ArticleMolecular psychiatry2023
Aβ1-6
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Exploiting blood-based biomarkers to align preclinical models with human traumatic brain injury.Brain : a journal of neurology · 2025Pooled it
- Peptide-Functionalized Hydroxypropyl Cellulose Mitigates Amyloid-β Protein Induced Endothelial Leakiness and Enhances Cognitive Function in Alzheimer's Disease.Angewandte Chemie (International ed. in English) · 2026Article
- Effect of the Icelandic Mutation APPBiomolecules · 2025Article
- The NOX2-ROS-NLRP3 inflammasome axis in traumatic brain injury.Journal of neuroinflammation · 2025Article
- Mesenchymal Stromal Cell Secretome and Its Key Bioactive Metabolites Induce Long-Term Neuroprotection After Traumatic Brain Injury in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Potential Correlation Between Molecular Biomarkers and Oxidative Stress in Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- Podoplanin-positive cell-derived small extracellular vesicles contribute to cardiac amyloidosis after myocardial infarction.Cell reports · 2025Article
- Transmissible long-term neuroprotective and pro-cognitive effects of 1-42 beta-amyloid with A2T icelandic mutation in an Alzheimer's disease mouse model.Molecular psychiatry · 2024Article
- Recent insights from non-mammalian models of brain injuries: an emerging literature.Frontiers in neurology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 2 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD), the leading cause of dementia in older adults, is a double proteinopathy characterized by amyloid-β (Aβ) and tau pathology. Despite enormous efforts that have been spent in the last decades to find effective therapies, late pharmacological interventions along the course of the disease, inaccurate clinical methodologies in the enrollment of patients, and inadequate biomarkers for evaluating drug efficacy have not allowed the development of an effective therapeutic strategy. The approaches followed so far for developing drugs or antibodies focused solely on targeting Aβ or tau protein. This paper explores the potential therapeutic capacity of an all-D-isomer synthetic peptide limited to the first six amino acids of the N-terminal sequence of the A2V-mutated Aβ, Aβ1-6
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.