ReviewBrain pathology (Zurich, Switzerland)2004
Apolipoprotein Abeta: black sheep in a good family.
Review in Brain pathology (Zurich, Switzerland), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 21 citations in OpenAlex.
- ABCA1- and ABCG1-mediated cholesterol efflux capacity of cerebrospinal fluid is impaired in Alzheimer's disease.Journal of lipid research · 2019Article
- Green Tea Seed Oil Suppressed AβInternational journal of molecular sciences · 2019Article
- Phospholipid transfer protein is expressed in cerebrovascular endothelial cells and involved in high density lipoprotein biogenesis and remodeling at the blood-brain barrier.The Journal of biological chemistry · 2014Article
- Neurobiological pathways to Alzheimer's disease: Amyloid-beta, TAU protein or both?Dementia & neuropsychologiaReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid-beta (Abeta) has for a long time been thought to play a central role in the pathogenesis of Alzheimer disease (AD). Analysis of available data indicates that Abeta possesses properties of a metal-binding apolipoprotein influencing lipid transport and metabolism. Protection of lipoproteins from oxidation by transition metals, synaptic activity and role in the acute phase response represent plausible physiological functions of Abeta. However, these important biochemical qualities which may critically influence the development of AD, have been largely ignored by mainstream AD researchers, making Abeta appear to be a "black sheep" in a "good apolipoprotein" family. New studies are needed to shed further light on the physiological role of Abeta in lipid metabolism in the brain.
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.