ArticleAlzheimer's research & therapy2012
Lipidomics of Alzheimer's disease: current status.
Article in Alzheimer's research & therapy, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
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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
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Who cites it
89 citing papers in PubMed, 163 citations in OpenAlex.
- Is Lipidomic the Answer to the Search of a Biomarker for Organ Preservation Protocol in Head and Neck Squamous Cell Carcinoma?Pathology oncology research : POR · 2018Trial
- Reframing Alzheimer's Disease Through a Redox-Metabolic Framework.International journal of molecular sciences · 2026Review
- Causal Links Between the Plasma Lipidome and Cognitive Performance: Targets, Pathways, and Lifestyle Influences.Molecular neurobiology · 2026Article
- Review
- Lipidomic Analysis of Human Plasma and Hippocampus Across Alzheimer's Progression and Preclinical 5xFAD Mouse Model.Molecular neurobiology · 2026Article
- Alzheimer's disease: from molecular pathways to therapies.Molecular biomedicine · 2026Review
- Lipidomic signatures reveal biomarkers of mild cognitive impairment.Translational psychiatry · 2026Article
- Plasma lipidomic fingerprinting enables high-accuracy biomarker discovery for Alzheimer's disease: a targeted LC-MRM/MS approach.GeroScience · 2026Article
- Microglial GM3 accumulation impairs Aβ phagocytic activity and promotes neuroinflammation in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Loss of Nuclear TDP-43 Impairs Lipid Metabolism in Microglia-Like Cells.Research square · 2025Article
- Loss of Nuclear TDP-43 Impairs Lipid Metabolism in Microglia-Like Cells.bioRxiv : the preprint server for biology · 2025Article
- Artificial intelligence-driven multi-omics approaches in Alzheimer's disease: Progress, challenges, and future directions.Acta pharmaceutica Sinica. B · 2025Review
- Lipidomic Network Analysis Reveals Amyloid-β-Induced Lysosomal Lipid Accumulation in the Cortex and Hippocampus of 5xFAD Mice.Journal of proteome research · 2025Article
- Novel insights from comprehensive analysis: The role of cuproptosis and peripheral immune infiltration in Alzheimer's disease.PloS one · 2025Article
- Article
- Differential effect of an evolving amyloid and tau pathology on brain phospholipids and bioactive lipid mediators in rat models of Alzheimer-like pathology.Journal of neuroinflammation · 2024Article
- Protein restriction slows the development and progression of pathology in a mouse model of Alzheimer's disease.Nature communications · 2024Article
- Phospholipidomics in Clinical Trials for Brain Disorders: Advancing our Understanding and Therapeutic Potentials.Molecular neurobiology · 2024Review
- Brain cholesterol and Alzheimer's disease: challenges and opportunities in probe and drug development.Brain : a journal of neurology · 2024Review
- Protein restriction slows the development and progression of Alzheimer's disease in mice.Research square · 2024Article
29 more citing papers are in PubMed but not listed here.
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
Alzheimer's disease (AD) is a cognitive disorder with a number of complex neuropathologies, including, but not limited to, neurofibrillary tangles, neuritic plaques, neuronal shrinkage, hypomyelination, neuroinflammation and cholinergic dysfunction. The role of underlying pathological processes in the evolution of the cholinergic deficit responsible for cognitive decline has not been elucidated. Furthermore, generation of testable hypotheses for defining points of pharmacological intervention in AD are complicated by the large scale occurrence of older individuals dying with no cognitive impairment despite having a high burden of AD pathology (plaques and tangles). To further complicate these research challenges, there is no animal model that reproduces the combined hallmark neuropathologies of AD. These research limitations have stimulated the application of 'omics' technologies in AD research with the goals of defining biologic markers of disease and disease progression and uncovering potential points of pharmacological intervention for the design of AD therapeutics. In the case of sporadic AD, the dominant form of dementia, genomics has revealed that the ε4 allele of apolipoprotein E, a lipid transport/chaperone protein, is a susceptibility factor. This seminal observation points to the importance of lipid dynamics as an area of investigation in AD. In this regard, lipidomics studies have demonstrated that there are major deficits in brain structural glycerophospholipids and sphingolipids, as well as alterations in metabolites of these complex structural lipids, which act as signaling molecules. Peroxisomal dysfunction appears to be a key component of the changes in glycerophospholipid deficits. In this review, lipid alterations and their potential roles in the pathophysiology of AD are discussed.
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.