BDNF

Official Full Name

brain derived neurotrophic factor

Organism

Homo sapiens

GeneID

627

Background

This gene encodes a member of the nerve growth factor family of proteins. Alternative splicing results in multiple transcript variants, at least one of which encodes a preproprotein that is proteolytically processed to generate the mature protein. Binding of this protein to its cognate receptor promotes neuronal survival in the adult brain. Expression of this gene is reduced in Alzheimer's, Parkinson's, and Huntington's disease patients. This gene may play a role in the regulation of the stress response and in the biology of mood disorders. [provided by RefSeq, Nov 2015]

Synonyms

ANON2; BULN2;

Bio Chemical Class

Growth factor

Protein Sequence

MTILFLTMVISYFGCMKAAPMKEANIRGQGGLAYPGVRTHGTLESVNGPKAGSRGLTSLADTFEHVIEELLDEDQKVRPNEENNKDADLYTSRVMLSSQVPLEPPLLFLLEEYKNYLDAANMSMRVRRHSDPARRGELSVCDSISEWVTAADKKTAVDMSGGTVTVLEKVPVSKGQLKQYFYETKCNPMGYTKEGCRGIDKRHWNSQCRTTQSYVRALTMDSKKRIGWRFIRIDTSCVCTLTIKRGR

Open

Disease

Dissociative neurological symptom disorder

Approved Drug

Clinical Trial Drug

1 +

Discontinued Drug

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Detailed Information

Essential for the survival, development, and differentiation of neurons, brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family. Originally extracted from the pig brain in 1982 by neuroscientist Hans Barde, BDNF has since been a main focus in neurobiological studies because of its many functions in the nervous system. A gene marked by a complex structure containing many exons and distinct promoters codes BDNF, which allows alternative splicing to produce several transcript variants. Among them, at least one type codes for a precursor protein that undergoes proteolytic processing to produce the BDNF protein of maturity. This protein is essential for neuroplasticity as it hooks to its corresponding receptor, TrkB (tropomyosin receptor kinase B), therefore fostering neuronal survival.

BDNF expression is important in maturity as well as throughout development. It is engaged in many activities, including synaptic transmission, axonal development, and dendritic morphology modification. Crucially, BDNF has been shown to affect long-term potentiation (LTP) and long-term depression (LTD), fundamental processes underpinning memory and learning. Reduced levels of BDNF are linked to neurodegenerative illnesses such as Alzheimer's disease, Parkinson's disease, and Huntington's disease, many studies have underlined, thereby stressing its relevance in preserving neuronal health and functioning.

BDNF and Neurodegenerative Diseases

With age, a main risk factor, neurodegenerative disorders are defined by persistent, gradual neuronal deterioration and loss. Illnesses including Huntington's, Parkinson's, and Alzheimer's show aberrant BDNF expression. Studies show that BDNF is important for neuronal survival, development, and repair as well as for indicating possible therapeutic consequences in reducing neurodegenerative disorders symptoms. BDNF has been the subject of a great study aiming at comprehending its processes and finding treatments as its link with neuronal health suggests something about the neurological condition.

The interaction of BDNF with neurodegenerative disorders tells a striking story. For example, Alzheimer's illness is characterized by synapse and neuron loss, which corresponds with low BDNF levels. In Parkinson's disease, when dopaminergic neurons are compromised, the regulation of BDNF expression may also help to neuro-protect. Researchers are concentrating more and more on how raising BDNF levels can perhaps stop or slow down the development of several illnesses.

BDNF in Learning and Memory

The participation of BDNF in cognitive processes is very remarkable. Particularly about learning and memory, BDNF correlates with cognitive ability. Research on animals with enhanced memory capacity reveals that BDNF levels in the hippocampus dentate gyrus are much greater than those of less competent animals. Memory formation is intimately related to synaptic plasticity, which BDNF controls by affecting synapse structure and function.

Released BDNF improves synaptic connection during learning, therefore enabling the required neuronal changes for memory creation. The fact that this protein can regulate LTP and LTD emphasizes its key importance in preserving cognitive capacity. The complex interaction between BDNF signaling and synaptic plasticity points to treatments meant to raise BDNF levels improving memory and learning capacity, therefore offering a therapeutic path for cognitive problems.

BDNF and Mood Disorders

Apart from its neurogenic functions, BDNF has been linked to emotional stability and control. Mood disorders, marked by symptoms like anxiety and sadness, often correspond with low BDNF levels in the brain. Particularly in areas linked to mood control, studies on the brains of suicide victims found far lower BDNF concentration.

Fascinatingly, raising BDNF levels has been demonstrated to help brain areas damaged by depression recover, indicating a possible treatment target. Studies on people with anxiety disorders show that their blood BDNF levels are much lower; these levels rise with good therapy, therefore highlighting the function of the protein in mood control. Therefore, changing BDNF expression offers a good approach to treating mood disorders.

Mechanism of Action

BDNF is composed of a precursor protein that passes through numerous processing stages to get the physiologically active version. The protein first exists as a pre-pro-BDNF after transcription and translation; it is then cleaved into pro-BDNF and then handled to produce mature BDNF. Comprising a dimeric protein, the mature BDNF binds with TrkB receptors on neuronal surfaces to start signaling cascades essential for neuronal survival.

Figure 1 illustrates the BDNF (brain-derived neurotrophic factor)-related signaling pathways involved in Alzheimer disease (AD), highlighting how the interaction between BDNF and TrkB activates multiple downstream pathways that play a crucial role in neuronal excitability, synaptic plasticity, and the neurodegenerative changes that ultimately lead to AD. Figure 1. BDNF-related signaling pathways in AD. (Gao L, et al., 2022)

BDNF stimulates many intracellular signaling systems, including the Ras-MAPK and PI3K pathways, when it binds to TrkB. Many proteins, including CREB (cAMP response element-binding protein), phosphorylated as a result of this activation, therefore improving the transcription of BDNF itself and other neuroprotective genes such as BCL-2. Emphasizing the vital function of BDNF in neurobiology, these signaling processes together support neuronal survival, differentiation, and enhanced synaptic plasticity.

References:

Camuso S, Canterini S. Brain-derived neurotrophic factor in main neurodegenerative diseases. Neural Regen Res. 2023 Mar;18(3):554-555.
Gao L, Zhang Y, Sterling K, Song W. Brain-derived neurotrophic factor in Alzheimer's disease and its pharmaceutical potential. Transl Neurodegener. 2022 Jan 28;11(1):4.
Li Y, Li F, Qin D, et al. The role of brain derived neurotrophic factor in central nervous system. Front Aging Neurosci. 2022;14:986443.
Chow R, Wessels JM, Foster WG. Brain-derived neurotrophic factor (BDNF) expression and function in the mammalian reproductive Tract. Hum Reprod Update. 2020;26(4):545-564.

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