scholarly journals Parkinson’s Disease: Possible Mechanisms for Nutritional Approaches

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Christine E. Cherpak-Castagna ◽  
Sherryl J. Van Lare

Parkinson’s disease (PD) is among the most common chronic neurodegenerative conditions, affecting 1% of those over 60 years of age, and involves motor and non-motor impairments. Alterations in normal physiology may become apparent years – in some cases, 10–20 years – before established diagnostic criteria are met. Thus, better clinical outcomes may result when practitioners utilize nutritional and supplement interventions that support reductions in neuroinflammation and neurodegeneration as early as possible. PD is a devastating, progressive neurodegenerative condition that has both hereditary and environmental components to its pathogenesis, and early identification of risk factors and onset is critical. The purpose of this review is to highlight various nutrition and supplement interventions that may positively affect disease onset and progression, and that warrant further research.

2010 ◽  
Vol 469 (1) ◽  
pp. 155-158 ◽  
Author(s):  
Clecio Godeiro ◽  
Patricia M. de Carvalho Aguiar ◽  
Andre C. Felício ◽  
Orlando G.P. Barsottini ◽  
Sonia M.A. Silva ◽  
...  

2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A60.1-A60
Author(s):  
Susan Peters ◽  
Douglas Walker ◽  
Gary Miller ◽  
Marc Chadeau-Hyam ◽  
Paolo Vineis ◽  
...  

Parkinson’s disease (PD) is the second most common neurodegenerative disorder after Alzheimer disease and is imposing an increasing social and economic burden in ageing populations. Although the role of environmental factors has been recognised, few established risk factors have been consistently identified. Evidence that exposure to pesticides, herbicides and metals increase PD risk is suggestive, but further research is needed to identify specific compounds that may play a causal role.Large established prospective population studies offer an important opportunity for investigating risk factors in relatively rare diseases such as PD. Within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort, 734 incident PD cases have been ascertained, for whom pre-diagnostic blood has been stored. A nested case-control study will be conducted, where one control per case will be selected by incidence density sampling matched by age at recruitment, sex and study centre.Untargeted metabolomics can simultaneously characterize thousands of endogenous and exogenous compounds within a biological sample: the metabolome. Metabolome wide association studies (MWAS) have identified significant differences in the metabolomic profile of older adults with and without PD. We will employ an innovative approach combining liquid and gas phase chromatography with ultra-high-resolution mass spectrometry (LC/GC-UHRMS), to identify exogenous chemical exposures (e.g. pollutants, pesticides and medications), the exposome, in addition to the metabolome.Disease specific variability in blood metabolite compositions may signify the presence of mechanistic aberrations contributing to PD pathogenesis. The combination of metabolome and exposome profiling provides a measure of the continuum from exposure to disease. Allowing previously unavailable richness and depth for characterizing the metabolome and exposome upon which novel discoveries in PD can be made.The EPIC cohort allows us to perform a to study the metabolome and exposome well before disease onset, to eliminate possible effects of levodopa medication or disease-related processes.


2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Muhammad Aslam ◽  
Nirosiya Kandasamy ◽  
Anwar Ullah ◽  
Nagarajan Paramasivam ◽  
Mehmet Ali Öztürk ◽  
...  

AbstractRare variants in the beta-glucocerebrosidase gene (GBA1) are common genetic risk factors for alpha synucleinopathy, which often manifests clinically as GBA-associated Parkinson’s disease (GBA-PD). Clinically, GBA-PD closely mimics idiopathic PD, but it may present at a younger age and often aggregates in families. Most carriers of GBA variants are, however, asymptomatic. Moreover, symptomatic PD patients without GBA variant have been reported in families with seemingly GBA-PD. These observations obscure the link between GBA variants and PD pathogenesis and point towards a role for unidentified additional genetic and/or environmental risk factors or second hits in GBA-PD. In this study, we explored whether rare genetic variants may be additional risk factors for PD in two families segregating the PD-associated GBA1 variants c.115+1G>A (ClinVar ID: 93445) and p.L444P (ClinVar ID: 4288). Our analysis identified rare genetic variants of the HSP70 co-chaperone DnaJ homolog subfamily B member 6 (DNAJB6) and lysosomal protein prosaposin (PSAP) as additional factors possibly influencing PD risk in the two families. In comparison to the wild-type proteins, variant DNAJB6 and PSAP proteins show altered functions in the context of cellular alpha-synuclein homeostasis when expressed in reporter cells. Furthermore, the segregation pattern of the rare variants in the genes encoding DNAJB6 and PSAP indicated a possible association with PD in the respective families. The occurrence of second hits or additional PD cosegregating rare variants has important implications for genetic counseling in PD families with GBA1 variant carriers and for the selection of PD patients for GBA targeted treatments.


