Evidence map›Paper›PMID 26749150›Full record

ReviewJournal of neurochemistry2016

Therapeutic approaches in Parkinson's disease and related disorders.

Elvira Valera, Eliezer Masliah

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of neurochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
6.1field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  17. Modulation of Amyloid States by Molecular Chaperones.Cold Spring Harbor perspectives in biology · 2019
    Review
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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

2 authors at 1 institution in 1 country.

Elvira ValeraDepartment of Neurosciences, University of California, San Diego, La Jolla, California, USA.
Eliezer MasliahDepartment of Neurosciences, University of California, San Diego, La Jolla, California, USA. emasliah@ucsd.edu.
University of California, San Diego · US

Funding

VIRUS-INDUCED BRAIN PATHOLOGYP50AG005131 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BREWER, JAMES B · 1985 to 2018
$55.4M
Tissue Culture CoreP01AG022074 · NIA · J. DAVID GLADSTONE INSTITUTES · PI FINKBEINER, STEVEN M · 2003 to 2012
$27.0M
Studies on Diagnosis, Pathophysiology, and Treatment of Autonomic Failure in MSAP01NS044233 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2003 to 2014
$12.4M
Mechanisms of Neuroprotection in HIV EncephalitisR01MH062962 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2002 to 2016
$5.2M
B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
Clearance Pathways in the CNS in Aging and HIVR01AG043384 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DESPLATS, PAULA ALEJANDRA · 2012 to 2016
$1.9M
NIA NIH HHS P01 AG022074NIA NIH HHS P50 AG005131NIA NIH HHS R01 AG018440NIA NIH HHS R01 AG043384NIA NIH HHS R37 AG018440NIMH NIH HHS R01 MH062962NINDS NIH HHS P01 NS044233
6 · The paper itself

Abstract

The lack of effective therapies for neurodegenerative disorders is one of the most relevant challenges of this century, considering that, as the global population ages, the incidence of these type of diseases is quickly on the rise. Among these disorders, synucleinopathies, which are characterized by the abnormal accumulation and spreading of the synaptic protein alpha-synuclein in the brain, already constitute the second leading cause of parkinsonism and dementia in the elderly population. Disorders with alpha-synuclein accumulation include Parkinson's disease, dementia with Lewy bodies and multiple system atrophy. Numerous therapeutic alternatives for synucleinopathies are being tested in pre-clinical models and in the clinic; however, only palliative treatments addressing the dopaminergic deficits are approved to date, and no disease-modifying options are available yet. In this article, we provide a brief overview of therapeutic approaches currently being explored for synucleinopathies, and suggest possible explanations to the clinical trials outcomes. Finally, we propose that a deeper understanding of the pathophysiology of synucleinopathies, together with a combination of therapies tailored to each disease stage, may lead to better therapeutic outcomes in synucleinopathy patients. Synucleinopathies, neurodegenerative disorders characterized by the abnormal accumulation of the protein alpha-synuclein, constitute the second leading cause of parkinsonism and dementia in the elderly population, however, no disease-modifying options are available yet. In this review, we summarize the therapeutic approaches currently being explored for synucleinopathies, suggest possible explanations to the clinical outcomes, and propose areas of further therapeutic improvement. This article is part of a special issue on Parkinson disease.

Indexed as

alpha-SynucleinAnimalsClinical Trials as TopicDementiaGenetic TherapyHumansLewy Body DiseaseMultiple System AtrophyParkinson DiseaseStem Cell Transplantationalpha-Synuclein

Identifiers

PMID26749150
PMCPMC4939141
OpenAlexW2226926731

What OpenQuestion holds

Textmetadata
LicenceTDM
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.