ReviewExperimental neurology2010
Beyond the signaling effect role of amyloid-ß42 on the processing of APP, and its clinical implications.
Review in Experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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
18 citing papers in PubMed, 46 citations in OpenAlex.
- Dexmedetomidine Exerts Multi-level Effects to Ameliorate Alzheimer's Disease Pathology in the Adult Zebrafish Brain.Molecular neurobiology · 2026Article
- Advances in the Exploration of Coordination Complexes of Vanadium in the Realm of Alzheimer's Disease: A Mini Review.Molecules (Basel, Switzerland) · 2025Review
- Neurodevelopmental disorders and microcephaly: how apoptosis, the cell cycle, tau and amyloid-β precursor protein APPly.Frontiers in molecular neuroscience · 2023Review
- APPlications of amyloid-β precursor protein metabolites in macrocephaly and autism spectrum disorder.Frontiers in molecular neuroscience · 2023Review
- Synaptosome microRNAs regulate synapse functions in Alzheimer's disease.NPJ genomic medicine · 2022Article
- The synthesized transporter K16APoE enabled the therapeutic HAYED peptide to cross the blood-brain barrier and remove excess iron and radicals in the brain, thus easing Alzheimer's disease.Drug delivery and translational research · 2019Article
- The Transcriptional Regulatory Properties of Amyloid Beta 1-42 may Include Regulation of Genes Related to Neurodegeneration.Neuromolecular medicine · 2018Article
- (-)-Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury.Brain research · 2017Article
- Diabetic Microvascular Disease: An Endocrine Society Scientific Statement.The Journal of clinical endocrinology and metabolism · 2017Review
- Altered protein phosphorylation as a resource for potential AD biomarkers.Scientific reports · 2016Article
- Finding novel distinctions between the sAPPα-mediated anabolic biochemical pathways in Autism Spectrum Disorder and Fragile X Syndrome plasma and brain tissue.Scientific reports · 2016Article
- Alzheimer's disease: Unique markers for diagnosis & new treatment modalities.The Indian journal of medical research · 2015Review
- AAD-2004 Attenuates Progressive Neuronal Loss in the Brain of Tg-betaCTF99/B6 Mouse Model of Alzheimer Disease.Experimental neurobiology · 2013Article
- Article
- A case of cellular alchemy: lineage reprogramming and its potential in regenerative medicine.Journal of molecular cell biology · 2012Review
- Axonal transport of APP and the spatial regulation of APP cleavage and function in neuronal cells.Experimental brain research · 2012Review
- Article
- Article
Corrections and comments
- Comment on
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) currently has over 6 million victims in the USA, alone. The recently FDA approved drugs for AD only provide mild, transient relief for symptoms without addressing underlying mechanisms to a significant extent. Basic understanding of the activities of the amyloid beta peptide (Abeta) and associated proteins such as beta-site APP-cleaving enzyme 1 (BACE1) is necessary to develop effective medical responses to AD. Recently (Exper. Neurol. 2010. 221, 18-25), Tabaton et al. have presented a model of both non-pathological and pathological Abeta activities and suggest potential therapeutic pathways based on their proposed framework of Abeta acting as the signal that induces a kinase cascade, ultimately stimulating transcription factors that upregulate genes such as BACE1. We respond by presenting evidence of Abeta's other activities, including protection against metal-induced reactive oxidizing species (ROS), modification of cholesterol transport, and potential activity as a transcription factor in its own right. We touch upon clinical implications of each of these functions and highlight the currently unexplored implications of our suggested novel function of Abeta as a transcription factor. Abeta appears to be a highly multi-functional peptide, and any or all of the pathways it engages in is a likely candidate for antiAD drug development.
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.