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Brain-derived neurotrophic factor and its clinical implications.

Bathina S, Das UN - Arch Med Sci (2015)

Bottom Line: It is widely expressed in the CNS, gut and other tissues.BDNF binds to its high affinity receptor TrkB (tyrosine kinase B) and activates signal transduction cascades (IRS1/2, PI3K, Akt), crucial for CREB and CBP production, that encode proteins involved in β cell survival.Thus, BDNF may be useful in the prevention and management of several diseases including diabetes mellitus.

View Article: PubMed Central - PubMed

Affiliation: Bio-Science Research Center, Gayatri Vidya Parishad College of Engineering, Visakhapatnam, India.

ABSTRACT
Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal survival and growth, serves as a neurotransmitter modulator, and participates in neuronal plasticity, which is essential for learning and memory. It is widely expressed in the CNS, gut and other tissues. BDNF binds to its high affinity receptor TrkB (tyrosine kinase B) and activates signal transduction cascades (IRS1/2, PI3K, Akt), crucial for CREB and CBP production, that encode proteins involved in β cell survival. BDNF and insulin-like growth factor-1 have similar downstream signaling mechanisms incorporating both p-CAMK and MAPK that increase the expression of pro-survival genes. Brain-derived neurotrophic factor regulates glucose and energy metabolism and prevents exhaustion of β cells. Decreased levels of BDNF are associated with neurodegenerative diseases with neuronal loss, such as Parkinson's disease, Alzheimer's disease, multiple sclerosis and Huntington's disease. Thus, BDNF may be useful in the prevention and management of several diseases including diabetes mellitus.

No MeSH data available.


Related in: MedlinePlus

Interaction between omega 3-fatty acids and BDNF that may underlie their cytoprotective actions. Mechanism of cytoprotection may involve: a) prevention of degradation of membrane phospholipids; b) reduction of oxidative stress that helps maintain synaptic plasticity; and c) normalization of levels of BDNF and its downstream effectors synapsin I and CREB, which are important in learning, memory and LTP. This figure is adapted and modified from refs. [89–91]
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Figure 0005: Interaction between omega 3-fatty acids and BDNF that may underlie their cytoprotective actions. Mechanism of cytoprotection may involve: a) prevention of degradation of membrane phospholipids; b) reduction of oxidative stress that helps maintain synaptic plasticity; and c) normalization of levels of BDNF and its downstream effectors synapsin I and CREB, which are important in learning, memory and LTP. This figure is adapted and modified from refs. [89–91]

Mentions: BDNF showed a positive correlation with low-density lipid (LDL) cholesterol, total cholesterol and triglycerides [86]. BDNF treatment of diabetic animals resulted in a decrease of plasma glucose, non-esterified fat, phospholipids and liver weight, along with an increase in β-oxidation, peroxisome proliferator activator receptor (PPAR-α) activation and level of fibroblast growth factor [87]. TrkB activation is essential for appetite regulation and energy homeostasis. It was reported that dietary omega-3 fatty acids normalize BDNF levels (Figure 5), reduce oxidative damage and improve learning ability after traumatic brain injury [88].


Brain-derived neurotrophic factor and its clinical implications.

Bathina S, Das UN - Arch Med Sci (2015)

Interaction between omega 3-fatty acids and BDNF that may underlie their cytoprotective actions. Mechanism of cytoprotection may involve: a) prevention of degradation of membrane phospholipids; b) reduction of oxidative stress that helps maintain synaptic plasticity; and c) normalization of levels of BDNF and its downstream effectors synapsin I and CREB, which are important in learning, memory and LTP. This figure is adapted and modified from refs. [89–91]
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4697050&req=5

Figure 0005: Interaction between omega 3-fatty acids and BDNF that may underlie their cytoprotective actions. Mechanism of cytoprotection may involve: a) prevention of degradation of membrane phospholipids; b) reduction of oxidative stress that helps maintain synaptic plasticity; and c) normalization of levels of BDNF and its downstream effectors synapsin I and CREB, which are important in learning, memory and LTP. This figure is adapted and modified from refs. [89–91]
Mentions: BDNF showed a positive correlation with low-density lipid (LDL) cholesterol, total cholesterol and triglycerides [86]. BDNF treatment of diabetic animals resulted in a decrease of plasma glucose, non-esterified fat, phospholipids and liver weight, along with an increase in β-oxidation, peroxisome proliferator activator receptor (PPAR-α) activation and level of fibroblast growth factor [87]. TrkB activation is essential for appetite regulation and energy homeostasis. It was reported that dietary omega-3 fatty acids normalize BDNF levels (Figure 5), reduce oxidative damage and improve learning ability after traumatic brain injury [88].

Bottom Line: It is widely expressed in the CNS, gut and other tissues.BDNF binds to its high affinity receptor TrkB (tyrosine kinase B) and activates signal transduction cascades (IRS1/2, PI3K, Akt), crucial for CREB and CBP production, that encode proteins involved in β cell survival.Thus, BDNF may be useful in the prevention and management of several diseases including diabetes mellitus.

View Article: PubMed Central - PubMed

Affiliation: Bio-Science Research Center, Gayatri Vidya Parishad College of Engineering, Visakhapatnam, India.

ABSTRACT
Brain-derived neurotrophic factor (BDNF) plays an important role in neuronal survival and growth, serves as a neurotransmitter modulator, and participates in neuronal plasticity, which is essential for learning and memory. It is widely expressed in the CNS, gut and other tissues. BDNF binds to its high affinity receptor TrkB (tyrosine kinase B) and activates signal transduction cascades (IRS1/2, PI3K, Akt), crucial for CREB and CBP production, that encode proteins involved in β cell survival. BDNF and insulin-like growth factor-1 have similar downstream signaling mechanisms incorporating both p-CAMK and MAPK that increase the expression of pro-survival genes. Brain-derived neurotrophic factor regulates glucose and energy metabolism and prevents exhaustion of β cells. Decreased levels of BDNF are associated with neurodegenerative diseases with neuronal loss, such as Parkinson's disease, Alzheimer's disease, multiple sclerosis and Huntington's disease. Thus, BDNF may be useful in the prevention and management of several diseases including diabetes mellitus.

No MeSH data available.


Related in: MedlinePlus