of three cysteine bonds in the structure, confirming them as ␣-defensins. Quantification of ␣-defensins in T cell lysates from six patients and 18 healthy controls was carried out by ELISA, which also showed that ␣-defensin levels were significantly increased in patient lysates when com- Schizophrenia is worldwide one of the most severe psychiatric disorders with a prevalence of 1% in the general population. The causes of this devastating disorder are still undetermined, although schizophrenia is widely believed to have a multifactorial etiology with contribution from both heritable and environmental factors. Despite decades of research, we have failed to find consistent pathological features across cases, making laboratory-based diagnosis impossible at the present time. Among the most widely reported findings in schizophrenia are decreased cerebral volume with ventricular enlargement (for a review, see Ref. 1) and a greater prevalence of neurological soft signs (2) as well as hypofrontality (3). There is robust evidence to support a heritable risk to the development of schizophrenia, and individuals with an affected relative have an increased chance of developing schizophrenia. The risk increases with the closeness of the relative but only reaches ϳ50% concordance in monozygotic twins (4), suggesting that environmental risk factors play an important role. Patterns of in...

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“…[20][21][22] In addition, polymorphisms in this gene have relevance for several aspects of the phenomenology of schizophrenia including negative symptoms 23 and treatment responsiveness. 24,25 Moreover, post-mortem studies indicated that BDNF levels are abnormal in patients with schizophrenia [26][27][28] and several studies reported an association between neonatal rat hippocampal lesions and BDNF mRNA.…”

mentioning

confidence: 99%

Brain-derived neurotrophic factor Val66met polymorphism and volume of the hippocampal formation

et al. 2005

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Magnetic resonance (MR) imaging studies have identified hippocampal structural alterations in the pathogenesis of schizophrenia. Brain-derived neurotrophic factor (BDNF) is one of the neurotrophins that is widely expressed in the hippocampal formation and has been implicated in the neurobiology of schizophrenia. Polymorphisms in the BDNF gene may therefore confer risk for schizophrenia through hippocampal pathogenesis and/or making the hippocampus more susceptible to environmental insults. In this study, we investigated whether val66met, a functional and abundant missense polymorphism in the coding region of the BDNF gene, was associated with the volume of the hippocampal formation in 19 patients with first-episode schizophrenia and 25 healthy volunteers. A total of 124 contiguous T1-weighted coronal MR images (slice thickness ¼ 1.5 mm) were acquired through the whole head using a 3D Fast SPGR IR Prep sequence on a 1.5 T GE imaging system. Volumes of the right and left hippocampal formation were measured manually by an operator blind to group status and genotype. All participants were genotyped for the BDNF val66met locus. Mixed model analyses revealed a main effect of BDNF val66met genotype such that in the combined sample of patients and healthy volunteers, val/val homozygotes (N ¼ 27) had larger volumes of the hippocampal formation compared to val/met heterozygotes (N ¼ 17). In separate analyses by group, however, val66met genotype accounted for a greater proportion of the variance in the volume of the hippocampal formation in patients compared to healthy volunteers. These findings implicate genetic involvement of BDNF in variation of human hippocampal volume and suggest that this effect may be greater among patients compared to healthy volunteers. Molecular Psychiatry (2005) 10, 631-636.

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Association between the BDNF gene and schizophrenia

Cited by 77 publications

References 12 publications

Expanding the ‘central dogma’: the regulatory role of nonprotein coding genes and implications for the genetic liability to schizophrenia

Expanding the ‘central dogma’: the regulatory role of nonprotein coding genes and implications for the genetic liability to schizophrenia

Increased α-Defensins as a Blood Marker for Schizophrenia Susceptibility

Brain-derived neurotrophic factor Val66met polymorphism and volume of the hippocampal formation

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