Evidence map›Paper›PMID 31527516›Full record

ReviewMolecules (Basel, Switzerland)2019

Autophagy Modulation as a Treatment of Amyloid Diseases.

Zoe Mputhia, Eugene Hone, Timir Tripathi, Tim Sargeant, Ralph Martins, Prashant Bharadwaj

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Regulation of autophagy-mediated pathways by diet, physical activity, and sleep in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. The role of autophagy in the progression of HIV infected cardiomyopathy.Frontiers in cell and developmental biology · 2024
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Frontiers in neuroscience · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review
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

6 authors at 3 institutions in 2 countries.

Zoe MputhiaCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Nedlands, WA 6009, Australia. zoe.mputhia@gmail.com.
Eugene HoneCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Nedlands, WA 6009, Australia. e.hone@ecu.edu.au.
Timir TripathiDepartment of Biochemistry, North-Eastern Hill University, Meghalaya 793022, India. timir.tripathi@gmail.com.ORCID 0000-0001-5559-289X
Tim SargeantHopwood Centre for Neurobiology, SAHMRI, Adelaide, SA 5000, Australia. tim.sargeant@sahmri.com.
Ralph MartinsCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Nedlands, WA 6009, Australia. r.martins@ecu.edu.au.
Prashant BharadwajCentre of Excellence for Alzheimer's Disease Research and Care, School of Medical and Health Sciences, Edith Cowan University, Nedlands, WA 6009, Australia. p.bharadwaj@ecu.edu.au.
Edith Cowan University · AUNorth Eastern Hill University · INSouth Australian Health and Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyloids are fibrous proteins aggregated into toxic forms that are implicated in several chronic disorders. More than 30 diseases show deposition of fibrous amyloid proteins associated with cell loss and degeneration in the affected tissues. Evidence demonstrates that amyloid diseases result from protein aggregation or impaired amyloid clearance, but the connection between amyloid accumulation and tissue degeneration is not clear. Common examples of amyloid diseases are Alzheimer's disease (AD), Parkinson's disease (PD) and tauopathies, which are the most common forms of neurodegenerative diseases, as well as polyglutamine disorders and certain peripheral metabolic diseases. In these diseases, increased accumulation of toxic amyloid proteins is suspected to be one of the main causative factors in the disease pathogenesis. It is therefore important to more clearly understand how these toxic amyloid proteins accumulate as this will aide in the development of more effective preventive and therapeutic strategies. Protein homeostasis, or proteostasis, is maintained by multiple cellular pathways-including protein synthesis, quality control, and clearance-which are collectively responsible for preventing protein misfolding or aggregation. Modulating protein degradation is a very complex but attractive treatment strategy used to remove amyloid and improve cell survival. This review will focus on autophagy, an important clearance pathway of amyloid proteins, and strategies for using it as a potential therapeutic target for amyloid diseases. The physiological role of autophagy in cells, pathways for its modulation, its connection with apoptosis, cell models and caveats in developing autophagy as a treatment and as a biomarker is discussed.

Indexed as

AmyloidAmyloidogenic ProteinsAnimalsApoptosisAutophagyBiomarkersDisease SusceptibilityHumansNeurodegenerative DiseasesProtein AggregatesProtein Aggregation, PathologicalSignal TransductionAmyloidAmyloidogenic ProteinsBiomarkersProtein AggregatesAlzheimer’s diseaseamyloidautophagybeta amyloidclearanceHuntington’s diseaselysosomeParkinson’s diseasepolyglutamineTau proteintoxicityα-synuclein

Identifiers

PMID31527516
PMCPMC6766836
OpenAlexW2972585421

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.