Evidence map›Paper›PMID 31225476›Full record

ArticleCell stress2018

Endolysosomal dysfunction and exosome secretion: implications for neurodegenerative disorders.

André M Miranda, Gilbert Di Paolo

Open access · goldAbstract readComment
In one paragraph

Article in Cell stress, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 42 citations in OpenAlex.

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  9. Phosphatidylinositol-3-phosphate mediates Arc capsid secretion through the multivesicular body pathway.Proceedings of the National Academy of Sciences of the United States of America · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

André M MirandaDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York City, NY 10032, USA.
Gilbert Di PaoloDepartment of Pathology and Cell Biology, Columbia University Medical Center, New York City, NY 10032, USA.
Columbia University Irving Medical Center · USUniversity of Minho · PT

Funding

Satellite Diagnostic and Treatment Clinic CoreP50AG008702 · NIA · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI DE JAGER, PHILIP L · 1989 to 2019
$46.3M
Role of phospholipids in membrane traffic at the synapseR01NS056049 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI LIEM, RONALD K. · 2006 to 2016
$3.7M
NIA NIH HHS P50 AG008702NINDS NIH HHS R01 NS056049
6 · The paper itself

Abstract

Growing evidence suggests that endolysosomal and autophagic defects are key pathogenic processes in various neurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). The causal relationship between these defects and neurodegeneration is supported by human genetic studies identifying disease mutations in genes controlling endolysosomal function and autophagy. The canonical view is that defects in these processes lead to impaired lysosomal clearance of proteins prone to form toxic oligomeric assemblies and/or aggregates, ultimately resulting in cellular pathologies that define these disorders. Because lysosomes mediate the clearance of a large number of lipids, lipid storage is frequently associated with compromised endolysosomal and autophagic function. However, an emerging notion, supported by our recent study on class III phosphatidylinositol 3-kinase (PI3K) Vps34, is that neuronal endolysosomal and autophagic dysfunction can manifest itself with the occurrence of physically damaged endomembranes and with the release of exosomes enriched for Amyloid Precursor Protein COOH-terminal fragments (APP-CTFs) as well as atypical phospholipid bis(monoacylglycero)phosphate (BMP). Here, we summarize our recent findings and their potential implications in the context of lysosomal biology, lipid signaling and neurodegenerative diseases.

Indexed as

endomembrane damageextracellular vesiclesgalectinLBPAlysobisphosphatidic acidphosphatidylinositol-3-phosphatephosphoinositidephospholipidssphingolipids

Identifiers

PMID31225476
PMCPMC6551703
OpenAlexW2802452640

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.