Sudden unexpected death in Parkinson’s disease: why is drinking water important?

2019 ◽  
Vol 9 (4) ◽  
pp. 241-246 ◽  
Author(s):  
Francisco S Menezes-Rodrigues ◽  
Cristiane S Scorza ◽  
Ana C Fiorini ◽  
Afonso Caricati-Neto ◽  
Carla A Scorza ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Drinking Water ◽  
Neurodegenerative Disorders ◽  
Premature Death ◽  
Healthy Controls ◽  
Unexpected Death ◽  
Age Related ◽  
Daily Water ◽  
Daily Water Consumption

Parkinson’s disease (PD) is one of the most common age-related neurodegenerative disorders. Several studies over the last few years have shown that PD is accompanied by high rates of premature death compared with healthy controls. Death in PD patients is usually caused by determinant factors such as pneumonia, and cerebrovascular and cardiovascular diseases. During recent years it has emerged that dehydration may also contribute to mortality in PD. Interestingly, it has been documented that a substantial proportion of patients with PD die suddenly (known as sudden and unexpected death in PD). In this article, we focus on the magnitude of the problem of sudden and unexpected death in PD, with special reference to the daily water consumption of PD patients.

scholarly journals The Contribution ofα-Synuclein Spreading to Parkinson’s Disease Synaptopathy

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Francesca Longhena ◽  
Gaia Faustini ◽  
Cristina Missale ◽  
Marina Pizzi ◽  
PierFranco Spano ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorders ◽  
Physiological Conditions ◽  
Age Related ◽  
Endogenous Protein ◽  
Synaptic Failure ◽  
Nigrostriatal Neurons ◽  
Somatic Nervous System ◽  
The Brain

Synaptopathies are diseases with synapse defects as shared pathogenic features, encompassing neurodegenerative disorders such as Parkinson’s disease (PD). In sporadic PD, the most common age-related neurodegenerative movement disorder, nigrostriatal dopaminergic deficits are responsible for the onset of motor symptoms that have been related toα-synuclein deposition at synaptic sites. Indeed,α-synuclein accumulation can impair synaptic dopamine release and induces the death of nigrostriatal neurons. While in physiological conditions the protein can interact with and modulate synaptic vesicle proteins and membranes, numerous experimental evidences have confirmed that its pathological aggregation can compromise correct neuronal functioning. In addition, recent findings indicate thatα-synuclein pathology spreads into the brain and can affect the peripheral autonomic and somatic nervous system. Indeed, monomeric, oligomeric, and fibrillaryα-synuclein can move from cell to cell and can trigger the aggregation of the endogenous protein in recipient neurons. This novel “prion-like” behavior could further contribute to synaptic failure in PD and other synucleinopathies. This review describes the major findings supporting the occurrence ofα-synuclein pathology propagation in PD and discusses how this phenomenon could induce or contribute to synaptic injury and degeneration.

scholarly journals Dual Task Performance in Parkinson’s Disease

2013 ◽  
Vol 27 (2) ◽  
pp. 183-191 ◽  
Author(s):  
Jennifer A. Foley ◽  
Reiner Kaschel ◽  
Sergio Della Sala
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Task Performance ◽  
Dual Task ◽  
Neurodegenerative Disorders ◽  
Later Life ◽  
Healthy Controls ◽  
Dual Tasking ◽  
The People ◽  
Dual Task Performance

Several studies have found dual tasking to be impaired in Alzheimer's disease (AD), but unaffected by healthy ageing. It is not known if this deficit is specific to AD, or also present in other neurodegenerative disorders that can occur in later life, such as Parkinson's disease (PD). Therefore, this study investigated dual tasking in 13 people with PD, 26 AD and 42 healthy age-matched controls. The people with AD demonstrated a specific impairment in dual tasking, which worsened with increasing disease severity. The people with PD did not demonstrate any deficits in dual tasking ability, when compared to healthy controls, suggesting that the dual task impairment is specific to AD.

scholarly journals Expression Profiling of Blood microRNAs 885, 361, and 17 in the Patients with the Parkinson’s disease: Integrating Interaction Data to Uncover the Possible Triggering Age-Related Mechanisms

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Molood Behbahanipour ◽  
Maryam Peymani ◽  
Mehri Salari ◽  
Motahare-Sadat Hashemi ◽  
Mohammad Hossein Nasr-Esfahani ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Disease Severity ◽  
Cellular Senescence ◽  
Healthy Subjects ◽  
Target Genes ◽  
Healthy Controls ◽  
Early Stages ◽  
Age Related ◽  
Advanced Stages

