We investigated the potential protective effects of EA on dopaminergic neurons in a mouse model of PD and whether these effects are associated with the promotion of endogenous brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF).
Strikingly, in contrast to BDNF and GDNF mRNA levels, BDNF and GDNF protein levels were lower in almost all PD-derived TDNs than in HD-derived cells, thus indicating the dysregulation of NTF expression at the post-transcriptional level.
These results suggest that the neuroprotection and modulation of NE on dopaminergic neurons are mediated via BDNF and MAPK/ERK pathways, as well as through epigenetic histone modification, which may have implications for the improvement of therapeutic strategies for Parkinson's disease.
Specifically, in this randomized controlled trial, we will determine the effects of the HiBalance program on balance, gait and cognition and relate this to task-evoked functional MRI (fMRI), as well as brain-derived neurotrophic factor (BDNF) in participants with mild-moderate PD.
Brain-derived neurotrophic factor (BDNF) is associated with onset of several central nervous system disorders, e.g., Parkinson's disease, Alzheimer's disease, depression, epilepsy, and chronic pain.
The lower level of BDNF in Alzheimer's and Parkinson's disease has been found to be related to cognitive and other neuropsychological impairments, whereas, its higher levels are associated with the tumour growth and metastasis and poor survival rate in the cancer patients.
Overall, these findings suggest that harboring the BDNF val/val genotype in PD leads to a set of cortical and subcortical brain alterations that could promote cognitive decline in this population.
Reduced nigral brain-derived neurotrophic factor (BDNF) has been postulated to contribute to the loss of nigral dopaminergic neurons in PD by causing a lack of trophic support.
Gami-Chunggan Formula Prevents Motor Dysfunction in MPTP/p-Induced and A53T α-Synuclein Overexpressed Parkinson's Disease Mouse Model Though DJ-1 and BDNF Expression.
These results suggest that the decreased peripheral alteration of BDNF/TrkB levels found in patients with PD is directly related to the dopaminergic neurons neurodegeneration and that decreased expression of BDNF/TrkB may lead to the development of innovative biomarkers of PD, whereas the increased level of BDNF and phosphorylated TrkB at advanced stages may due to L-DOPA medication.
Our meta-analysis implicates Val66MetBDNF polymorphism may be associated with Parkinson's disease cognitive impairment, further well-designed studies with larger populations are required to validate these results owing to the limited research.
Levels of brain-derived neurotrophic factor (BDNF), known to promote the survival of dopaminergic neurons, were increased in PD mice after FMD, suggesting an involvement of BDNF in FMD-mediated neuroprotection.
Expression of BDNF for the 'T/T' variant was significantly lower (p-value = 0.012) than the 'C/C' variant, suggesting a possible role in PD pathogenesis.
The research provides evidence of moderate quality that blood levels of BDNF are decreased in PD patients despite various influencing factors, supporting an association between decreased level of peripheral BDNF and PD.
The objective was to investigate if high cadence cycling altered non-motor cognition and depression symptoms in individuals with Parkinson's disease (PD) and whether exercise responses were influenced by brain-derived neurotrophic factor (BDNF) Val66Met polymorphism.
Our studies demonstrate that VPA exerts neuroprotective effects in a rat model of 6-OHDA-induced Parkinson's disease (PD), likely in part by up-regulation BDNF.
These results suggest that the beneficial effects on the neuroplasticity of PD model mice treated with TMAS could possibly be conducted through postsynaptic regulations and mediated by BDNF.
These findings indicate that miRNA-7 regulates the BDNF/α-syn axis in the early stages of PD and can serve as a biomarker or therapeutic target for disease treatment.