To determine whether dopaminergic (rs1076560 DRD2 G > T and rs4680 catechole-o-methyltranspherase (COMT) Val158Met) or brain derived neurotrophic factor (rs6265BDNFVal66Met) genetic polymorphisms are associated with gait function and medication responsiveness in Parkinson's disease.
The influence of a common functional polymorphism of the BDNF gene on the risk of developing dyskinesias in a large cohort of patients with PD (n = 315), who were independently and variably treated with levodopa and/or other dopaminergic treatments, was investigated.
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.
Several genetic studies have shown a significant association between schizophrenia, Alzheimer's disease, and Parkinson's disease and certain BDNF polymorphisms, specifically rs6265;rs759834365" genes_norm="627">G196A (rs6265) and C270T (rs56164415).
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.
We studied two genetic polymorphisms (240C/T and 480G/A) of the brain-derived neurotrophic factor (BDNF) gene in Japanese patients with Alzheimer's disease (AD, n = 172), Parkinson's disease (PD, n = 327), and multiple system atrophy (MSA, n = 122), as well as controls (n = 275).
Sixteen polymorphisms in candidate genes belonging to five neurotransmitter systems (dopaminergic, catecholaminergic, serotonergic, glutamatergic, opioidergic) and the BDNF were screened in 154 PD patients with addictive behaviors and 288 PD control subjects.
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.
To determine the role of the BDNF gene in the development of familial and sporadic PD, we sequenced the promoter region of the gene using genomic DNA from patients with familial PD.
We found that the APOE ε4 allele is associated with a higher risk for PD-D. Gene-gene interaction analysis revealed that three significant gene-gene interactions, including BDNF and CLU, APOE and CR1, and DYRK1A and CD2AP increase the risk for PD.
Thus, our negative findings suggest that it is unlikely that the BDNFVal66Met polymorphism plays a major role in the pathogenesis of PD in the Chinese population.
Here we review the role and relevance of the BDNFVal66Met polymorphism in neurodegenerative diseases, with particular emphasis on glaucoma, multiple sclerosis (MS), Alzheimer's disease (AD) and Parkinson's disease (PD).
To date, there have been several conflicting reports on the correlation between AD or PD and Val66Met or C270T polymorphism in the BDNF promoter region, although no data on this relationship have been published with respect to dementia with Lewy bodies (DLB).