Evidence map›Paper›PMID 34572087›Full record

ReviewCells2021

All Roads Lead to Rome: Different Molecular Players Converge to Common Toxic Pathways in Neurodegeneration.

Shirel Argueti-Ostrovsky, Leenor Alfahel, Joy Kahn, Adrian Israelson

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. 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
3.0field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

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  14. New Insights into Mitochondria in Health and Diseases.International journal of molecular sciences · 2024
    Review
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  16. Article
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  20. Brain Effects ofInternational journal of molecular sciences · 2022
    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

4 authors at 1 institution in 1 country.

Shirel Argueti-OstrovskyDepartment of Physiology and Cell Biology, Faculty of Health Sciences and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, Israel.
Leenor AlfahelDepartment of Physiology and Cell Biology, Faculty of Health Sciences and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, Israel.
Joy KahnDepartment of Physiology and Cell Biology, Faculty of Health Sciences and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, Israel.
Adrian IsraelsonDepartment of Physiology and Cell Biology, Faculty of Health Sciences and The Zlotowski Center for Neuroscience, Ben-Gurion University of the Negev, P.O. Box 653, Beer Sheva 84105, Israel.ORCID 0000-0002-8289-7653
Ben-Gurion University of the Negev · IL

Funding

German-Israeli Foundation for Scientific Research and Development 1-1425-415.13/2017Israel Science Foundation 284/19United States - Israel Binational Science Foundation 2017118
6 · The paper itself

Abstract

Multiple neurodegenerative diseases (NDDs) such as Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and Huntington's disease (HD) are being suggested to have common cellular and molecular pathological mechanisms, characterized mainly by protein misfolding and aggregation. These large inclusions, most likely, represent an end stage of a molecular cascade; however, the soluble misfolded proteins, which take part in earlier steps of this cascade, are the more toxic players. These pathological proteins, which characterize each specific disease, lead to the selective vulnerability of different neurons, likely resulting from a combination of different intracellular mechanisms, including mitochondrial dysfunction, ER stress, proteasome inhibition, excitotoxicity, oxidative damage, defects in nucleocytoplasmic transport, defective axonal transport and neuroinflammation. Damage within these neurons is enhanced by damage from the nonneuronal cells, via inflammatory processes that accelerate the progression of these diseases. In this review, while acknowledging the hallmark proteins which characterize the most common NDDs; we place specific focus on the common overlapping mechanisms leading to disease pathology despite these different molecular players and discuss how this convergence may occur, with the ultimate hope that therapies effective in one disease may successfully translate to another.

Indexed as

Active Transport, Cell NucleusEndoplasmic Reticulum StressOxidative StressAnimalsHumansMitochondriaNeurodegenerative DiseasesALSAlzheimer’s diseasesHuntington’s diseasemisfolded proteinsneurodegenerative diseasesParkinson’s diseasesproteostasis

Identifiers

PMID34572087
PMCPMC8468417
OpenAlexW3200519851

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.