ReviewNeuroscience bulletin2011
Screening of treatment targets for Alzheimer's disease from the molecular mechanisms of impairment by β-amyloid aggregation and tau hyperphosphorylation.
Review in Neuroscience bulletin, 2011. 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, 6 citations in OpenAlex.
- Combination of schisandrin and nootkatone exerts neuroprotective effect in Alzheimer's disease mice model.Metabolic brain disease · 2019Article
- Clusterin in Alzheimer's disease: a player in the biological behavior of amyloid-beta.Neuroscience bulletin · 2014Review
- Combination of Aβ clearance and neurotrophic factors as a potential treatment for Alzheimer's disease.Neuroscience bulletin · 2013Review
- Regulation of cerebral cholesterol metabolism in Alzheimer disease.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2012Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Amyloid (Aβ) over-expression and tau hyperphosphorylation are considered to be the central events in the pathogenesis of Alzheimer's disease (AD). Studies on them may help elucidate the precise molecular pathogenesis of AD. Until now, although tau protein and Aβ remain the foci of AD research, the etiopathogenesis of AD and effective drugs for AD treatment are still largely unsolved. The present review was mainly focused on the molecular mechanism of Aβ aggregation-related impairment and the pathways leading to tau hyperphosphorylation, based on which some promising therapeutic targets for AD were also proposed.
Indexed as
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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.