ReviewNeurochemical research
Alzheimer disease--no target for statin treatment. A mini review.
Review in Neurochemical research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 26 citations in OpenAlex.
- Univ.-Prof. Dr. med. Siegfried Hoyer 1933-2014.Journal of neural transmission (Vienna, Austria : 1996) · 2014Article
- Intracerebral propagation of Alzheimer's disease: strengthening evidence of a herpes simplex virus etiology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2013Review
- What have we learned from the streptozotocin-induced animal model of sporadic Alzheimer's disease, about the therapeutic strategies in Alzheimer's research.Journal of neural transmission (Vienna, Austria : 1996) · 2013Review
- Bryostatin-1 vs. TPPB: dose-dependent APP processing and PKC-α, -δ, and -ε isoform activation in SH-SY5Y neuronal cells.Journal of molecular neuroscience : MN · 2012Article
- Free cholesterol induces higher β-sheet content in Aβ peptide oligomers by aromatic interaction with Phe19.PloS one · 2012Article
- Prescription of lipophilic statins to Alzheimer's disease patients: some controversies to consider.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2011Review
- Lipid Rafts: Linking Alzheimer's Amyloid-β Production, Aggregation, and Toxicity at Neuronal Membranes.International journal of Alzheimer's disease · 2010Article
- Membrane rafts in Alzheimer's disease beta-amyloid production.Biochimica et biophysica acta · 2010Review
- The effects of cholesterol on learning and memory.Neuroscience and biobehavioral reviews · 2010Review
- Mechanisms of disease: new therapeutic strategies for Alzheimer's disease--targeting APP processing in lipid rafts.Nature clinical practice. Neurology · 2007Review
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nosologically, Alzheimer disease (AD) is not a single disorder. A minority of around 400 families worldwide can be grouped as hereditary in origin, whereas the majority of all Alzheimer cases (approx. 25 million worldwide) are sporadic in origin. In the pathophysiology of the latter type, a number of susceptibility genes contribute to the disease among which are allelic abnormalities of the apolipoprotein E4 gene pointing to a link between disturbed cholesterol metabolism and sporadic AD. Cholesterol is a main component of membrane composition enriched in microdomains and is functionally linked to the proteolytic processing of amyloid precursor protein (APP). In sporadic AD, a marked diminution of both membrane phospholipids and cholesterol has been found. Evidence has been provided that high plasma cholesterol may protect from AD. In contrast to these well documented abnormalities observed in AD patients, it was assumed that an elevated cholesterol concentration might favour the generation of beta-amyloid and, thus, AD. However, a series of in vitro-and in vivo-studies did not provide evidence for the assumption that an enhanced cholesterol concentration increased betaA4-production. A harsh reduction of membrane cholesterol only caused a "beneficial" effect of APP metabolism. However, this experimentally induced condition may not be compatible to sporadic AD. The application of statins in sporadic AD did not yield results to assume that this therapeutic strategy may prevent or treat successfully sporadic AD.
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.