7,8-Dihydroxyflavone (7,8-DHF), as a high-affinity TrkB receptor agonist, has been extensively explored in many human disorders involving brain-derived neurotrophic factor (BDNF) such as Alzheimer's disease, Parkinson's disease, depression, and obesity.
Alzheimer's disease (AD), most tauopathies, and other neurodegenerative diseases are highly associated with impaired neurotrophin regulation and imbalanced neutrophin distribution.
Alzheimer's disease (AD) models were established by injecting Aβ(1-42) into the rat hippocampus and the effects of learning and memory were observed by a Morris water maze test, immunohistological alterations, and correlative indicators covering nerve growth (brain-derived neurotrophic factor, glial-cell-derived trophic factor, and nerve growth factor), interleukin 1β, tumor necrosis factor, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), glial fibrillary acidic protein (GFAP), and microglial CD11b in AD rats.
Alzheimer's disease is marked by the presence of amyloid-beta (Aβ) plaques, elevated central cytokine levels, dysregulation of BDNF-related gene expression, and cognitive decline.
Brain-derived neurotrophic factor gene polymorphisms in Japanese patients with sporadic Alzheimer's disease, Parkinson's disease, and multiple system atrophy.
Brain-derived neurotrophic factor (BDNF) is a neurotrophic factor and is known to possess anti-obesity, anti-diabetic actions and is believed to have a role in memory and Alzheimer's disease.
Brain-derived neurotrophic factor (BDNF) and its receptor, tropomyosin-related kinase B (TrkB), have emerged as key regulators of brain plasticity and represent disease-modifying targets for several brain disorders, including Alzheimer's disease and major depressive disorder.
Brain-derived neurotrophic factor (BDNF) gene delivery to the entorhinal cortex is a candidate for treatment of Alzheimer's disease (AD) to reduce neurodegeneration that is associated with memory loss.
Brain-derived neurotrophic factor (BDNF) is a neutrotrophic factor essential for the survival and differentiation of neurons and is considered a key target in the pathophysiology of various neurodegenerative diseases, as for example AD.
Brain-derived neurotrophic factor (BDNF), an essential factor for maintaining brain functions, has been reported to be reduced in various neurological diseases, including Alzheimer's disease and major depression.
BDNF total long 3' transcript expression was significantly lower in those with early AD neuropathology, compared to those without any neuropathology (p = 0.021).
Neurotrophin receptor p75 (p75<sup>NTR</sup>) is a receptor for Aβ and mediates Aβ neurotoxicity, implying that p75<sup>NTR</sup> may mediate Aβ-induced tau phosphorylation in AD.
Val66Met Polymorphism in BDNF Has No Sexual and APOE ε4 Status-Based Dimorphic Effects on Susceptibility to Alzheimer's Disease: Evidence From an Updated Meta-Analysis of Case-Control Studies and High-Throughput Genotyping Cohorts.
A marked decrease in the expression of miR-29c was observed in the AD group compared with the normal control group, accompanied by a decreased in the expression of BDNF.
A meta-analysis of BDNF levels between early AD and controls showed statistically significantly higher levels (SMD [95 % CI]: 0.72 [0.31, 1.13]) with no heterogeneity.
A molecular fingerprint strikingly similar to that of diminished network activity occurs in the human brain during aging and in AD, and opposite changes occur in response to activation of N-methyl-D-aspartate (NMDA) and brain-derived neurotrophic factor (BDNF) receptors in cultured cortical neurons and in mice in response to an enriched environment or electroconvulsive shock.