Evidence map›Paper›PMID 33340068›Full record

ReviewCellular and molecular life sciences : CMLS2021

Autophagy and the endolysosomal system in presynaptic function.

Maria Andres-Alonso, Michael R Kreutz, Anna Karpova

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.1field-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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Fiber-basedNeurophotonics · 2024
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. The Key Role of Lysosomal Protease Cathepsins in Viral Infections.International journal of molecular sciences · 2022
    Review
  15. Article
  16. Autophagy in Human Retinal Neurons in Glaucoma.Bulletin of experimental biology and medicine · 2022
    Article
  17. A Quantitative Model of Sporadic Axonal Degeneration in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  18. Review
  19. Review
  20. 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

3 authors at 2 institutions in 1 country.

Maria Andres-AlonsoResearch Group Neuroplasticity, Leibniz Institute for Neurobiology, 39118, Magdeburg, Germany.ORCID http://orcid.org/0000-0002-1585-539X
Michael R KreutzResearch Group Neuroplasticity, Leibniz Institute for Neurobiology, 39118, Magdeburg, Germany. Michael.Kreutz@zmnh.uni-hamburg.de.ORCID http://orcid.org/0000-0003-0575-6950
Anna KarpovaResearch Group Neuroplasticity, Leibniz Institute for Neurobiology, 39118, Magdeburg, Germany. akarpova@lin-magdeburg.de.ORCID http://orcid.org/0000-0001-7423-4764
Universität Hamburg · DECenter for Behavioral Brain Sciences · DE

Funding

Bundesministerium für Bildung und Forschung ENERGIDeutsche Forschungsgemeinschaft KR1879 6-1, 9-1, 10-1
6 · The paper itself

Abstract

The complex morphology of neurons, the specific requirements of synaptic neurotransmission and the accompanying metabolic demands create a unique challenge for proteostasis. The main machineries for neuronal protein synthesis and degradation are localized in the soma, while synaptic junctions are found at vast distances from the cell body. Sophisticated mechanisms must, therefore, ensure efficient delivery of newly synthesized proteins and removal of faulty proteins. These requirements are exacerbated at presynaptic sites, where the demands for protein turnover are especially high due to synaptic vesicle release and recycling that induces protein damage in an intricate molecular machinery, and where replacement of material is hampered by the extreme length of the axon. In this review, we will discuss the contribution of the two major pathways in place, autophagy and the endolysosomal system, to presynaptic protein turnover and presynaptic function. Although clearly different in their biogenesis, both pathways are characterized by cargo collection and transport into distinct membrane-bound organelles that eventually fuse with lysosomes for cargo degradation. We summarize the available evidence with regard to their degradative function, their regulation by presynaptic machinery and the cargo for each pathway. Finally, we will discuss the interplay of both pathways in neurons and very recent findings that suggest non-canonical functions of degradative organelles in synaptic signalling and plasticity.

Indexed as

AutophagyAnimalsHumansLysosomesNerve Growth FactorsNeuronal PlasticityNeuronsPresynaptic TerminalsSynapsesSynaptic VesiclesNerve Growth FactorsAutophagyAxonal boutonsEndolysosomal systemProteostasisSynaptic plasticity

Identifiers

PMID33340068
PMCPMC8004491
OpenAlexW3117895140

What Socratic 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 Socratic graph.