ArticleAlzheimer's & dementia (New York, N. Y.)2019
Decrease in p3-Alcβ37 and p3-Alcβ40, products of Alcadein β generated by γ-secretase cleavages, in aged monkeys and patients with Alzheimer's disease.
Article in Alzheimer's & dementia (New York, N. Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- The Potential Regulators of Amyloidogenic Pathway of APP Processing in Alzheimer's Disease.Biomedicines · 2025Review
- Suppression of the amyloidogenic metabolism of APP and the accumulation of Aβ by alcadein α in the brain during aging.Scientific reports · 2024Article
- Axonal transport of Frizzled5 by Alcadein α-containing vesicles is associated with kinesin-1.Molecular biology of the cell · 2023Article
- Brain p3-Alcβ peptide restores neuronal viability impaired by Alzheimer's amyloid β-peptide.EMBO molecular medicine · 2023Article
- Amyloidogenic processing of amyloid β protein precursor (APP) is enhanced in the brains of alcadein α-deficient mice.The Journal of biological chemistry · 2020Article
Corrections and comments
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Authors and funding
26 authors at 16 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionNeuronal p3-Alcβ peptides are generated from the precursor protein Alcadein β (Alcβ) through cleavage by α- and γ-secretases of the amyloid β (Aβ) protein precursor (APP). To reveal whether p3-Alcβ is involved in Alzheimer's disease (AD) contributes for the development of novel therapy and/or drug targets.
methodsWe developed new sandwich enzyme-linked immunosorbent assay (sELISA) systems to quantitate levels of p3-Alcβ in the cerebrospinal fluid (CSF).
resultsIn monkeys, CSF p3-Alcβ decreases with age, and the aging is also accompanied by decreased brain expression of Alcβ. In humans, CSF p3-Alcβ levels decrease to a greater extent in those with AD than in age-matched controls. Subjects carrying presenilin gene mutations show a significantly lower CSF p3-Alcβ level. A cell study with an inverse modulator of γ-secretase remarkably reduces the generation of p3-Alcβ37 while increasing the production of Aβ42. DISCUSSION: Aging decreases the generation of p3-Alcβ, and further significant decrease of p3-Alcβ caused by aberrant γ-secretase activity may accelerate pathogenesis in AD.
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