Evidence map›Paper›PMID 29492779›Full record

ReviewCNS drugs2018

Activating Autophagy as a Therapeutic Strategy for Parkinson's Disease.

Alan J Fowler, Charbel E-H Moussa

Abstract readReview
PubMed Publisher
In one paragraph

Review in CNS drugs, 2018. 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
4.6field-weighted citation impact, top 5% 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, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Disease modification in Parkinsonism: obstacles and ways forward.Journal of neural transmission (Vienna, Austria : 1996) · 2022
    Review
  11. Article
  12. Article
  13. Inhibition of the TLR/NF-Oxidative medicine and cellular longevity · 2022
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Alan J FowlerDepartment of Neurology, Laboratory for Dementia and Parkinsonism, Translational Neurotherapeutics Program, Room 203-C, Building D, 4000 Reservoir Rd. NW, Washington, DC, USA.
Charbel E-H MoussaDepartment of Neurology, Laboratory for Dementia and Parkinsonism, Translational Neurotherapeutics Program, Room 203-C, Building D, 4000 Reservoir Rd. NW, Washington, DC, USA. cem46@georgetown.edu.
Nanotherapeutics (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease is a progressive neurodegenerative disease characterized by Lewy body pathology of which the primary constituent is aggregated misfolded alpha-synuclein protein. Currently, there are no clinical therapies for treatment of the underlying alpha-synuclein dysfunction and accumulation, and the standard of care for patients with Parkinson's disease focuses only on symptom management, creating an immense therapeutic gap that needs to be filled. Defects in autophagy have been strongly implicated in Parkinson's disease. Here, we review evidence from human, mouse, and cell culture studies to briefly explain these defects in autophagy in Parkinson's disease and the necessity for autophagy to be carefully and precisely tuned to maintain neuron survival. We summarize recent experimental agents for treating alpha-synuclein accumulation in α-synuclein Parkinson's disease and related synucleinopathies. Most of the efforts for developing experimental agents have focused on immunotherapeutic strategies, but we discuss why those efforts are misplaced. Finally, we emphasize why increasing autophagy flux for alpha-synuclein clearance is the most promising therapeutic strategy. Activating autophagy has been successful in preclinical models of Parkinson's disease and yields promising results in clinical trials.

Indexed as

alpha-SynucleinAnimalsAntiparkinson AgentsAutophagyDrug DevelopmentDrug Evaluation, PreclinicalHumansMiceParkinson Diseasealpha-SynucleinAntiparkinson Agents

Identifiers

PMID29492779
OpenAlexW2791130706

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.