Evidence map›Paper›PMID 36965025›Full record

ReviewBritish journal of pharmacology2023

Novel therapeutic approaches to target neurodegeneration.

Alerie G de la Fuente, Silvia Pelucchi, Jerome Mertens, Monica Di Luca, Daniela Mauceri, Elena Marcello

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
4.6field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.Apoptosis : an international journal on programmed cell death · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Synthetic Cyclic CAntioxidants (Basel, Switzerland) · 2025
    Article
  12. Review
  13. Dopamine Depletion in Parkinson's Disease and Therapeutic Options.CNS & neurological disorders drug targets · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  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 4 institutions in 6 countries.

Alerie G de la FuenteInstituto de Investigación Sanitaria y Biomédica de Alicante (ISABIAL), Alicante, Spain.ORCID 0000-0001-8366-4969
Silvia PelucchiDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy.ORCID 0000-0002-5994-487X
Jerome MertensInstitute of Molecular Biology, Leopold-Franzens-Universität Innsbruck, Innsbruck, Austria.ORCID 0000-0002-4291-4121
Monica Di LucaDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy.ORCID 0000-0003-2298-615X
Daniela MauceriInstitute of Anatomy and Cell Biology, Department of Molecular and Cellular Neuroscience, University of Marburg, Marburg, Germany.ORCID 0000-0003-1225-4633
Elena MarcelloDepartment of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy.ORCID 0000-0003-0452-762X
University of Milan · ITPhilipps University of Marburg · DEQueen's University Belfast · GBUniversität Innsbruck · AT

Funding

UCSD Shiley-Marcos Alzheimer's Disease Research Center P30P30AG062429 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Steven Dyal Edland · 2019 to 2026
$34.9M
ConProject-002RF1AG056306 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI GAGE, FRED H · 2022 to 2025
$2.8M
Assessing cellular aging in old and rejuvenated neurons from Alzheimer patientsR01AG056306 · NIA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI GAGE, FRED H · 2017 to 2021
$2.4M
NIA NIH HHS AG056306NIA NIH HHS AG062429NIA NIH HHS P30 AG062429NIA NIH HHS R01 AG056306NIA NIH HHS RF1 AG056306Wellcome Trust
6 · The paper itself

Abstract

Ageing is the main risk factor common to most primary neurodegenerative disorders. Indeed, age-related brain alterations have been long considered to predispose to neurodegeneration. Although protein misfolding and the accumulation of toxic protein aggregates have been considered as causative events in neurodegeneration, several other biological pathways affected by brain ageing also contribute to pathogenesis. Here, we discuss the evidence showing the involvement of the mechanisms controlling neuronal structure, gene expression, autophagy, cell metabolism and neuroinflammation in the onset and progression of neurodegenerative disorders. Furthermore, we review the therapeutic strategies currently under development or as future approaches designed to normalize these pathways, which may then increase brain resilience to cope with toxic protein species. In addition to therapies targeting the insoluble protein aggregates specifically associated with each neurodegenerative disorder, these novel pharmacological approaches may be part of combined therapies designed to rescue brain function.

Indexed as

Neurodegenerative DiseasesProtein AggregatesAutophagyHumansProteinsProtein AggregatesProteinsautophagydendritegene expressionmetabolismneurodegenerative disordersneuroinflammationsynapse

Identifiers

PMID36965025
PMCPMC10952850
OpenAlexW4360946340

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.