2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Velma T. E. Aho ◽  
Madelyn C. Houser ◽  
Pedro A. B. Pereira ◽  
Jianjun Chang ◽  
Knut Rudi ◽  
...  

Abstract Background Previous studies have reported that gut microbiota, permeability, short-chain fatty acids (SCFAs), and inflammation are altered in Parkinson’s disease (PD), but how these factors are linked and how they contribute to disease processes and symptoms remains uncertain. This study sought to compare and identify associations among these factors in PD patients and controls to elucidate their interrelations and links to clinical manifestations of PD. Methods Stool and plasma samples and clinical data were collected from 55 PD patients and 56 controls. Levels of stool SCFAs and stool and plasma inflammatory and permeability markers were compared between patients and controls and related to one another and to the gut microbiota. Results Calprotectin was increased and SCFAs decreased in stool in PD in a sex-dependent manner. Inflammatory markers in plasma and stool were neither intercorrelated nor strongly associated with SCFA levels. Age at PD onset was positively correlated with SCFAs and negatively correlated with CXCL8 and IL-1β in stool. Fecal zonulin correlated positively with fecal NGAL and negatively with PD motor and non-motor symptoms. Microbiota diversity and composition were linked to levels of SCFAs, inflammatory factors, and zonulin in stool. Certain relationships differed between patients and controls and by sex. Conclusions Intestinal inflammatory responses and reductions in fecal SCFAs occur in PD, are related to the microbiota and to disease onset, and are not reflected in plasma inflammatory profiles. Some of these relationships are distinct in PD and are sex-dependent. This study revealed potential alterations in microbiota-host interactions and links between earlier PD onset and intestinal inflammatory responses and reduced SCFA levels, highlighting candidate molecules and pathways which may contribute to PD pathogenesis and clinical presentation and which warrant further investigation.


Author(s):  
Iván Galtier ◽  
Antonieta Nieto ◽  
María Mata ◽  
Jesús N. Lorenzo ◽  
José Barroso

ABSTRACT Objective: Subjective cognitive decline (SCD) and mild cognitive impairment (MCI) in Parkinson’s disease (PD) are considered as the risk factors for dementia (PDD). Posterior cortically based functions, such as visuospatial and visuoperceptual (VS-VP) processing, have been described as predictors of PDD. However, no investigations have focused on the qualitative analysis of the Judgment of Line Orientation Test (JLOT) and the Facial Recognition Test (FRT) in PD-SCD and PD-MCI. The aim of this work was to study the VS-VP errors in JLOT and FRT. Moreover, these variables are considered as predictors of PDD. Method: Forty-two PD patients and 19 controls were evaluated with a neuropsychological protocol. Patients were classified as PD-SCD and PD-MCI. Analyses of errors were conducted following the procedure described by Ska, Poissant, and Joanette (1990). Follow-up assessment was conducted to a mean of 7.5 years after the baseline. Results: PD-MCI patients showed a poor performance in JLOT and FRT total score and made a greater proportion of severe intraquadrant (QO2) and interquadrant errors (IQO). PD-SCD showed a poor performance in FRT and made mild errors in JLOT. PD-MCI and QO2/IQO errors were independent risk factors for PDD during the follow-up. Moreover, the combination of both PD-MCI diagnosis and QO2/IQO errors was associated with a greater risk. Conclusions: PD-MCI patients presented a greater alteration in VS-VP processing observable by the presence of severe misjudgments. PD-SCD patients also showed mild difficulties in VS-SP functions. Finally, QO2/IQO errors in PD-MCI are a useful predictor of PDD, more than PD-MCI diagnosis alone.


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