Parkinson's disease: Molecular risk factors

Grünblatt, Edna

doi:10.1016/s1353-8020(11)70016-5

Cited by 14 publications

(7 citation statements)

References 18 publications

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“…Following these findings, more specifically, the down-regulation of ALDH1A1 mRNA was found by our group using genomewide transcriptomic assay in SN from PD patients compared to controls (Grünblatt et al 2004). Following this report, many other groups could consistently confirm ALDH1A1 down-regulation in the SN of PD patients (Durrenberger et al 2012;Grünblatt 2012;Kotraiah et al 2013). In the last report by Kotraiah et al the analysis was extended to the various splice variants of ALDH1A1, which all showed similar down-regulation (Kotraiah et al 2013).…”

Section: Transcriptomic Alterationssupporting

confidence: 71%

Aldehyde dehydrogenase (ALDH) in Alzheimer’s and Parkinson’s disease

Grünblatt

Riederer

2014

J Neural Transm

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Evidence suggests that aldehyde dehydrogenase (ALDH; E.C. 1.2.1.3) gene, protein expression and activity are substantially decreased in the substantia nigra of patients with Parkinson's disease (PD). This holds especially true for cytosolic ALDH1A1, while mitochondrial ALDH2 is increased in the putamen of PD. Similarly, in Alzheimer's disease (AD) several studies in genetic, transcriptomic, protein and animal models suggest ALDH involvement in the neurodegeneration processes. Such data are in line with findings of increased toxic aldehydes, like for example malondialdehyde, nonenal, 3,4-dihydroxyphenylacetaldehyde and others. Genetic, transcriptomic and protein alterations may contribute to such data. Also in vitro and in vivo experimental work points to an important role of ALDH in the pathology of neurodegenerative disorders. Aims at investigating dysfunctions of aldehyde detoxification are suitable to define genetic/molecular targets for new therapeutic strategies balancing amine metabolism in devastating disorders like PD and probably also AD.

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Section: Transcriptomic Alterationssupporting

confidence: 71%

Aldehyde dehydrogenase (ALDH) in Alzheimer’s and Parkinson’s disease

Grünblatt

Riederer

2014

J Neural Transm

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“…Not only will these biomarkers be useful for diagnosing the disease in affected persons, it will be useful for identifying family members or populations at risk, thus providing an opportunity to initiate neuroprotective therapy at an asymptomatic stage. Literatures have reported the transcription (RNA) profiles in peripheral blood samples might be of diagnostic value for estimating the risk of developing sporadic PD [ 16 , 22 ]. Mitochondrial dysfunction, reactive oxygen species (ROS), proteasome dysfunction and neuroinflammation are implicated in PD [ 23 – 26 ], as the mutations or changes of genes related with these processes, such as PINK1, Parkin, DJ-1, SNCA, UCHL1, LRRK2, TRIM24, MUL1 and USP30, are found to be widely present in PD [ 27 – 29 ].…”

Section: Discussionmentioning

confidence: 99%

Pilot study: molecular risk factors for diagnosing sporadic Parkinson's disease based on gene expression in blood in MPTP-induced rhesus monkeys

et al. 2017

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Clinical diagnosis of Parkinson's disease (PD) is characterized by the classical features of tremor, bradykinesia and rigidity, which are present only when more than 70%-80% degeneration of dopaminergic (DA) neurons in the substantia nigra. The lack of means for early diagnosis of PD has elicited interest in searching for its risk factors, which, by now, are almost obtained at a single time point in PD process, and little developing risk factors, obtained from completely normal situation to the onset or even advanced stage of PD in individual person which could monitor the progress of PD, are present. Here we have detected some potential factors in the blood of MPTP induced PD monkeys along with the progress of the disease. All the PD monkeys showed mild PD symptoms since the 9th week and gradually reached a classic and stable parkinsonism stage at the 18th week. Our results have found that the expression of Parkin, USP30, MUL1, PINK1, and LRRK2 significantly increased at 1st, 3th, 3th, 5th, and 8th week respectively and remained high till the end; The expression of UCHL1 and TRIM24 significantly increased at the 1st and 18th week, respectively, then gradually decreased and significantly lower than normal value; DJ-1 showed significantly decreased since the 12th week, while SNCA showed no significantly changed excepted at the 5th week. And, the terminal results of whole blood were highly consistent with those of in SN. These results support that these genes change may as biomarkers to monitor the progress of PD, and may facilitate the development of biomarkers for early diagnosis.

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“…Various risk and protective factors of PD have been extensively investigated over several decades, however the etiology remains largely unclear [ 3 ]. There is a great interest in identifying at-risk individuals early, to potentially slow down or prevent neurodegeneration [ 4 ]. While genetic and familial environmental exposures are often cited to contribute to PD risk, lifestyle exposures such as smoking, coffee/tea and alcohol consumption have been the focus of research for several decades with varying and often conflicting results.…”

Section: Introductionmentioning

confidence: 99%

Alcohol Consumption and Parkinson’s Disease Risk: A Review of Recent Findings

Bettiol

Rose

Hughes

et al. 2015

JPD

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Background: The association between Parkinson’s disease and lifestyle exposures such as smoking, coffee and alcohol consumption have been the focus of research for several decades, with varying and often conflicting results. Objective: This paper reviews the key features of observational studies investigating the relationship between alcohol drinking and PD risk, to determine potential sources of variability between the results. Methods: Relevant literature from 2000–2014 was systematically retrieved using three databases. Primary research articles were included if they reported a measure of association between quantity and frequency of alcohol intake and PD risk, and adjusted at least for the potential confounding factors of smoking and age. Results: Sixteen articles were identified. The seven case-control studies were more likely to report a weak protective association by level of alcohol consumption compared to the studies with prospective designs. Two studies reported the relationship between heavy (harmful to health) drinking and PD. There was weak evidence that associations varied by type of alcoholic beverage. Smoking may modify the association between alcohol intake and PD risk, however, the evidence does not support the theory that a confounder (such as an addiction-avoiding personality trait) produced the inverse associations between smoking, coffee and alcohol intake and PD risk. Methodological weaknesses of the studies, including selection and recall bias, residual confounding and lack of statistical power may in part account for their differences. Conclusion: The weak association between alcohol drinking and PD risk was found in studies at greater risk of selection and recall bias.

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Parkinson's disease: Molecular risk factors

Cited by 14 publications

References 18 publications

Aldehyde dehydrogenase (ALDH) in Alzheimer’s and Parkinson’s disease

Aldehyde dehydrogenase (ALDH) in Alzheimer’s and Parkinson’s disease

Pilot study: molecular risk factors for diagnosing sporadic Parkinson's disease based on gene expression in blood in MPTP-induced rhesus monkeys

Alcohol Consumption and Parkinson’s Disease Risk: A Review of Recent Findings

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