ReviewBMC neuroscience2008
Preventing beta-amyloid fibrillization and deposition: beta-sheet breakers and pathological chaperone inhibitors.
Review in BMC neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 41 citations in OpenAlex.
- Blocking the apolipoprotein E/amyloid β interaction in triple transgenic mice ameliorates Alzheimer's disease related amyloid β and tau pathology.Journal of neurochemistry · 2014Article
- Immunotherapy for the treatment of Alzheimer's disease: amyloid-β or tau, which is the right target?ImmunoTargets and therapy · 2014Review
- Target- and mechanism-based therapeutics for neurodegenerative diseases: strength in numbers.Journal of medicinal chemistry · 2013Review
- Treating Alzheimer's disease with monoclonal antibodies: current status and outlook for the future.Alzheimer's research & therapy · 2013Review
- Development of a new DNA vaccine for Alzheimer disease targeting a wide range of aβ species and amyloidogenic peptides.PloS one · 2013Article
- Molecular plasticity regulates oligomerization and cytotoxicity of the multipeptide-length amyloid-β peptide pool.The Journal of biological chemistry · 2012Article
- Recent advances in the development of immunotherapies for tauopathies.Experimental neurology · 2011Article
- Blocking the apolipoprotein E/amyloid-β interaction reduces fibrillar vascular amyloid deposition and cerebral microhemorrhages in TgSwDI mice.Journal of Alzheimer's disease : JAD · 2011Article
- Prevention of autosomal dominant retinitis pigmentosa by systemic drug therapy targeting heat shock protein 90 (Hsp90).Human molecular genetics · 2010Article
- Murine models of Alzheimer's disease and their use in developing immunotherapies.Biochimica et biophysica acta · 2010Review
- Immunotherapeutic approaches for Alzheimer's disease in transgenic mouse models.Brain structure & function · 2010Review
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 1 institution in 1 country.
Funding
Abstract
Central to the pathogenesis of Alzheimer's disease (AD) is the conversion of normal, soluble beta-amyloid (sAbeta) to oligomeric, fibrillar Abeta. This process of conformational conversion can be influenced by interactions with other proteins that can stabilize the disease-associated state; these proteins have been termed 'pathological chaperones'. In a number of AD models, intervention that block soluble Abeta aggregation, including beta-sheet breakers, and compounds that block interactions with pathological chaperones, have been shown to be highly effective. When combined with early pathology detection, these therapeutic strategies hold great promise as effective and relatively toxicity free methods of preventing AD related pathology.
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.