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      Role of homocysteine in the development and progression of Parkinson’s disease

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          Abstract

          Homocysteine is an essential intermediate product of biochemical reactions that is present in various tissues of the human body. Homocysteine may be associated with the development and progression of Parkinson’s disease. Plasma homocysteine levels in patients with Parkinson’s disease are elevated compared to those of healthy individuals. High homocysteine drives PD development and progression while aggregating the clinical symptoms of PD patients. The relationship between PD and homocysteine involves multiple pathways, including nerve cell apoptosis, oxidative stress, and DNA damage. This is crucial for explaining how high homocysteine drives the PD procession. Elevated homocysteine level during PD development and progression offers a new strategy for the diagnosis and treatment of this disease.

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          MDS clinical diagnostic criteria for Parkinson's disease.

          Ronald Postuma, Daniela Berg, Matthew Stern … (2015)
          This document presents the Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's disease (PD). The Movement Disorder Society PD Criteria are intended for use in clinical research but also may be used to guide clinical diagnosis. The benchmark for these criteria is expert clinical diagnosis; the criteria aim to systematize the diagnostic process, to make it reproducible across centers and applicable by clinicians with less expertise in PD diagnosis. Although motor abnormalities remain central, increasing recognition has been given to nonmotor manifestations; these are incorporated into both the current criteria and particularly into separate criteria for prodromal PD. Similar to previous criteria, the Movement Disorder Society PD Criteria retain motor parkinsonism as the core feature of the disease, defined as bradykinesia plus rest tremor or rigidity. Explicit instructions for defining these cardinal features are included. After documentation of parkinsonism, determination of PD as the cause of parkinsonism relies on three categories of diagnostic features: absolute exclusion criteria (which rule out PD), red flags (which must be counterbalanced by additional supportive criteria to allow diagnosis of PD), and supportive criteria (positive features that increase confidence of the PD diagnosis). Two levels of certainty are delineated: clinically established PD (maximizing specificity at the expense of reduced sensitivity) and probable PD (which balances sensitivity and specificity). The Movement Disorder Society criteria retain elements proven valuable in previous criteria and omit aspects that are no longer justified, thereby encapsulating diagnosis according to current knowledge. As understanding of PD expands, the Movement Disorder Society criteria will need continuous revision to accommodate these advances.
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            Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases.

            Michael T. Lin, M. Flint Beal (2006)
            Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. Mitochondria are critical regulators of cell death, a key feature of neurodegeneration. Mutations in mitochondrial DNA and oxidative stress both contribute to ageing, which is the greatest risk factor for neurodegenerative diseases. In all major examples of these diseases there is strong evidence that mitochondrial dysfunction occurs early and acts causally in disease pathogenesis. Moreover, an impressive number of disease-specific proteins interact with mitochondria. Thus, therapies targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria, hold great promise.
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              Epidemiology of Parkinson's disease.

              Ole-Bjørn Tysnes, Anette Storstein (2017)
              Parkinson's disease (PD) affects 1-2 per 1000 of the population at any time. PD prevalence is increasing with age and PD affects 1% of the population above 60 years. The main neuropathological finding is α-synuclein-containing Lewy bodies and loss of dopaminergic neurons in the substantia nigra, manifesting as reduced facilitation of voluntary movements. With progression of PD, Lewy body pathology spreads to neocortical and cortical regions. PD is regarded as a movement disorder with three cardinal signs: tremor, rigidity and bradykinesia. A recent revision of the diagnostic criteria excludes postural instability as a fourth hallmark and defines supportive criteria, absolute exclusion criteria and red flags. Non-motor symptoms in PD have gained increasing attention and both motor and non-motor signs are now included among the supportive criteria. The cause of PD is unknown in most cases. Genetic risk factors have been identified, including monogenetic causes that are rare in unselected populations. Some genetic factor can be identified in 5-10% of the patients. Several environmental factors are associated with increased risk of PD. Autopsy studies show that the clinical diagnosis of PD is not confirmed at autopsy in a significant proportion of patients. Revised diagnostic criteria are expected to improve the clinician´s accuracy in diagnosing PD. Increasing knowledge on genetic and environmental risk factors of PD will probably elucidate the cause of this disease within the near future.
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                Author and article information

                Contributors
                Yuelei Jin:
                ORCID: https://orcid.org/0000-0003-3677-3235
                jinyuelei_001@163.com
                Journal
                Journal ID (nlm-ta): Ann Clin Transl Neurol
                Journal ID (iso-abbrev): Ann Clin Transl Neurol
                Journal ID (doi): 10.1002/(ISSN)2328-9503
                Journal ID (publisher-id): ACN3
                Title: Annals of Clinical and Translational Neurology
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Electronic): 2328-9503
                Publication date (Electronic): 21 October 2020
                Publication date Collection: November 2020
                Volume: 7
                Issue: 11 ( doiID: 10.1002/acn3.v7.11 )
                Pages: 2332-2338
                Affiliations
                [ 1 ] Department of Basic Medical Sciences Taizhou University Taizhou China
                [ 2 ] Department of Neurology Taizhou Second People’s Hospital Taizhou China
                [ 3 ] Department of Sleep Medicine Center Taizhou Second People’s Hospital Taizhou China
                [ 4 ] Department of Respiratory Medicine Municipal Hospital Affiliated to Medical School of Taizhou University Taizhou China
                Author notes
                [*] [* ] Correspondence

                Yuelei Jin, Department of Basic Medical Sciences, Taizhou University, No. 1139 Shifu Road, Jiaojiang District, Taizhou 318000, Zhejiang Province, China. Tel: (86)‐576‐88665198; Fax: XXXX; E‐mail: jinyuelei_001@ 123456163.com

                [a]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0003-3677-3235
                Article
                Publisher ID: ACN351227
                DOI: 10.1002/acn3.51227
                PMC ID: 7664283
                PubMed ID: 33085841
                SO-VID: 34f2c509-e219-4a1d-ae7e-40992adf5df4
                Copyright © © 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                History
                Date received : 23 July 2020
                Date revision received : 22 September 2020
                Date accepted : 30 September 2020
                Page count
                Figures: 0, Tables: 0, Pages: 7, Words: 12743
                Funding
                Funded by: Scientific Research Project of Taizhou Municipal Science and Technology Bureau
                Award ID: 20ywb100
                Award ID: 20ywb101
                Award ID: 1902ky100
                This work was funded by Scientific Research Project of Taizhou Municipal Science and Technology Bureau grants 20ywb100, 20ywb101, and 1902ky100.
                Categories
                Subject: Review
                Subject: Review
                Custom metadata
                source-schema-version-number 2.0
                cover-date November 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.9.4 mode:remove_FC converted:13.11.2020

                Keywords: apoptosis,hyperhomocysteinemia,oxidative stress,parkinson’s disease
                Data availability:
                Keywords: apoptosis, hyperhomocysteinemia, oxidative stress, parkinson’s disease

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