Abstract MicroRNAs (miRNAs) have been reported to contribute to the pathophysiology of the Parkinson’s disease (PD), an age related-neurodegenerative disorder. The aim of present study was to compare the expression profiles of a new set of candidate miRNAs related to aging and cellular senescence in peripheral blood mononuclear cells (PBMCs) obtained from the PD patients with healthy controls and then in the early and advanced stages of the PD patients with their controls to clarify whether their expression was correlated with the disease severity. We have also proposed a consensus-based strategy to interpret the miRNAs expression data to gain a better insight into the molecular regulatory alterations during the incidence of PD. We evaluated the miRNA expression levels in the PBMCs obtained from 36 patients with PD and 16 healthy controls by the reverse transcription-quantitative real-time PCR and their performance to discriminate the PD patients from the healthy subjects assessed using the receiver operating characteristic curve analysis. Also, we applied our consensus and integration approach to construct a deregulated miRNA-based network in PD with the respective targets and transcription factors, and the enriched gene ontology and pathways using the enrichment analysis approach were obtained. There was a significant overexpression of miR-885 and miR-17 and the downregulation of miR-361 in the PD patients compared to the controls. The blood expression of miR-885 and miR-17 tended to increase along with the disease severity. On the other hand, the lower levels of miR-361 in the early stages of the PD patients, as compared to controls, and its higher levels in the advanced stages of PD patients, as compared to the early stages of the PD patients, were observed. Combination of all three miRNAs showed an appropriate value of AUC (0.985) to discriminate the PD patients from the healthy subjects. Also, the deregulated miRNAs were linked to the known PD pathways and the candidate related target genes were presented. We revealed 3 candidate biomarkers related to aging and cellular senescence for the first time in the patients with PD. Our in-silico analysis identified candidate target genes and TFs, including those related to neurodegeneration and PD. Overall, our findings provided novel insights into the probable age-regulatory mechanisms underlying PD and a rationale to further clarify the role of the identified miRNAs in the PD pathogenesis.

scholarly journals S-nitrosylation-impaired autophagy: An alternative mechanism underlying aging?

2013 ◽  
Author(s):  
Qing-Ping Zeng
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorders ◽  
Alternative Mechanism ◽  
Age Related ◽  
Surprising Finding

Aging is mysterious with unknown managing patterns. A surprising finding on the tune mode of autophagy by S-nitrosylation is a distinctive step towards the interpretation of the mechanism underlying aging and age-related diseases. This commentary article will discuss, in a wider sense, the implications of S-nitrosylation- and nitration-switched dysfunction of proteins/enzymes in neurodegenerative disorders including Alzheimer's disease (AD), Huntington's diseases (HD) and Parkinson's disease (PD).

scholarly journals S-nitrosylation-impaired autophagy: An alternative mechanism underlying aging?

2013 ◽  
Author(s):  
Qing-Ping Zeng
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorders ◽  
Alternative Mechanism ◽  
Age Related ◽  
Surprising Finding

Aging is mysterious with unknown managing patterns. A surprising finding on the tune mode of autophagy by S-nitrosylation is a distinctive step towards the interpretation of the mechanism underlying aging and age-related diseases. This commentary article will discuss, in a wider sense, the implications of S-nitrosylation- and nitration-switched dysfunction of proteins/enzymes in neurodegenerative disorders including Alzheimer's disease (AD), Huntington's diseases (HD) and Parkinson's disease (PD).

scholarly journals Bidirectional Mendelian randomization analysis of shared genetic signals between coexisting neurodegenerative disorders to decipher underlying causal pathways

2019 ◽  
Author(s):  
Sandeep Grover ◽  
Keyword(s):  
Multiple Sclerosis ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Macular Degeneration ◽  
Neurodegenerative Disorders ◽  
Mendelian Randomization ◽  
Age Related Macular Degeneration ◽  
European Ancestry ◽  
Age Related

