However, genotyping of 300 PD patients and 302 healthy controls did not reveal a significant association between coding MDR1 gene polymorphisms and PD.
Decreased blood-brain barrier (BBB) P-glycoprotein (P-gp) efflux function has been proposed as a possible causative link between toxin exposure and PD neurodegeneration.
With aging, AD and PD, there is growing evidence of altered structure and function of the blood-brain barrier (BBB), including modifications to tight junctions and efflux transporters, such as P-glycoprotein.
Fifty-nine participants with PD were classified as avoiders (n = 27) or nonavoiders (n = 32) by using the Fear of Falling Avoidance Behavior Questionnaire and compared across 5 domains: demographic characteristics; PD-specific symptoms (subtype, Movement Disorder Society-Unified Parkinson's Disease Rating Scale [MDS-UPDRS], Hoehn and Yahr Scale, Parkinson's Disease Questionnaire-39 [PDQ-39]); balance and falls (fall history, Berg Balance Scale [BBS], Activities-Specific Balance Confidence [ABC] Scale, Impact of Events Scale, Consequences of Falling Questionnaire [CoFQ]); physical performance (30 Second Sit-to-Stand Test, Timed Up and Go Test, physical activity monitoring); and psychological factors (Zung Anxiety Scale, Beck Depression Inventory [BDI]).
In summary, Pluronic P85/F68 micelles could be considered as a promising drug delivery system to reverse MRP2-mediated efflux and improve the bioactivity of this MRP2 substrate, baicalein, for the treatment of PD.
Recently, some studies have indicated that the levels and activation of Abelson non-receptor tyrosine kinase (c-Abl, Abl1) were up-regulated in the brain tissue of patients with PD and demonstrated that c-Abl inhibitors could improve motor behavior, prevent the loss of dopamine neurons, inhibit phosphorylation of Cdk5, regulate α-synuclein phosphorylation and clearance, inhibit the tyrosine phosphorylation of parkin and decrease parkin substrate, for example, PARIS (zinc finger protein 746), AIMP2 (aminoacyl-tRNA synthetase-interacting multifunctional protein type2), FBP1 (fuse-binding protein 1), and synphilin-1.
For this study of a sample population consisting of 101 PD patients and 108 controls, we tested the hypothesis that an ACC --> ACT transversion (2664(th) nucleotide of the coding sequence) affecting codon 888 (tyrosine) of GRIN2B confers susceptibility to PD, or relates to the age of onset.
We found widespread, decreased expression of nDNA Complex-I genes that correlated in some cases with mitochondrial Complex-I protein levels, and of ACAD9, a Complex-I assembly factor. mtDNA-transcribed Complex-I genes showed ~ constant expression within each PD sample but variable expression across PD samples that correlated with NRF1.
Genetic polymorphism of Angiotensin-Converting Enzyme is not associated with the development of Parkinson's disease and of L-dopa-induced adverse effects.
We thus conclude that, in Finns, interaction between DCP1 *I and epsilon4 increases the risk of AD as well as of PD with coexisting Alzheimer pathology, which underlines the importance of the DCP1 I/D polymorphism in the development of Alzheimer neuropathology, whereas the wild type BCHE genotype in combination with epsilon4 had a combined effect with regard to the risk of AD.
Neuroprotective effects in animal PD models have been shown for the angiotensin-converting enzyme (ACE) inhibitors captopril and perindopril, and the AT1 receptor antagonists losartan, candesartan and telmisartan.
In conclusion, results of our study support the hypothesis that the ACE gene may indicate genetic susceptibility to PD, particularly in older individuals.
The meta-analysis revealed no association between the ACE D allele and schizophrenia (OR = 0.990, 95% CI = 0.889-1.102, p = 0.856) or PD (OR = 1.067, 95% CI = 0.907-1.255, p = 0.433).