Evidence map›Paper›PMID 39456257›Full record

ReviewBiomolecules2024

Targeting Protein Aggregation in ALS.

Michele Perni, Benedetta Mannini

Abstract readReview
In one paragraph

Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. 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

2 authors.

Michele PerniBaz-Therapeutics Inc., 810 Rittenhouse Square, Suite 412, Philadelphia, PA 19103, USA.ORCID 0000-0001-7593-8376
Benedetta ManniniDepartment of Experimental and Clinical Biomedical Sciences Mario Serio, University of Florence, Viale Morgagni 50, 50134 Florence, Italy.ORCID 0000-0001-6812-7348

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteinopathies involve the abnormal accumulation of specific proteins. Maintaining the balance of the proteome is a finely regulated process managed by a complex network of cellular machinery responsible for protein synthesis, folding, and degradation. However, stress and ageing can disrupt this balance, leading to widespread protein aggregation. Currently, several therapies targeting protein aggregation are in clinical trials for ALS. These approaches mainly focus on two strategies: addressing proteins that are prone to aggregation due to mutations and targeting the cellular mechanisms that maintain protein homeostasis to prevent aggregation. This review will cover these emerging drugs. Advances in ALS research not only offer hope for better outcomes for ALS patients but also provide valuable insights and methodologies that can benefit the broader field of neurodegenerative disease drug discovery.

Indexed as

Amyotrophic Lateral SclerosisProtein Aggregation, PathologicalAnimalsHumansProtein AggregatesProtein Aggregatesamyotrophic lateral sclerosisclinical trialsdrug discoveryinflammationneurodegenerationprotein aggregationprotein homeostasistherapeutics

Identifiers

PMID39456257
PMCPMC11506292

What OpenQuestion holds

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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.