ArticleAnalytical biochemistry2013
Amyloid-beta isoform metabolism quantitation by stable isotope-labeled kinetics.
Article in Analytical biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed.
- Plasma MCP-1 and changes on cognitive function in community-dwelling older adults.Alzheimer's research & therapy · 2022Trial
- Prospective Associations between Plasma Amyloid-Beta 42/40 and Frailty in Community-Dwelling Older Adults.The journal of prevention of Alzheimer's disease · 2021Trial
- Assessment of Plasma Amyloid-β42/40 and Cognitive Decline Among Community-Dwelling Older Adults.JAMA network open · 2020Trial
- Regional Cerebrospinal Fluid Motility as a Key Determinant of Soluble Amyloid-β Levels and Kinetics.Research square · 2026Article
- Neuronal Death and Biomolecular Condensates: Are There Any New Treatment Options for Alzheimer's Disease?Cells · 2025Review
- Lipid-induced condensate formation from the Alzheimer's Aβ peptide triggers amyloid aggregation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Active Immunization Targeting Amyloid β for the Treatment of Alzheimer's Disease.Neuro-degenerative diseases · 2025Review
- Review
- Amyloid-β and Phosphorylated Tau are the Key Biomarkers and Predictors of Alzheimer's Disease.Aging and disease · 2024Review
- Unraveling the therapeutic efficacy of resveratrol in Alzheimer's disease: an umbrella review of systematic evidence.Nutrition & metabolism · 2024Review
- Alzheimer's Disease Biomarker Analysis Using Targeted Mass Spectrometry.Molecular & cellular proteomics : MCP · 2024Review
- Amyloid-β and caspase-1 are indicators of sepsis and organ injury.ERJ open research · 2024Article
- Re-Arranging the Puzzle between the Amyloid-Beta and Tau Pathology: An APP-Centric Approach.International journal of molecular sciences · 2023Review
- Advances in sample preparation and HPLC-MS/MS methods for determining amyloid-β peptide in biological samples: a review.Analytical and bioanalytical chemistry · 2023Review
- Review
- TNFR-1 and GDF-15 Are Associated With Plasma Neurofilament Light Chain and Progranulin Among Community-Dwelling Older Adults: A Secondary Analysis of the MAPT Study.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- Interactions Between Weight Loss and Plasma Neurodegenerative Markers for Determining Cognitive Decline Among Community-Dwelling Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Observational
- Amyloid-β peptide 37, 38 and 40 individually and cooperatively inhibit amyloid-β 42 aggregation.Chemical science · 2022Article
- Validation of Plasma Amyloid-β 42/40 for Detecting Alzheimer Disease Amyloid Plaques.Neurology · 2022Article
- Is liquid biopsy mature enough for the diagnosis of Alzheimer's disease?Frontiers in aging neuroscience · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Abundant evidence suggests a central role for the amyloid-beta (Aβ) peptide in Alzheimer's disease (AD) pathogenesis. Production and clearance of different Aβ isoforms have been established as targets of proposed disease-modifying therapeutic treatments of AD. However, previous studies used multiple sequential purification steps to isolate the isoforms individually and quantitate them based on a common mid-domain peptide. We created a method to simultaneously purify Aβ isoforms and quantitate them by the specific C-terminal peptides in order to investigate Aβ isoform physiology in the central nervous system. By using standards generated from in vitro metabolic labeling, the relative quantitation of four peptides representing total amount of Aβ (Aβ-Total), Aβ38, Aβ40, and Aβ42 were achieved both in cell culture and in human cerebrospinal fluid (CSF). Standard curves for each isoform demonstrated good sensitivity with very low limits of detection and high accuracy. Because the assay does not require antibody development for each Aβ isoform peptide, significant improvements in the throughput and accuracy of isoform quantitation were achieved.
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.