Evidence map›Paper›PMID 30756362›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2019

Nucleic Acid-Based Therapeutics for Parkinson's Disease.

Masayuki Nakamori, Eunsung Junn, Hideki Mochizuki, M Maral Mouradian

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
5.3field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Long non-coding RNA UCA1 regulates MPPMetabolic brain disease · 2023
    Article
  9. Review
  10. Review
  11. Intronic enhancers of the humanScience advances · 2022
    Article
  12. Targeted Molecular Therapeutics for Parkinson's Disease: A Role for Antisense Oligonucleotides?Movement disorders : official journal of the Movement Disorder Society · 2022
    Article
  13. Article
  14. MiR-9-5p Inhibits the MMPOxidative medicine and cellular longevity · 2022
    Article
  15. Review
  16. Noncoding RNA therapeutics for substance use disorder.Advances in drug and alcohol research · 2022
    Article
  17. Review
  18. Epigenetic Regulation of Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2021
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Masayuki NakamoriDepartment of Neurology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Eunsung JunnRobert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ, 08854, USA.
Hideki MochizukiDepartment of Neurology, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
M Maral MouradianRobert Wood Johnson Medical School Institute for Neurological Therapeutics, and Department of Neurology, Rutgers Biomedical and Health Sciences, Piscataway, NJ, 08854, USA. m.mouradian@rutgers.edu.ORCID 0000-0002-9937-412X
Rutgers, The State University of New Jersey · USThe University of Osaka · JP

Funding

Manipulating Gene Expression in the Dyskinesias of Parkinson's DiseaseR01NS073994 · NINDS · EMORY UNIVERSITY · PI MOURADIAN, M. MARAL, PAPA, STELLA M · 2011 to 2016
$2.4M
PP2A Dysregulation in the Pathogenesis of alpha-SynucleinopathiesR01NS101134 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI MOURADIAN, M. MARAL, NICHOLLS, RUSSELL E · 2017 to 2021
$2.3M
Synergistic Neuroprotective Mechanisms of Coffee Components in Parkinson's DiseasR01AT006868 · NCCIH · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI MOURADIAN, M. MARAL, STOCK, JEFFRY B · 2012 to 2016
$2.2M
Alpha-Synuclein Regulation by microRNAsR01NS070898 · NINDS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI JUNN, EUNSUNG · 2011 to 2015
$1.7M
Developing Novel RNA-Based Therapeutics for Parkinson's DiseaseR33NS096032 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI DISNEY, MATTHEW D, MOURADIAN, M. MARAL · 2018 to 2019
$843k
Developing Novel RNA-Based Therapeutics for Parkinson's DiseaseR21NS096032 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI DISNEY, MATTHEW D, MOURADIAN, M. MARAL · 2017 to 2017
$452k
Translational regulation by DJ-1R21NS095003 · NINDS · RBHS-ROBERT WOOD JOHNSON MEDICAL SCHOOL · PI JUNN, EUNSUNG · 2016 to 2017
$437k
Japan Agency for Medical Research and Development JP17ek0109195National Center for Complementary and Alternative Medicine AT006868NCCIH NIH HHS R01 AT006868NINDS NIH HHS NS070898NINDS NIH HHS NS073994NINDS NIH HHS NS095003NINDS NIH HHS NS096032NINDS NIH HHS NS101134NINDS NIH HHS R01 NS070898NINDS NIH HHS R01 NS073994NINDS NIH HHS R01 NS101134NINDS NIH HHS R21 NS095003NINDS NIH HHS R21 NS096032NINDS NIH HHS R33 NS096032
6 · The paper itself

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder that is diagnosed largely on clinical grounds due to characteristic motor manifestations that result from the loss of nigrostriatal dopaminergic neurons. While traditional pharmacological approaches to enhance dopamine levels, such as with L-dopa, can be very effective initially, the chronic use of this dopamine precursor is commonly plagued with motor response complications. Additionally, with advancing disease, non-motor manifestations emerge, including psychosis and dementia that compound patient disability. The pathology includes hallmark intraneuronal inclusions known as Lewy bodies and Lewy neurites that contain fibrillar α-synuclein aggregates. Evidence has also accumulated that these aggregates can propagate across synaptically connected brain regions, a phenomenon that can explain the progressive nature of the disease and the emergence of additional symptoms over time. The level of α-synuclein is believed to play a critical role in its fibrillization and aggregation. Accordingly, nucleic acid-based therapeutics for PD include strategies to deliver dopamine biosynthetic enzymes to boost dopamine production or modulate the basal ganglia circuitry in order to improve motor symptoms. Delivery of trophic factors that might enhance the survival of dopamine neurons is another strategy that has been attempted. These gene therapy approaches utilize viral vectors and are delivered stereotaxically in the brain. Alternative disease-modifying strategies focus on downregulating the expression of the α-synuclein gene using various techniques, including modified antisense oligonucleotides, short hairpin RNA, short interfering RNA, and microRNA. The latter approaches also have implications for dementia with Lewy bodies. Other PD genes can also be targeted using nucleic acids. In this review, we detail these various strategies that are still experimental, and discuss the challenges and opportunities of nucleic acid-based therapeutics for PD.

Indexed as

alpha-SynucleinAnimalsGenetic TherapyHumansMicroRNAsOligonucleotides, AntisenseParkinson DiseaseRNA, Small Interferingalpha-SynucleinMicroRNAsOligonucleotides, AntisenseRNA, Small InterferingAntisense oligonucleotidesGene therapyMicroRNANeurodegenerationα-Synuclein

Identifiers

PMID30756362
PMCPMC6554378
OpenAlexW2911646467

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.