- In the adult brain, BDNF is maintained at high levels of expression and regulates both excitatory and inhibitory synaptic transmission and activity-dependent plasticity.
- The expression of specific BDNF exons can be regulated by epigenetic mechanisms, suggesting that environmental experiences dynamically influence mature BDNFs.
- There are high levels of BDNF in the hippocampus, amygdala, cerebellum, and cerebral cortex.
- Regulation of BDNF modulated by neuronal activity, exercise, antidepressants, stress, and hormones.
- BDNF is synthesized as the precursor, proBDNF, and is stored in dendrites and axons; can undergo cleavage intra- or extracellularly to produce mature BDNF protein.

University of Minnesota - Twin Cities

- BDNF encodes a member of the nerve growth factor family of proteins, otherwise known as brain-derived neurotrophic factor.
- Binding of this protein to its cognate receptor promotes neuronal survival in the adult brain.
   - Influences the growth, maturation (differentiation), and maintenance of these cells. 
- May play a role in the regulation of the stress response and in the biology of mood disorders.

BDNF Gene

Miranda, M., Morici, J. F., Zanoni, M. B., & Bekinschtein, P. (2019). Brain-derived neurotrophic factor: A key molecule for memory in the healthy and the pathological brain. Frontiers in Cellular Neuroscience, 13(363), 1-25, https://doi.org/10.3389/fncel.2019.00363

Brain-derived neurotrophic factor: A key molecule for memory in the healthy and the pathological brain

- HTR1B was repeatedly found to be involved in the regulation of impulsive-aggressive behavior.
- SNPs of the HTR1B gene have been associated with various impulsivity-related clinical features such as suicidal behavior, substance abuse, and ADHD.
- The regulation and growth of 5-HT neurons and 5-HT signaling is strongly regulated by BDNF.
- Results of the study support the hypothesis that this gene–gene interaction could play a role in the susceptibility to BPD.
- Consider whether the HTR1B × BDNF interaction modulates the risk of developing BPD symptoms as a function of life events (e.g., childhood trauma).

HTR1B x BDNF Interaction

- SNP in the BDNF gene resulting in a valine (Val) to methionine (Met) substitution at codon 66 negatively influences activity-dependent release of the BDNF protein, playing an important role in neuroplasticity.
- Val66Met SNP reported to be associated with cognitive and emotional dysfunctions by modifying cerebral cortex excitability, gray matter structures, or white matter integrities.
- Met-allele carriers, in comparison to Val homozygotes, had gray matter volume deficits found in the temporal, frontal areas, and thalamus.
- White matter structural networks of the Met-allele carrier group showed higher vulnerability to targeted removal of central nodes as compared with those of the Val homozygous group.
- Increased susceptibility to brain disorders in Met-allele carriers may correlate to the limited stability in white matter structural connectivity.

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