Evidence map›Paper›PMID 39401987›Full record

ArticleAutophagy2024

Clustering lysosomes around the MTOC: a promising strategy for SNCA/alpha-synuclein breakdown leading to parkinson disease treatment.

Yukiko Sasazawa, Yuki Date, Nobutaka Hattori, Shinji Saiki

Abstract read
In one paragraph

Article in Autophagy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. 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.

Yukiko SasazawaResearch Institute for Diseases of Old Age Juntendo, University Graduate School of Medicine, Tokyo, Japan.
Yuki DateDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo, Japan.
Shinji SaikiDepartment of Neurology, Juntendo University Faculty of Medicine, Tokyo, Japan.ORCID 0000-0002-9732-8488

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy maintains cellular homeostasis by degrading cytoplasmic components and its disruption is linked to Parkinson disease (PD), which is characterized by dopamine depletion and the accumulation of SNCA/α-synuclein aggregates in neurons. Therefore, activation of autophagy is considered a therapeutic strategy for PD; however, autophagy inducers have not yet been developed as therapeutic drugs because they are involved in a wide range of signaling pathways. Here, we focused on the lysosomal clustering around the microtubule-organizing center (MTOC) that can regulate the process of autophagosome-lysosome fusion, the final step of autophagy, and examined how lysosomal clustering affects protein degradation through autophagy. Our study identified six compounds from a high-content screen of 1,200 clinically approved drugs that induce both lysosomal clustering and autophagy. Notably, albendazole reduced SNCA aggregates in a PD model by lysosomal clustering and autophagy. These findings suggest that targeting lysosomal clustering could offer new therapeutic insights for PD.

Indexed as

alpha-SynucleinAutophagyLysosomesMicrotubule-Organizing CenterParkinson DiseaseAnimalsAutophagosomesHumansMicealpha-SynucleinAlpha-synucleinautophagylysosomal clusteringlysosomal traffickingParkinson disease

Identifiers

PMID39401987
PMCPMC11587859

What Socratic 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 Socratic graph.