Evidence map›Paper›PMID 38899624›Full record

ArticleAutophagy2024

Secretory autophagy - a new paradigm regulating synaptic plasticity.

Yen-Ching Chang, Karen T Chang

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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

2 authors.

Yen-Ching ChangZilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.
Karen T ChangZilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

Funding

Role of DYRK1A/MNB in Synaptic growth and functionR01NS080946 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAREN T CHANG · 2013 to 2026
$5.0M
Molecular mechanisms underlying activity-induced synaptic remodelingR01NS102260 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI CHANG, KAREN T · 2018 to 2022
$2.2M
NINDS NIH HHS R01 NS080946NINDS NIH HHS R01 NS102260
6 · The paper itself

Abstract

When exposed to new experiences or changes in the environment, neurons rapidly remodel their synaptic structure and function in a process called activity-induced synaptic remodeling. This process is necessary for transforming transient experiences into stable, lasting memories. The molecular mechanisms underlying acute, activity-dependent synaptic changes are not well understood, partly because processes regulating synaptic plasticity and neurodevelopment are intricately linked. By using an RNAi screen in

Indexed as

AutophagyNeuronal PlasticityAnimalsAutophagosomesDrosophila melanogasterDrosophila ProteinsHumansLysosomesNeuronsSynapsesDrosophila ProteinsActivity-induced synaptic remodelingDrosophilaMacroautophagysecretory autophagysynaptic plasticity

Identifiers

PMID38899624
PMCPMC11423689

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.