ReviewProceedings of the Japan Academy. Series B, Physical and biological sciences2013
Metabolism of amyloid β peptide and pathogenesis of Alzheimer's disease.
Review in Proceedings of the Japan Academy. Series B, Physical and biological sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed.
- Lipopolysaccharides fromJournal of Alzheimer's disease : JAD · 2025Article
- Dietary Strategies to Mitigate Alzheimer's Disease: Insights into Antioxidant Vitamin Intake and Supplementation with Microbiota-Gut-Brain Axis Cross-Talk.Antioxidants (Basel, Switzerland) · 2024Review
- Recent advances in therapeutic strategies for Alzheimer's and Parkinson's disease using protein/peptide co-modified polymer nanoparticles.Neuroprotection (Chichester, England) · 2024Review
- Multi-Protective Effects of Petunidin-3-O-(International journal of molecular sciences · 2024Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Predicting Key Genes and Therapeutic Molecular Modelling to Explain the Association betweenInternational journal of molecular sciences · 2023Article
- Role of Chemokines in the Development and Progression of Alzheimer's Disease.Journal of molecular neuroscience : MN · 2022Review
- Gene Therapy Approach with an Emphasis on Growth Factors: Theoretical and Clinical Outcomes in Neurodegenerative Diseases.Molecular neurobiology · 2022Review
- Distinguishing Amyloid β-Protein in a Mouse Model of Alzheimer's Disease by Label-Free Vibrational Imaging.Biosensors · 2021Article
- Research and prospect of peptides for use in obesity treatment (Review).Experimental and therapeutic medicine · 2020Review
- Kai-Xin-San, a Chinese Herbal Decoction, Accelerates the Degradation ofEvidence-based complementary and alternative medicine : eCAM · 2020Article
- Effect of Varying Concentrations of Docosahexaenoic Acid on Amyloid Beta (1⁻42) Aggregation: An Atomic Force Microscopy Study.Molecules (Basel, Switzerland) · 2018Article
- Article
- Current Therapeutic Molecules and Targets in Neurodegenerative Diseases Based on in silico Drug Design.Current neuropharmacology · 2018Review
- Neuroprotective mechanism ofNeural regeneration research · 2017Article
- Mutations in MME cause an autosomal-recessive Charcot-Marie-Tooth disease type 2.Annals of neurology · 2016Article
- Coffee and caffeine potentiate the antiamyloidogenic activity of melatonin via inhibition of Aβ oligomerization and modulation of the Tau-mediated pathway in N2a/APP cells.Drug design, development and therapy · 2015Article
- Aβ degradation or cerebral perfusion? Divergent effects of multifunctional enzymes.Frontiers in aging neuroscience · 2014Review
- Amyloid-clearing proteins and their epigenetic regulation as a therapeutic target in Alzheimer's disease.Frontiers in aging neuroscience · 2014Review
- Thymoquinone recovers learning function in a rat model of Alzheimer's disease.Avicenna journal of phytomedicineArticle
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The conversion of what has been interpreted as "normal brain aging" to Alzheimer's disease (AD) via transition states, i.e., preclinical AD and mild cognitive impairment, appears to be a continuous process caused primarily by aging-dependent accumulation of amyloid β peptide (Aβ) in the brain. This notion however gives us a hope that, by manipulating the Aβ levels in the brain, we may be able not only to prevent and cure the disease but also to partially control some very significant aspects of brain aging. Aβ is constantly produced from its precursor and immediately catabolized under normal conditions, whereas dysmetabolism of Aβ seems to lead to pathological deposition upon aging. We have focused our attention on elucidation of the unresolved mechanism of Aβ catabolism in the brain. In this review, I describe a new approach to prevent AD development by reducing Aβ burdens in aging brains through up-regulation of the catabolic mechanism involving neprilysin that can degrade both monomeric and oligomeric forms of Aβ. The strategy of combining presymptomatic diagnosis with preventive medicine seems to be the most pragmatic in both medical and socioeconomical terms.(Communicated by Kunihiko SUZUKI, M.J.A.).
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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.