scholarly journals Biomarker in Parkinson’s Disease: Clinical and Biochemical Biomarker

2021 ◽  
Vol 39 (4) ◽  
pp. 287-297
Author(s):  
Ju-Young Lee ◽  
Hyeo-il Ma ◽  
Young Eun Kim
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disease ◽  
Biological Tissue ◽  
Disease Course ◽  
Prodromal Stage ◽  
Successful Development ◽  
Disease Modifying Therapy ◽  
Clinical Biomarkers ◽  
Disease Modifying

Parkinson’s disease is a neurodegenerative disease compromising progressive motor and non-motor features for a long disease course. Although many drugs controlling parkinsonian symptoms were discovered, treatment with disease-modifying or halting effect was not developed to date. The exploration of reliable biomarkers would be helpful for better predicting disease progression and thereby successful development of disease-modifying therapy. In this review, we will review the clinical biomarkers in the prodromal stage and biomarkers using biological tissue in Parkinson’s disease.

scholarly journals Parkinson’s Disease: Available Clinical and Promising Omics Tests for Diagnostics, Disease Risk Assessment, and Pharmacotherapy Personalization

Diagnostics ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 339 ◽  
Author(s):  
Oxana P. Trifonova ◽  
Dmitri L. Maslov ◽  
Elena E. Balashova ◽  
Guzel R. Urazgildeeva ◽  
Denis A. Abaimov ◽  
...  
Keyword(s):  
Risk Assessment ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disease ◽  
Disease Risk ◽  
Modern Medicine ◽  
Economic Problem ◽  
Prodromal Stage ◽  
Effective System ◽  
Diagnostics And Therapy

Parkinson’s disease is the second most frequent neurodegenerative disease, representing a significant medical and socio-economic problem. Modern medicine still has no answer to the question of why Parkinson’s disease develops and whether it is possible to develop an effective system of prevention. Therefore, active work is currently underway to find ways to assess the risks of the disease, as well as a means to extend the life of patients and improve its quality. Modern studies aim to create a method of assessing the risk of occurrence of Parkinson’s disease (PD), to search for the specific ways of correction of biochemical disorders occurring in the prodromal stage of Parkinson’s disease, and to personalize approaches to antiparkinsonian pharmacotherapy. In this review, we summarized all available clinically approved tests and techniques for PD diagnostics. Then, we reviewed major improvements and recent advancements in genomics, transcriptomics, and proteomics studies and application of metabolomics in PD research, and discussed the major metabolomics findings for diagnostics and therapy of the disease.

scholarly journals Poly(ADP-ribose) drives pathologic α-synuclein neurodegeneration in Parkinson’s disease

Science ◽  
2018 ◽  
Vol 362 (6414) ◽  
pp. eaat8407 ◽  
Author(s):  
Tae-In Kam ◽  
Xiaobo Mao ◽  
Hyejin Park ◽  
Shih-Ching Chou ◽  
Senthilkumar S. Karuppagounder ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Mechanisms ◽  
Parp Inhibitors ◽  
Dopamine Neurons ◽  
Parp Activation ◽  
Disease Modifying Therapy ◽  
Genetic Deletion ◽  
Disease Modifying ◽  
Parp 1

The pathologic accumulation and aggregation of α-synuclein (α-syn) underlies Parkinson’s disease (PD). The molecular mechanisms by which pathologic α-syn causes neurodegeneration in PD are not known. Here, we found that pathologic α-syn activates poly(adenosine 5′-diphosphate–ribose) (PAR) polymerase-1 (PARP-1), and PAR generation accelerates the formation of pathologic α-syn, resulting in cell death via parthanatos. PARP inhibitors or genetic deletion of PARP-1 prevented pathologic α-syn toxicity. In a feed-forward loop, PAR converted pathologic α-syn to a more toxic strain. PAR levels were increased in the cerebrospinal fluid and brains of patients with PD, suggesting that PARP activation plays a role in PD pathogenesis. Thus, strategies aimed at inhibiting PARP-1 activation could hold promise as a disease-modifying therapy to prevent the loss of dopamine neurons in PD.

scholarly journals Alpha-synuclein antisense oligonucleotides as a disease-modifying therapy for Parkinson’s disease

2019 ◽  
Author(s):  
Tracy A. Cole ◽  
Hien Zhao ◽  
Timothy J. Collier ◽  
Ivette Sandoval ◽  
Caryl E. Sortwell ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Antisense Oligonucleotides ◽  
Alpha Synuclein ◽  
Nucleotide Polymorphisms ◽  
Gene Encoding ◽  
Disease Modifying Therapy ◽  
Increase Risk ◽  
Disease Modifying

AbstractParkinson’s disease (PD) is a prevalent neurodegenerative disease with no approved disease-modifying therapies. Multiplications, mutations, and single nucleotide polymorphisms in the SNCA gene, encoding alpha-synuclein protein (aSyn), either cause or increase risk for PD. Intracellular accumulations of aSyn are pathological hallmarks of PD. Taken together, reduction of aSyn production may provide a disease-modifying therapy for PD. We show that antisense oligonucleotides (ASOs) reduce production of aSyn in rodent pre-formed fibril (PFF) models of PD. Reduced aSyn production leads to prevention and removal of established aSyn pathology and prevents dopaminergic cell dysfunction. In addition, we address the translational potential of the approach through characterization of human SNCA targeting ASOs that efficiently suppress the human SNCA transcript in vivo. We demonstrate broad activity and distribution of the human SNCA ASOs throughout the non-human primate brain and a corresponding decrease in aSyn cerebral spinal fluid (CSF) levels. Taken together, these data suggest that by inhibiting production of aSyn it may be possible to reverse established pathology and thus supports the development of SNCA ASOs as a potentially disease modifying therapy for PD and related synucleinopathies.SummaryAntisense oligonucleotides designed against SNCA, which are progressing to the clinic, have the potential to be a disease modifying therapeutic for Parkinson’s disease patients.

scholarly journals Nigral Iron Elevation Is an Invariable Feature of Parkinson’s Disease and Is a Sufficient Cause of Neurodegeneration

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Scott Ayton ◽  
Peng Lei
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Substantia Nigra ◽  
Neurodegenerative Disorder ◽  
Motor Deficits ◽  
Disease Mechanism ◽  
Disease Modifying Therapy ◽  
Disease Modifying Therapies ◽  
Sufficient Cause ◽  
Disease Modifying

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by motor deficits accompanying degeneration of substantia nigra pars compactor (SNc) neurons. Although familial forms of the disease exist, the cause of sporadic PD is unknown. Symptomatic treatments are available for PD, but there are no disease modifying therapies. While the neurodegenerative processes in PD may be multifactorial, this paper will review the evidence that prooxidant iron elevation in the SNc is an invariable feature of sporadic and familial PD forms, participates in the disease mechanism, and presents as a tractable target for a disease modifying therapy.

Promising disease-modifying therapies for Parkinson’s disease

2019 ◽  
Vol 11 (520) ◽  
pp. eaba1659 ◽  
Author(s):  
Valina L. Dawson ◽  
Ted M. Dawson
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Trials ◽  
New Agents ◽  
Disease Modifying Therapy ◽  
Disease Modifying Therapies ◽  
Disease Modifying

To date, there is no disease-modifying therapy for Parkinson’s disease; however, promising new agents have advanced into clinical trials.

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