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. 2022 Jun 19;23(12):6827. doi: 10.3390/ijms23126827

Table 2.

Role of BDNF in Parkinson’s disease.

Observations References
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]