ArticleScientific reports2021
The Aβ(1-38) peptide is a negative regulator of the Aβ(1-42) peptide implicated in Alzheimer disease progression.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.
- Systematic review and meta-analysis of randomized controlled trials on the effects of exercise interventions on amyloid beta levels in humans.Experimental brain research · 2024Pooled it
- Autophagy Activators Normalize Aberrant Tau Proteostasis and Rescue Synapses in Human Familial Alzheimer's Disease iPSC-Derived Cortical Organoids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- BACE-1 and ADAM-10 as Potential Peripheral Biomarkers for Alzheimer's Disease.Current pharmaceutical design · 2026Review
- Modeling Alzheimer's Disease: A Review of Gene-Modified and Induced Animal Models, Complex Cell Culture Models, and Computational Modeling.Brain sciences · 2025Review
- Target Validation Studies of PS48, a PDK-1 Allosteric Agonist, for the Treatment of Alzheimer's Disease Phenotype in APP/PS1 Transgenic Mice.International journal of molecular sciences · 2025Article
- γ-Secretase modulator resistance of an aggressive Alzheimer-causing presenilin mutant can be overcome in the heterozygous patient state by a set of advanced compounds.Alzheimer's research & therapy · 2025Article
- Human brain organoids containing microglia that have arisen innately adapt to a β-amyloid challenge better than those in which microglia are integrated by co-culture.Stem cell research & therapy · 2024Article
- Drug-Target Interaction Prediction Based on an Interactive Inference Network.International journal of molecular sciences · 2024Article
- Distinctive contribution of two additional residues in protein aggregation of Aβ42 and Aβ40 isoforms.BMB reports · 2024Review
- Review
- Amyloid fibril proteomics of AD brains reveals modifiers of aggregation and toxicity.Molecular neurodegeneration · 2023Article
- Advanced Overview of Biomarkers and Techniques for Early Diagnosis of Alzheimer's Disease.Cellular and molecular neurobiology · 2023Review
- Oxidative Damages on the Alzheimer's Related-Aβ Peptide Alters Its Ability to Assemble.Antioxidants (Basel, Switzerland) · 2023Article
- Gamma-secretase modulators: a promising route for the treatment of Alzheimer's disease.Frontiers in molecular neuroscience · 2023Review
- Unveiling the Potential of Polyphenols as Anti-Amyloid Molecules in Alzheimer's Disease.Current neuropharmacology · 2023Review
- Review
- Cognitive Impairment in Idiopathic Normal Pressure Hydrocephalus.Neuroscience bulletin · 2022Review
- Dynamic observations of various oligomers in amyloidBiochemistry and biophysics reports · 2022Article
- The Effects of Physical Running on Dendritic Spines and Amyloid-beta Pathology in 3xTg-AD Male Mice.Aging and disease · 2022Article
- Recent Advances Towards Diagnosis and Therapeutic Fingerprinting for Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pool of β-Amyloid (Aβ) length variants detected in preclinical and clinical Alzheimer disease (AD) samples suggests a diversity of roles for Aβ peptides. We examined how a naturally occurring variant, e.g. Aβ(1-38), interacts with the AD-related variant, Aβ(1-42), and the predominant physiological variant, Aβ(1-40). Atomic force microscopy, Thioflavin T fluorescence, circular dichroism, dynamic light scattering, and surface plasmon resonance reveal that Aβ(1-38) interacts differently with Aβ(1-40) and Aβ(1-42) and, in general, Aβ(1-38) interferes with the conversion of Aβ(1-42) to a β-sheet-rich aggregate. Functionally, Aβ(1-38) reverses the negative impact of Aβ(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an Aβ(1-42) phenotype in Caenorhabditis elegans. Aβ(1-38) also reverses any loss of MTT conversion induced by Aβ(1-40) and Aβ(1-42) in HT-22 hippocampal neurons and APOE ε4-positive human fibroblasts, although the combination of Aβ(1-38) and Aβ(1-42) inhibits MTT conversion in APOE ε4-negative fibroblasts. A greater ratio of soluble Aβ(1-42)/Aβ(1-38) [and Aβ(1-42)/Aβ(1-40)] in autopsied brain extracts correlates with an earlier age-at-death in males (but not females) with a diagnosis of AD. These results suggest that Aβ(1-38) is capable of physically counteracting, potentially in a sex-dependent manner, the neuropathological effects of the AD-relevant Aβ(1-42).
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