Brain-derived neurotrophic factor

Laske, Christoph; Eschweiler, Gerhard W.

doi:10.1007/s00115-005-1971-0

Cited by 35 publications

(7 citation statements)

References 111 publications

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“…In our recent study we demonstrated implication of genetic variation of brain-derived neurotropic factor, modulators of brain plasticity in cognitive processes [15] , in pathogenesis of schizophrenia [12] . Other important members of neurotrophin family are nerve growth factor (NGF) and its receptor (NGFR), the essential mediators of synaptic and morphological plasticity, neuronal growth, survival, and differentiation, especially in the developing brain [18] , [22] .…”

Section: Introductionmentioning

confidence: 95%

“…Promising studies suggest that defects in synaptic plasticity detected in schizophrenia [9] may be linked to neurodevelopmental and neurodegenerative abnormalities [10] , [11] , [12] , [13] and contribute to cognitive impairment associated with this disease [14] , [15] , [16] , [17] . Therefore, study of synaptic plasticity regulatory genes in schizophrenia represents a special interest, as it can provide insight into molecular mechanisms of schizophrenia-associated cognitive dysfunction and sufficiently contribute to development of target-oriented therapy for this disorder.…”

Section: Introductionmentioning

confidence: 99%

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Nerve growth factor and its receptor in schizophrenia

et al. 2014

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Promising studies suggest that defects in synaptic plasticity detected in schizophrenia may be linked to neurodevelopmental and neurodegenerative abnormalities and contribute to disease-associated cognitive impairment. We aimed to clarify the role of the synaptic plasticity regulatory proteins, nerve growth factor (NGF) and its receptor (NGFR) in the pathogenesis of schizophrenia by comparative analysis of their blood levels and functional single nucleotide polymorphisms (SNPs) in genes encoding these proteins (NGF and NGFR) in schizophrenia-affected and healthy subjects. Relationships between the selected SNPs' genotypes and NGF and NGFR plasma levels were also assessed. Our results demonstrated a positive association between schizophrenia and the NGF rs6330 as well as the NGFR rs11466155 and rs2072446 SNPs. Also, a negative association between this disorder and NGF rs4839435 as well as NGFR rs734194 was found. In both, haloperidol-treated and antipsychotic-free patients decreased blood levels of the NGF and NGFR were found, and a positive interrelation between rs6330 and rs2072446 carriage and decreased NGF and NGFR levels, respectively, was revealed. In conclusion, our results demonstrate association of schizophrenia with the rs6330, rs4839435 and rs734194, rs11466155, rs2072446 as well as with the decreased blood levels of corresponding proteins. Our findings indicate the implication of alterations in NGFR and NGFR genes in schizophrenia, particularly, in defects of synaptic plasticity. Furthermore, the data obtained suggests that at least in Armenian population the NGF rs6330*T and NGFR rs11466155*T, rs2072446*T alleles might be nominated as risk factors, whereas the NGF rs4839435*A and NGFR rs734194*G alleles might be protective against developing schizophrenia.

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Section: Introductionmentioning

confidence: 95%

Section: Introductionmentioning

confidence: 99%

Nerve growth factor and its receptor in schizophrenia

et al. 2014

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“…It is essential for cell growth, synaptic connectivity, and neuronal repair and survival [5]. BDNF is abundant in the brain and periphery.…”

Section: Introductionmentioning

confidence: 99%

Electroconvulsive Therapy Improves Clinical Manifestation with Plasma BDNF Levels Unchanged in Treatment-Resistant Depression Patients

Lin

Chen

Lee³

et al. 2013

Neuropsychobiology

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Electroconvulsive therapy (ECT) is the most effective treatment in treatment-resistant depression; it may modulate intracellular processes in such patients. This study aimed to investigate the association between changes in plasma brain-derived neurotrophic factor (BDNF) levels and the clinical improvements after ECT for patients with treatment-resistant depression. Fifty-five inpatients with treatment-resistant depression were recruited. The severity of depression was measured using the 17-item Hamilton Rating Scale for Depression (HAMD-17) and the Clinical Global Impression-Severity (CGI-S) before ECT, after every 3 sessions of ECT, and at the end of ECT. Plasma BDNF levels were measured in all subjects before and after ECT. The severity of depression was significantly reduced on the HAMD-17 (p < 0.001) and the CGI-S (p < 0.001) after the end of ECT. There were no significant differences in plasma BDNF levels after ECT (p = 0.615). No significant correlation was found between changes in plasma BDNF levels and changes in HAMD-17 scores (r = 0.188, p = 0.169). Our results do not support the hypothesis that improvements in treatment-resistant depression patients after ECT are due to changes in BDNF levels.

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“…In addition, BDNF has been suggested to play a mediating role in schizophrenia ( Sokoloff et al, 2004 ; Guillin et al, 2007 ). Thus, several studies indicate an increase of the BDNF levels and gene expression in patients with schizophrenia ( Laske and Eschweiler, 2006 ). In conclusion, an intermittent normobaric hypoxia regimen that successfully increases the BDNF levels may offer a non-pharmacological treatment to patients with schizophrenia.…”

Section: Discussionmentioning

confidence: 99%

Daily Intermittent Normobaric Hypoxia Over 2 Weeks Reduces BDNF Plasma Levels in Young Adults – A Randomized Controlled Feasibility Study

et al. 2018

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Background: The results from animal and human research indicate that acute intermittent hypoxia can enhance brain-derived neurotrophic factor (BDNF) plasma levels and gene expression. As BDNF is known to promote the differentiation of new neurons and the formation of synapses, it has been proposed to mediate adult neuroplasticity. Thus, the present study aimed to analyze the long-term effects of daily intermittent exposure to normobaric hypoxia (simulating high altitude exposure at approximately 4000–5000 m) over 2 weeks on BDNF levels in young adults.Methods: Twenty-eight young adults (age: 19–33 years) were randomized into a hypoxic intervention group (N = 14) or the control group (N = 14). Participants in the intervention group breathed intermittent normobaric hypoxic air at resting conditions (5 min intervals, 80–85% SpO2 measured via a finger pulse oximeter, 12 sessions for 60 min/day for 2 weeks) via a hypoxic generator. BDNF plasma and serum levels were determined at baseline and at 2 weeks after intervention using sandwich ELISAs.Results: After 2 weeks of daily intermittent hypoxic treatment (IHT), we found a significant group x time interaction effect for BDNF plasma levels based on a significant decrease in BDNF levels in the hypoxia group.Conclusion: Our results demonstrate that daily intermittent administration of hypoxic air has a significant effect on BDNF regulation in healthy young adults. Contrary to other results reporting an increase in BDNF levels under hypoxic conditions, the present data suggest that hypoxic treatment using intensive IHT can reduce BDNF plasma levels for at least 2 weeks. This finding indicates that the daily application of hypoxic air is too frequent for the aimed physiological response, namely, an increase in BDNF levels.

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Brain-derived neurotrophic factor

Cited by 35 publications

References 111 publications

Nerve growth factor and its receptor in schizophrenia

Nerve growth factor and its receptor in schizophrenia

Electroconvulsive Therapy Improves Clinical Manifestation with Plasma BDNF Levels Unchanged in Treatment-Resistant Depression Patients

Daily Intermittent Normobaric Hypoxia Over 2 Weeks Reduces BDNF Plasma Levels in Young Adults – A Randomized Controlled Feasibility Study

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