ArticleCognitive sciences2010
CHOLESTEROL AND NEURONAL SUSCEPTIBILITY TO BETA-AMYLOID TOXICITY.
Article in Cognitive sciences, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 13 citations in OpenAlex.
- Effectiveness of Combinational Treatments for Alzheimer's Disease with Human Neural Stem Cells and Microglial Cells Over-Expressing Functional Genes.International journal of molecular sciences · 2023Article
- A New Hypothesis for Alzheimer's Disease: The Lipid Invasion Model.Journal of Alzheimer's disease reports · 2022Article
- Neuroprotective effects of statins against amyloid β-induced neurotoxicity.Neural regeneration research · 2018Review
- Mevastatin promotes neuronal survival against Aβ-induced neurotoxicity through AMPK activation.Metabolic brain disease · 2017Article
- Calpain dysregulation in Alzheimer's disease.ISRN biochemistry · 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 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a devastating neurocognitive disorder rapidly growing across the elderly population. Although few cases arise due to genetic mutations, sporadic AD is the most common form of this disease. Therefore, there is a continuing research effort to discover a unifying cause of this form of AD. To date, the only strong genetic correlate to the sporadic AD is inheritance of the apolipoprotein E4 (ApoE4) allele, whose encoded protein is involved in cholesterol transport in the central nervous system. This genetic link has prompted a series of studies on the potential molecular mechanisms by which cholesterol could modulate neuronal degeneration in the context of AD. In this review, we discussed the involvement of cholesterol in the production of the pathological hallmarks of the disease and how it might alter the susceptibility of cells to AD-related insult. Finally, we discussed the use of cholesterol-lowering drugs as a potential preventative approach in AD.
Indexed as
Identifiers
25339981PMC4203449W2256855138What 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.