Monoamine Levels and Parkinson’s Disease Progression: Evidence From a High-Performance Liquid Chromatography Study

Wichit, Patsorn; Thanprasertsuk, Sekh; Phokaewvarangkul, Onanong; Bhidayasiri, Roongroj; Bongsebandhu-phubhakdi, Saknan

doi:10.3389/fnins.2021.605887

Cited by 18 publications

(9 citation statements)

References 25 publications

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“…In addition to gut microbiome dysbiosis, another possible mechanism linking PD to IBS was dysregulation of neurotransmitters and neurotrophic factors. It is well-known that deficits in dopamine and 5-HT signaling are implicated in the initiation and progression of PD ( 46 , 47 ), but as for IBS, reduced levels of these neurotransmitters could mitigate pathological symptoms like diarrhea, abdominal pain and discomfort and stabilize intestinal permeability ( 48 – 51 ). Additionally, although decreased netrin-1 concentrations in the brain and gut of PD patients resulted in significant loss of motor function, it provided an obvious alleviation effect on visceral hypersensitivity, a core characteristic in approximately half of patients with IBS ( 52 , 53 ).…”

Section: Discussionmentioning

confidence: 99%

Investigation of the causal association between Parkinson’s disease and autoimmune disorders: a bidirectional Mendelian randomization study

Yang,

Lin,

et al. 2024

Front. Immunol.

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BackgroundTo date, an increasing number of epidemiological evidence has pointed to potential relationships between Parkinson’s disease (PD) and various autoimmune diseases (AIDs), however, no definitive conclusions has been drawn about whether PD is causally related to AIDs risk.MethodsBy employing summary statistics from the latest and most extensive genome-wide association studies (GWAS), we performed a bidirectional two-sample Mendelian randomization (MR) analysis to investigate the causal associations between PD and a variety of 17 AIDs, encompassing multiple sclerosis, neuromyelitis optica spectrum disorder, myasthenia gravis, asthma, inflammatory bowel disease, Crohn’s disease, ulcerative colitis, irritable bowel syndrome, celiac disease, primary biliary cirrhosis, primary sclerosing cholangitis, type 1 diabetes, ankylosing spondylitis, rheumatoid arthritis, systemic lupus erythematosus, psoriasis and vitiligo. Inverse-variance weighted (IVW) was adopted as the main statistical approach to obtain the causal estimates of PD on different AIDs, supplemented by a series of complementary analyses (weighted median, MR Egger regression, and MR-PRESSO) for further strengthening the robustness of results.ResultsOur MR findings suggested that genetically predicted higher liability to PD was causally associated with a decreased risk of irritable bowel syndrome (OR = 0.98; 95% CI: 0.96-0.99; P = 0.032). On the contrary, IVW analysis showed a potential positive correlation between genetically determined PD and the incidence of type 1 diabetes (OR = 1.10; 95%CI: 1.02-1.19; P = 0.010). Subsequent MR tests ended up in similar results, confirming our findings were reliable. Additionally, in the reverse MR analyses, we did not identify any evidence to support the causal relationship of genetic predisposition to AIDs with PD susceptibility.ConclusionIn general, a bifunctional role that PD exerted on the risk of developing AIDs was detected in our studies, both protecting against irritable bowel syndrome occurrence and raising the incidence of type 1 diabetes. Future studies, including population-based observational studies and molecular experiments in vitro and in vivo, are warranted to validate the results of our MR analyses and refine the underlying pathological mechanisms involved in PD-AIDs associations.

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Section: Discussionmentioning

confidence: 99%

Investigation of the causal association between Parkinson’s disease and autoimmune disorders: a bidirectional Mendelian randomization study

Yang,

Lin,

et al. 2024

Front. Immunol.

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“…[ 18 ] It was found that the blood level of norepinephrine in PD patients decreased significantly with the increase of the Hoehn&Yahr stage, suggesting severe disease conditions. [ 19 ] A retrospective study on 1318 patients with PD found that the risk of OH was higher in PD patients with longer disease course, higher Hoehn&Yahr stage, and more severe disease. [ 20 ] However, in this study, we found that there was no obvious correlation between OH and disease course.…”

Section: Discussionmentioning

confidence: 99%

The correlation of orthostatic hypotension in Parkinson disease with the disease course and severity and its impact on quality of life