ABSTRACTOBJECTIVETo investigate whether coexistence of various neurodegenerative disorders is coincidental or biologically connected.DESIGNTwo sample Mendelian randomization using summary effect estimatesSETTINGGenetic data taken on various neurodegenerative disorders from various cohorts comprising individuals predominantly of European ancestry.PARTICIPANTSInternational Genomics of Alzheimer’s patients (IGAP), project MinE, International Age-related Macular Degeneration Consortium (IAMDGC), International Multiple Sclerosis Genetics Consortium (IMSGC), International Parkinson’s Disease Genomics Consortium (IPDGC)MAIN OUTCOME MEASURESAlzheimer’s disease (AD), Amyotrophic lateral sclerosis (ALS), Age related macular degeneration (AMD), Multiple sclerosis (MS) and Parkinson’s disease (PD).RESULTSA Bonferroni corrected threshold of P=0.005 was considered to be significant, and P<0.05 was considered suggestive of evidence for a potential association. I observed a risky effect of PD on ALS (OR = 1.126, 95% CI = 1.059-1.198, P = 0.005). Using AD as exposure and PD as outcome, I observed a risky effect of AD on PD using all the MR methods with strongest results using MBE method (OR = 2.072, 95% CI = 1.006-4.028, P = 0.0416). Genetic predisposition to AD was further observed to be a risky for AMD (OR = 1.759, 95% CI = 1.040-1.974, P = 0.0363). On the contrary, AMD was observed to be strongly protective towards MS (OR = 0.861, 95% CI = 0.776-0.955, P = 0.0059).CONCLUSIONSMy findings are consistent with the previously observed relative occurrence of co-existing neurodegenerative diseases or overlapping symptoms among neurodegenerative diseases.

scholarly journals Global efficiency of the motor network is decreased in Parkinson's disease in comparison with essential tremor and healthy controls

2021 ◽  
Author(s):  
Natalia Pelizari Novaes ◽  
Joana Bisol Balardin ◽  
Fabiana Campos Hirata ◽  
Luciano Melo ◽  
Edson Amaro ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Essential Tremor ◽  
Healthy Controls ◽  
Global Efficiency ◽  
Motor Network

scholarly journals Imaging Familial and Sporadic Neurodegenerative Disorders Associated with Parkinsonism

2021 ◽  
Author(s):  
David J. Brooks
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorders ◽  
Lewy Body Dementia ◽  
Imaging Biomarkers ◽  
Imaging Findings ◽  
Subclinical Disease ◽  
Similarities And Differences ◽  
Potential Use

AbstractIn this paper, the structural and functional imaging changes associated with sporadic and genetic Parkinson’s disease and atypical Parkinsonian variants are reviewed. The role of imaging for supporting diagnosis and detecting subclinical disease is discussed, and the potential use and drawbacks of using imaging biomarkers for monitoring disease progression is debated. Imaging changes associated with nonmotor complications of PD are presented. The similarities and differences in imaging findings in Lewy body dementia, Parkinson’s disease dementia, and Alzheimer’s disease are discussed.

scholarly journals The TOMM40 ‘523’ polymorphism in disease risk and age of symptom onset in two independent cohorts of Parkinson’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Megan C. Bakeberg ◽  
Madison E. Hoes ◽  
Anastazja M. Gorecki ◽  
Frances Theunissen ◽  
Abigail L. Pfaff ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Symptom Onset ◽  
Disease Risk ◽  
Age Of Onset ◽  
Sequencing Analysis ◽  
Age Related ◽  
Australian Cohort ◽  
Progression Markers ◽  
Age Related Cognitive Decline

AbstractAbnormal mitochondrial function is a key process in the pathogenesis of Parkinson’s disease (PD). The central pore-forming protein TOM40 of the mitochondria is encoded by the translocase of outer mitochondrial membrane 40 homologue gene (TOMM40). The highly variant ‘523’ poly-T repeat is associated with age-related cognitive decline and age of onset in Alzheimer’s disease, but whether it plays a role in modifying the risk or clinical course of PD it yet to be elucidated. The TOMM40 ‘523’ allele length was determined in 634 people with PD and 422 healthy controls from an Australian cohort and the Parkinson’s Progression Markers Initiative (PPMI) cohort, using polymerase chain reaction or whole genome sequencing analysis. Genotype and allele frequencies of TOMM40 ‘523’ and APOE ε did not differ significantly between the cohorts. Analyses revealed TOMM40 ‘523’ allele groups were not associated with disease risk, while considering APOE ε genotype. Regression analyses revealed the TOMM40 S/S genotype was associated with a significantly later age of symptom onset in the PPMI PD cohort, but not after correction for covariates, or in the Australian cohort. Whilst variation in the TOMM40 ‘523’ polymorphism was not associated with PD risk, the possibility that it may be a modifying factor for age of symptom onset warrants further investigation in other PD populations.

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