ReviewCNS drug reviews2004
The cellular biochemistry of cholesterol and statins: insights into the pathophysiology and therapy of Alzheimer's disease.
Review in CNS drug reviews, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 49 citations in OpenAlex.
- Genetic evidence for a causal relationship between 179 lipid species and cognitive function and alzheimer's disease: a bidirectional Mendelian randomization study.European archives of psychiatry and clinical neuroscience · 2026Article
- Prenatal exposure to undernutrition is associated with a specific lipid profile predicting future brain aging.npj aging · 2024Review
- Involvement of Lipids in Alzheimer's Disease Pathology and Potential Therapies.Frontiers in physiology · 2020Review
- Effect of the SIRT3-AMPK/PPAR pathway on invasion and migration of cervical cancer cells.International journal of clinical and experimental pathology · 2020Article
- Statin use associated with lower risk of epilepsy after intracranial haemorrhage: A population-based cohort study.British journal of clinical pharmacology · 2018Article
- Overnutrition Determines LPS Regulation of Mycotoxin Induced Neurotoxicity in Neurodegenerative Diseases.International journal of molecular sciences · 2015Review
- Plasma 24S-hydroxycholesterol levels in elderly subjects with late onset Alzheimer's disease or vascular dementia: a case-control study.BMC neurology · 2011Article
- Intracranial atherosclerosis as a contributing factor to Alzheimer's disease dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2011Article
- Cardiovascular dementia - a different perspective.The open biochemistry journal · 2010Article
- The natural products beauveriolide I and III: a new class of beta-amyloid-lowering compounds.Chembiochem : a European journal of chemical biology · 2009Article
- Potential mechanisms linking cholesterol to Alzheimer's disease-like pathology in rabbit brain, hippocampal organotypic slices, and skeletal muscle.Journal of Alzheimer's disease : JAD · 2008Review
- "Skittish" Abca2 knockout mice display tremor, hyperactivity, and abnormal myelin ultrastructure in the central nervous system.Molecular and cellular biology · 2007Article
- The ABCA2 transporter: intracellular roles in trafficking and metabolism of LDL-derived cholesterol and sterol-related compounds.Current drug metabolism · 2007Review
- Apolipoprotein E, cholesterol metabolism, diabetes, and the convergence of risk factors for Alzheimer's disease and cardiovascular disease.Molecular psychiatry · 2006Review
- Is the LDL receptor involved in cortical amyloid protein clearance?Neurochemical research · 2006Review
- Potential role of acyl-coenzyme A:cholesterol transferase (ACAT) Inhibitors as hypolipidemic and antiatherosclerosis drugs.Pharmaceutical research · 2005Review
- Apolipoprotein Abeta: black sheep in a good family.Brain pathology (Zurich, Switzerland) · 2004Review
- Cholesterol and apolipoprotein E in Alzheimer's disease.American journal of Alzheimer's disease and other dementiasReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The causes of late onset Alzheimer disease (AD) are poorly understood. Although beta-amyloid (Abeta) is thought to play a critical role in the pathophysiology of AD, no genetic evidence directly ties Abeta to late onset AD. This suggests that the accumulation of Abeta and neurodegeneration associated with AD might result from an abnormality that indirectly affects Abeta production or accumulation. Increasing evidence suggests that abnormalities in the metabolism of cholesterol and related molecules, such as cholseterol esters and 24(S) hydroxycholesterol might contribute to the pathophysiology of late onset AD by increasing production of Abeta. 24(S) Hydroxycholesterol is a member of a family of oxidized cholesterol catabolites, termed oxysterols, which function to regulate export of cholesterol from the cell and transcription of genes related to cholesterol metabolism. Cholesterol esters are cholesterol derivatives used for cholesterol storage. Levels of 24(S) hydroxycholesterol increase with AD. Polymorphisms in several different genes important for cholesterol physiology are associated with an increased load or level of Abeta in AD. These genes include apolipoprotein E, cholesterol 24 hydroxylase (Cyp46), acyl-CoA:cholesterol acetyltransferase (ACAT), and the cholesterol transporter ABCA1. Other studies show that levels of cholesterol, or its precursors, are elevated in subjects early in the course of AD. Finally, studies of the processing of amyloid precursor protein show that cholesterol and its catabolites modulate amyloid precursor protein processing and Abeta production. These lines of evidence raise the possibility that genetic abnormalities in cholesterol metabolism might contribute to the pathophysiology of AD.
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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.