Biology of Brain-Derived Neurotrophic Factor: Relevance for Disorders of the Central Nervous System

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Developmental Neuroscience".

Deadline for manuscript submissions: closed (20 November 2019) | Viewed by 8820

Special Issue Editor


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Guest Editor
School of Psychology and Public Health, La Trobe University, Bundoora 3086, Australia
Interests: schizophrenia; pharmacology; psychiatry; hippocampus; cardiovascular; blood pressure; dopamine; genetic engineering; heart; hypertension

Special Issue Information

Dear Colleagues,

Clinical, animal model, and molecular studies have shown that the Brain-Derived Neurotrophic Factor (BDNF) plays an important role in brain development, neuroplasticity, and cognition. Deficits in BDNF signalling have been implicated in several neurological and psychiatric disorders, and cumulative research suggests targeting BDNF signalling may be a viable treatment option. Already, it is clear that the mechanisms of action of clinically used drugs, such as antidepressants, may include changes in BDNF signalling. The effects of more directly targeting BDNF receptors are also being studied increasingly. Polymorphisms in the BDNF gene result in differential risk of CNS disorders, and it is possible that stratifying patient populations based on BDNF genetic profiles may enhance treatment success. The role of BDNF in brain function is often sex-specific and depends on the age and developmental stage of the subject.

Recent literature has shown rapid developments in pre-clinical and clinical research into the role of BDNF in the CNS, including the use of novel sophisticated animal models. This Special Issue comprises a series of review and research papers providing both an overview and update of the multi-factorial role of BDNF in the CNS.

Prof. Maarten van den Buuse
Guest Editor

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Keywords

  • BDNF
  • Neuroplasticity
  • Brain development
  • Cognition
  • Depression
  • Estrogen
  • Val66met
  • TrkB

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Published Papers (2 papers)

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Research

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12 pages, 1135 KiB  
Article
7,8-Dihydroxyflavone Enhances Cue-Conditioned Alcohol Reinstatement in Rats
by Samuel J. Hogarth, Elvan Djouma and Maarten van den Buuse
Brain Sci. 2020, 10(5), 270; https://doi.org/10.3390/brainsci10050270 - 1 May 2020
Cited by 5 | Viewed by 3037
Abstract
Alcohol use disorder (AUD) is a detrimental disease that develops through chronic ethanol exposure. Reduced brain-derived neurotrophic factor (BDNF) expression has been associated with AUD and alcohol addiction, however the effects of activation of BDNF signalling in the brain on voluntary alcohol intake [...] Read more.
Alcohol use disorder (AUD) is a detrimental disease that develops through chronic ethanol exposure. Reduced brain-derived neurotrophic factor (BDNF) expression has been associated with AUD and alcohol addiction, however the effects of activation of BDNF signalling in the brain on voluntary alcohol intake reinstatement and relapse are unknown. We therefore trained male and female Sprague Dawley rats in operant chambers to self-administer a 10% ethanol solution. Following baseline acquisition and progressive ratio (PR) analysis, rats were split into drug and vehicle groups during alcohol lever extinction. The animals received two weeks of daily IP injection of either the BDNF receptor, TrkB, agonist, 7,8-dihydroxyflavone (7,8-DHF), or vehicle. During acquisition of alcohol self-administration, males had significantly higher absolute numbers of alcohol-paired lever presses and a higher PR breakpoint. However, after adjusting for body weight, the amount of ethanol was not different between the sexes and the PR breakpoint was higher in females than males. Following extinction, alcohol-primed reinstatement in male rats was not altered by pretreatment with 7,8-DHF when adjusted for body weight. In contrast, in female rats, the weight-adjusted potential amount of ethanol, but not absolute numbers of active lever presses, was significantly enhanced by 7,8-DHF treatment during reinstatement. Analysis of spontaneous locomotor activity in automated photocell cages suggested that the effect of 7,8-DHF was not associated with hyperactivity. These results suggest that stimulation of the TrkB receptor may contribute to reward craving and relapse in AUD, particularly in females. Full article
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16 pages, 344 KiB  
Review
The BDNF Val66Met Polymorphism Modulates Resilience of Neurological Functioning to Brain Ageing and Dementia: A Narrative Review
by Donnamay T. Brown, James C. Vickers, Kimberley E. Stuart, Katerina Cechova and David D. Ward
Brain Sci. 2020, 10(4), 195; https://doi.org/10.3390/brainsci10040195 - 25 Mar 2020
Cited by 31 | Viewed by 5359
Abstract
Brain-derived neurotropic factor (BDNF) is an abundant and multi-function neurotrophin in the brain. It is released following neuronal activity and is believed to be particularly important in strengthening neural networks. A common variation in the BDNF gene, a valine to methionine substitution at [...] Read more.
Brain-derived neurotropic factor (BDNF) is an abundant and multi-function neurotrophin in the brain. It is released following neuronal activity and is believed to be particularly important in strengthening neural networks. A common variation in the BDNF gene, a valine to methionine substitution at codon 66 (Val66Met), has been linked to differential expression of BDNF associated with experience-dependent plasticity. The Met allele has been associated with reduced production of BDNF following neuronal stimulation, which suggests a potential role of this variation with respect to how the nervous system may respond to challenges, such as brain ageing and related neurodegenerative conditions (e.g., dementia and Alzheimer’s disease). The current review examines the potential of the BDNF Val66Met variation to modulate an individual’s susceptibility and trajectory through cognitive changes associated with ageing and dementia. On balance, research to date indicates that the BDNF Met allele at this codon is potentially associated with a detrimental influence on the level of cognitive functioning in older adults and may also impart increased risk of progression to dementia. Furthermore, recent studies also show that this genetic variation may modulate an individual’s response to interventions targeted at building cognitive resilience to conditions that cause dementia. Full article
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