Parkinson’s disease patients |
|
Serum BDNF levels and cognitive function scores were significantly lower in Parkinson’s disease patients versus healthy controls. |
[71] |
Decreased serum BDNF may be involved in the pathophysiology of depression in Parkinson’s disease patients. |
[72] |
Serum BDNF levels were lower in recently diagnosed, untreated Parkinson’s disease patients compared to controls. These lower levels were significantly correlated with nigrostriatal system degeneration. |
[73] |
Low BDNF is associated with cognitive impairment in patients with Parkinson’s disease. |
[74] |
Decreased serum BDNF levels may be involved in the pathophysiology of restless legs syndrome (RLS) in Parkinson’s disease. |
[75] |
The serum BDNF levels were lower in depressed Parkinson’s disease patients compared to non-depressed Parkinson’s disease patients and controls. |
[76] |
The decreased peripheral alteration in BDNF/TrkB levels found in patients with Parkinson’s disease is directly related to dopaminergic neuron neurodegeneration. |
[77] |
BDNF genetic polymorphism greatly increases the risk of leucine-rich repeat kinase 2 (LRRK2) in Parkinson’s disease, particularly in subjects with older onset age. |
[79] |
BDNF Val66Met (rs6265, G196A) polymorphism was not associated with cognitive status in Parkinson’s disease patients, nor with Parkinson’s disease risk or onset. |
[81] |
The carriers of at least one BDNF 66Met allele presented a higher prevalence of cognitive impairment. |
[83] |
The BDNF Met allele is associated with a higher neuropsychiatric burden in Parkinson’s disease. |
[84] |
Carrying two copies of the BDNF rs6265 Met66 allele is associated with the reduced severity of motor symptoms and, potentially, a slower rate of progression. |
[85] |
The BDNF Met-allele carriers showed a significantly smaller decline in set-shifting compared with the homozygous BDNF Val-allele carriers. |
[86] |
The G/G genotype was significantly associated with depression and anxiety symptoms and the development of Parkinson’s disease. |
[87] |
The BDNF Val/Val genotype in Parkinson’s disease leads to a set of cortical and subcortical brain alterations that could promote cognitive decline. |
[88] |
Carriers of dopamine receptors DRD2 haplotypes and possibly the BDNF variants rs6265 and DRD3 haplotypes, were at increased risk of dyskinesia, suggesting that these genes may be involved in dyskinesia-related pathomechanisms. |
[89] |
Animal model |
|
CEBPβ (+/−) mice |
Gut inflammation induces C/EBPβ activation, which leads to both BDNF and Netrin-1 reduction and triggers non-motor and motor symptoms of Parkinson’s disease. |
[78] |
MPTP-induced mouse model |
LncRNA BDNF-AS promotes autophagy and apoptosis by ablating microRNA-125b-5p. |
[90] |
Cell culture |
|
MPP+-induced SH-SY5Y cell |
BDNF-AS knockdown significantly promotes cell proliferation and suppresses apoptosis and autophagy in SH-SY5Y cells treated by MPP+. miR-125b-5p, a putative target gene of BDNF-AS, is involved in the effects of BDNF-AS on SH-SY5Y cell apoptosis and autophagy. |
[90] |