Evidence map›Paper›PMID 32739009›Full record

ReviewInternational review of neurobiology2020

Endosomal-lysosomal dysfunction in metabolic diseases and Alzheimer's disease.

Michael F Almeida, Ben A Bahr, Stephen T Kinsey

Abstract readReview
In one paragraph

Review in International review of neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing 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

29 citing papers in PubMed.

  1. Article
  2. Review
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  4. Review
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  6. Ginseng extract improves synaptic resiliency: A key factor for healthy cognitive aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  7. Review
  8. Loss of lysosomal acid lipase contributes to Alzheimer's disease pathology and cognitive decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. Review
  10. Review
  11. Lysosomes' fallback strategies: more than just survival or death.Frontiers in cell and developmental biology · 2025
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Endo-lysosomal dysfunction in neurodegenerative diseases: opinion on current progress and future direction in the use of exosomes as biomarkers.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
  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.

Michael F AlmeidaBiotechnology Research and Training Center, University of North Carolina-Pembroke, Pembroke, NC, United States.
Ben A BahrBiotechnology Research and Training Center, University of North Carolina-Pembroke, Pembroke, NC, United States.
Stephen T KinseyDepartment of Biology and Marine Biology, University of North Carolina-Wilmington, Wilmington, NC, United States. Electronic address: kinseys@uncw.edu.

Funding

The effects of chronic AMPK activation on skeletal muscle protein turnover and satellite cell function in normal and obese juvenile miceR15DK106688 · NIDDK · UNIVERSITY OF NORTH CAROLINA WILMINGTON · PI KINSEY, STEPHEN T · 2015 to 2015
$371k
NIDDK NIH HHS R15 DK106688
6 · The paper itself

Abstract

The endosomal-lysosomal pathways and related autophagic processes are responsible for proteostasis, involving complexes between lysosomes and autophagosomes. Lysosomes are a key component of homeostasis, involved in cell signaling, metabolism, and quality control, and they experience functional compromise in metabolic diseases, aging, and neurodegenerative diseases. Many genetic mutations and risk factor genes associated with proteinopathies, as well as with metabolic diseases like diabetes, negatively influence endocytic trafficking and autophagic clearance. In contrast, health-improving exercise induces autophagy-lysosomal degradation, perhaps promoting efficient digestion of injured organelles so that undamaged organelles ensure cellular healthiness. Reductions in lysosomal hydrolases are implicated in Alzheimer's, Parkinson's, and lysosomal storage diseases, as well as obesity-related pathology, and members of the cathepsin enzyme family are involved in clearing both Aβ42 and α-synuclein. Upregulation of cathepsin hydrolases improves synaptic and memory functions in models of dementia and in exercising humans, thus identifying lysosomal-related systems as vital for healthy cognitive aging.

Indexed as

ExerciseMetabolic Networks and PathwaysProteostasisAgingAlzheimer DiseaseAnimalsDiabetes MellitusHumansLysosomesMetabolic DiseasesObesitySynucleinopathiesAge-related neurodegenerative disordersAutophagic-lysosomal pathwayAutophagyCathepsin BEndocytic traffickingProtein accumulation disordersProteinopathyQuality controlSynaptic pathologyTrafficking

Identifiers

PMID32739009
PMCPMC8428780

What OpenQuestion holds

Textmetadata
LicenceTDM
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.