Meng,

Tang,

Wang

et al. 2024

Medicine

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We investigated the correlation of orthostatic hypotension (OH) in Parkinson disease (PD) with the disease course and severity, and its possible impact on quality of life. 171 PD patients were recruited and divided into the PD-NOH (n = 91) and PD-OH groups (n = 80). Clinical data were collected. The severity and quality of life of PD patients were evaluated. The impact of disease severity was analyzed using logistic regression analysis. The ROC curve was plotted. There were significant differences (P < .05) between PD-NOH and PD-OH groups in terms of the disease course, non-motor symptoms (somnipathy), Hoehn&Yahr stage, LEDD score, RBDSQ score, PDQ-39 score, MMSE score, MoCA, MDS-UPDRS Part III scores during off- and on-periods, and NMSS score. Hoehn&Yahr stage (OR 4.950, 95% CI 1.516–16.157, P = .008) was closely associated with the risk of OH in PD. PDQ-39 score (OR 1.079, 95% CI 1.033–1.127, P = .001) in PD patients with OH further decreased. Patients with PD-OH experienced severe impairment in 4 dimensions of quality of life, including motor function, cognitive function, physical discomfort, and activities of daily living. Different clinical symptoms of PD-OH were positively correlated with PDQ39 subscales. The area under the ROC curve of the Hoehn&Yahr stage in predicting the occurrence of OH was 0.679 (95% CI 0.600–0.758), and that of the Hoehn&Yahr stage combined with levodopa equivalent dose, and MDS-UPDRS Part III score during off-period was 0.793 (95% CI 0.727–0.862). Higher Hoehn&Yahr stage is associated with increased risk of OH in PD patients, and deteriorated quality of life of PD patients. Patients with different OH symptoms are affected in different dimensions of their quality of life. The Hoehn & Yahr stage can independently predict the risk of OH in PD patients.

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“…On this basis, the istradefylline-induced epigenetic suppression of A 2A receptor upregulation may have interesting implications for the fundamental goals of LD therapy, although many areas remain to be investigated, including PET imaging of dopamine transporters and A 2A receptors in patients with PD receiving long-term istradefylline treatment [24][25][26][27][28][29][30]. If increased A 2A receptor expression in the indirect pathway contributes to the need for progressive increases in LDD, A 2A receptor epigenesis [21] data and the present real-world evidence (RWE) findings may explain the mechanism underpinning this correlation.…”

Section: Discussionmentioning

confidence: 99%

Real-world evidence on levodopa dose escalation in patients with Parkinson’s disease treated with istradefylline

Kabata

Asada

Kanda

et al. 2022

Preprint

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Objective Istradefylline, a selective adenosine A2A receptor antagonist, is indicated in the US and Japan as adjunctive treatment to levodopa/decarboxylase inhibitors in adults with Parkinson’s disease (PD) experiencing OFF time. This study aimed to observe patterns of dose escalation of levodopa over time in patients initiated on istradefylline. Methods Using Japanese electronic health record data, interrupted time series analyses were used to compare levodopa daily dose (LDD, mg/day) gradients in patients before and after initiation of istradefylline. Data were analyzed by period relative to istradefylline initiation (Month 1): pre-istradefylline (Months -72 to 0), early istradefylline (Months 1 to 24), and late istradefylline (Months 25 to 72). Subgroup analyses included LDD before istradefylline initiation (<400, >=400 to <600, >=600 mg/day) and treatment with or without monoamine oxidase-B inhibitors (MAO-BIs), catechol-O-methyltransferase inhibitors (COMTIs), or dopamine agonists before istradefylline initiation. Results The analysis included 4026 patients; mean (SD) baseline LDD was 419.27 mg (174.19). Patients receiving >=600 mg/day levodopa or not receiving MAO-BIs or COMTIs demonstrated a significant reduction in LDD increase gradient for pre-istradefylline vs late-phase istradefylline (>=600 mg/day levodopa, -6.259 mg/day each month, p<0.001; no MAO-BIs, -1.819 mg/day each month, p=0.004; no COMTIs, -1.412 mg/day each month, p=0.027). Conclusions This real-world analysis of Japanese prescription data indicated that slowing of LDD escalation was observed in patients initiated on istradefylline, particularly in those receiving >=600mg/day levodopa, suggesting istradefylline may slow progressive LDD increases. These findings suggest that initiating istradefylline before other levodopa-adjunctive therapies may mitigate LDD increases, potentially reducing occurrence or severity of levodopa-induced complications in long-term istradefylline treatment.

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Monoamine Levels and Parkinson’s Disease Progression: Evidence From a High-Performance Liquid Chromatography Study

Cited by 18 publications

References 25 publications

Investigation of the causal association between Parkinson’s disease and autoimmune disorders: a bidirectional Mendelian randomization study

Investigation of the causal association between Parkinson’s disease and autoimmune disorders: a bidirectional Mendelian randomization study

The correlation of orthostatic hypotension in Parkinson disease with the disease course and severity and its impact on quality of life

Real-world evidence on levodopa dose escalation in patients with Parkinson’s disease treated with istradefylline

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