ReviewDrugs & aging2003
Dietary lipids in the aetiology of Alzheimer's disease: implications for therapy.
Review in Drugs & aging, 2003. 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.
- Serum triglycerides in Alzheimer disease: Relation to neuroimaging and CSF biomarkers.Neurology · 2020Article
- Oleanolic Acid Exerts a Neuroprotective Effect Against Microglial Cell Activation by Modulating Cytokine Release and Antioxidant Defense Systems.Biomolecules · 2019Article
- Role of Copper in the Onset of Alzheimer's Disease Compared to Other Metals.Frontiers in aging neuroscience · 2017Review
- Hypertension, cerebrovascular impairment, and cognitive decline in aged AβPP/PS1 mice.Theranostics · 2017Article
- Amyloid-beta Alzheimer targets - protein processing, lipid rafts, and amyloid-beta pores.The Yale journal of biology and medicine · 2016Review
- Dietary omega 3 polyunsaturated fatty acids and Alzheimer's disease: interaction with apolipoprotein E genotype.Current Alzheimer research · 2011Review
- Evidence from solid-state NMR for nonhelical conformations in the transmembrane domain of the amyloid precursor protein.Biophysical journal · 2011Article
- Association between food and nutrient intakes and cognitive capacity in a group of institutionalized elderly people.European journal of nutrition · 2010Article
- Dynamics and Cleavability at the alpha-cleavage site of APP(684-726) in different lipid environments.Biophysical journal · 2008Article
- High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice.Journal of neurochemistry · 2008Article
- Effects of a saturated fat and high cholesterol diet on memory and hippocampal morphology in the middle-aged rat.Journal of Alzheimer's disease : JAD · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid plaques and neurofibrillary tangles are the neuropathological hallmarks of Alzheimer's disease (AD), but no conclusive evidence has emerged showing that these hallmarks are the cause and not a product of the disease. Many studies have implicated oxidation and inflammation in the AD process, and there is growing evidence that abnormalities of lipid metabolism also play a role. Using epidemiology to elucidate risk factors and histological changes to suggest possible mechanisms, the hypothesis is advanced that dietary lipids are the principal risk factor for the development of late-onset sporadic AD. The degree of saturation of fatty acids and the position of the first double bond in essential fatty acids are the most critical factors determining the effect of dietary fats on the risk of AD, with unsaturated fats and n-3 double bonds conferring protection and an overabundance of saturated fats or n-6 double bonds increasing the risk. The interaction of dietary lipids and apolipoprotein E isoforms may determine the risk and rate of sustained autoperoxidation within cellular membranes and the efficacy of membrane repair. Interventions involving dietary lipids and lipid metabolism show great promise in slowing or possibly averting the development of AD, including dietary changes, cholesterol-modifying agents and antioxidants.
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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 Socratic graph.