ReviewAlzheimer's research & therapy2013
Regulation of distinct pools of amyloid β-protein by multiple cellular proteases.
Review in Alzheimer's research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Prominent tauopathy and intracellular β-amyloid accumulation triggered by genetic deletion of cathepsin D: implications for Alzheimer disease pathogenesis.Alzheimer's research & therapy · 2024Article
- Disruption of the grid cell network in a mouse model of early Alzheimer's disease.Nature communications · 2022Article
- Recent progress (2015-2020) in the investigation of the pharmacological effects and mechanisms of ginsenoside RbJournal of ginseng research · 2022Review
- Can Animal Models Inform on the Relationship between Depression and Alzheimer Disease?Canadian journal of psychiatry. Revue canadienne de psychiatrie · 2019Review
- Ex vivoMolecular neurodegeneration · 2017Article
- Review
- Unraveling Alzheimer's: Making Sense of the Relationship between Diabetes and Alzheimer's Disease1.Journal of Alzheimer's disease : JAD · 2016Review
- CALHM1 ion channel elicits amyloid-β clearance by insulin-degrading enzyme in cell lines and in vivo in the mouse brain.Journal of cell science · 2015Article
- Hypoxia Affects Neprilysin Expression Through Caspase Activation and an APP Intracellular Domain-dependent Mechanism.Frontiers in neuroscience · 2015Article
- Aβ degradation-the inside story.Frontiers in aging neuroscience · 2014Article
- Identification and characterization of Aβ peptide interactors in Alzheimer's disease by structural approaches.Frontiers in aging neuroscience · 2014Article
- Amyloid-clearing proteins and their epigenetic regulation as a therapeutic target in Alzheimer's disease.Frontiers in aging neuroscience · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive, age-related neurodegenerative disorder characterized by extracellular and intracellular deposition of the amyloid β-protein (Aβ). The study of rare, familial forms of AD has shown that sustained elevations in the production of Aβ (either all forms or specific pathogenic variants thereof) are sufficient to trigger the full spectrum of cognitive and histopathological features of the disease. Although the exact cause or causes remain unknown, emerging evidence suggests that impairments in the clearance of Aβ, after it is produced, may underlie the vast majority of sporadic AD cases. This review focuses on Aβ-degrading proteases (AβDPs), which have emerged as particularly important mediators of Aβ clearance. A wide variety of proteases that - by virtue of their particular regional and subcellular localization profiles - define distinct pools of Aβ have been identified. Different pools of Aβ, in turn, may contribute differentially to the pathogenesis of the disease. The study of individual AβDPs, therefore, promises to offer new insights into the mechanistic basis of AD pathogenesis and, ultimately, may facilitate the development of effective methods for its prevention or treatment or both.
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.