ReviewMolecular neurodegeneration2013
Cross-talk of membrane lipids and Alzheimer-related proteins.
Review in Molecular neurodegeneration, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
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.
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Who cites it
40 citing papers in PubMed, 74 citations in OpenAlex.
- Uncovering lipid biomarkers linked to methylphenidate efficacy in treating apathy in Alzheimer's disease: insights from the ADMET 2 trial.Alzheimer's research & therapy · 2026Trial
- Lipid Composition Drives Mutant Huntingtin Dimerization and Membrane Association: Insights from Computational Simulations.Molecules (Basel, Switzerland) · 2026Article
- Clustering hinders APP α-secretase processing in the plasma membrane.Biophysical journal · 2026Article
- Unveiling ribosomal dysfunction and impaired signaling pathways in the cortical region of 5xFAD mice.Acta neuropathologica communications · 2026Article
- Systems-Level Interactome Mapping Reveals Actionable Protein Network Dysregulation Across the Alzheimer's Disease Spectrum.Research square · 2025Article
- Lipoproteins and metabolites in diagnosing and predicting Alzheimer's disease using machine learning.Lipids in health and disease · 2024Article
- Cross interactions between Apolipoprotein E and amyloid proteins in neurodegenerative diseases.Computational and structural biotechnology journal · 2023Review
- Lipidomics and proteomics: An integrative approach for early diagnosis of dementia and Alzheimer's disease.Frontiers in genetics · 2023Review
- Live-Cell Imaging of Single Neurotrophin Receptor Molecules on Human Neurons in Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Likelihood ratio statistics for gene set enrichment in Alzheimer's disease pathways.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Article
- Genetic defects in the sphingolipid degradation pathway and their effects on microglia in neurodegenerative disease.Cellular signalling · 2021Review
- Role of the Lipid Membrane and Membrane Proteins in Tau Pathology.Frontiers in cell and developmental biology · 2021Review
- Cerebrospinal Fluid C18 Ceramide Associates with Markers of Alzheimer's Disease and Inflammation at the Pre- and Early Stages of Dementia.Journal of Alzheimer's disease : JAD · 2021Article
- Preferred Endocytosis of Amyloid Precursor Protein from Cholesterol-Enriched Lipid Raft Microdomains.Molecules (Basel, Switzerland) · 2020Article
- Ceramide analog [Scientific reports · 2020Article
- Importance of γ-secretase in the regulation of liver X receptor and cellular lipid metabolism.Life science alliance · 2020Article
- Live-cell monitoring of protein localization to membrane rafts using protein-fragment complementation.Bioscience reports · 2020Article
- Tau Protein and Its Role in Blood-Brain Barrier Dysfunction.Frontiers in molecular neuroscience · 2020Review
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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
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is neuropathologically characterized by the combined occurrence of extracellular β-amyloid plaques and intracellular neurofibrillary tangles in the brain. While plaques contain aggregated forms of the amyloid β-peptide (Aβ), tangles are formed by fibrillar forms of the microtubule associated protein tau. All mutations identified so far to cause familial forms of early onset AD (FAD) are localized close to or within the Aβ domain of the amyloid precursor protein (APP) or in the presenilin proteins that are essential components of a protease complex involved in the generation of Aβ. Mutations in the tau gene are not associated with FAD, but can cause other forms of dementia. The genetics of FAD together with biochemical and cell biological data, led to the formulation of the amyloid hypothesis, stating that accumulation and aggregation of Aβ is the primary event in the pathogenesis of AD, while tau might mediate its toxicity and neurodegeneration.The generation of Aβ involves sequential proteolytic cleavages of the amyloid precursor protein (APP) by enzymes called β-and γ-secretases. Notably, APP itself as well as the secretases are integral membrane proteins. Thus, it is very likely that membrane lipids are involved in the regulation of subcellular transport, activity, and metabolism of AD related proteins.Indeed, several studies indicate that membrane lipids, including cholesterol and sphingolipids (SLs) affect Aβ generation and aggregation. Interestingly, APP and other AD associated proteins, including β-and γ-secretases can, in turn, influence lipid metabolic pathways. Here, we review the close connection of cellular lipid metabolism and AD associated proteins and discuss potential mechanisms that could contribute to initiation and progression 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.