ReviewExpert reviews in molecular medicine2010
Molecular insights into amyloid regulation by membrane cholesterol and sphingolipids: common mechanisms in neurodegenerative diseases.
Review in Expert reviews in molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 172 citations in OpenAlex.
- A lattice Monte Carlo model for amyloid fibril formation.Biophysics and physicobiology · 2026Article
- Amyloid β Peptide Modifies Membrane Architecture and Surface Electrostatic Properties of Human Red Blood Cells.International journal of molecular sciences · 2025Article
- Integrative Spatial Omics for Systems-Level Mapping of Pathological Niches.bioRxiv : the preprint server for biology · 2025Article
- Crossing Barriers: Advancements in Macromolecular Therapeutics for Neurodegenerative Diseases and Strategies to Overcome the Blood-Brain Barrier.ACS pharmacology & translational science · 2025Review
- Gut microbiota and serum metabolomics unveil the role of Phellinus ribis polysaccharides in improving Alzheimer's disease symptoms in senescence-accelerated mice.Metabolic brain disease · 2025Article
- Molecular dynamics simulations of amyloid-β(29-42) aggregation in bulk water and at the air-water interface.Biophysics and physicobiology · 2025Article
- The Effects of External Interfaces on Hydrophobic Interactions I: Smooth Surface.Molecules (Basel, Switzerland) · 2024Article
- Spatial neurolipidomics-MALDI mass spectrometry imaging of lipids in brain pathologies.Journal of mass spectrometry : JMS · 2024Review
- Lipid rafts and human diseases: why we need to target gangliosides.FEBS open bio · 2023Review
- Cholesterol in Class C GPCRs: Role, Relevance, and Localization.Membranes · 2023Article
- AmyP53 Prevents the Formation of Neurotoxic β-Amyloid Oligomers through an Unprecedent Mechanism of Interaction with Gangliosides: Insights for Alzheimer's Disease Therapy.International journal of molecular sciences · 2023Article
- Structural Analysis of Oligosaccharides and Glycoconjugates Using NMR.Advances in neurobiology · 2023Article
- The Epigenetic Dimension of Protein Structure Is an Intrinsic Weakness of the AlphaFold Program.Biomolecules · 2022Article
- Conformational Variability of Amyloid-β and the Morphological Diversity of Its Aggregates.Molecules (Basel, Switzerland) · 2022Review
- Molecular Dynamics Simulation Studies on the Aggregation of Amyloid-β Peptides and Their Disaggregation by Ultrasonic Wave and Infrared Laser Irradiation.Molecules (Basel, Switzerland) · 2022Review
- Free Cholesterol Accelerates Aβ Self-Assembly on Membranes at Physiological Concentration.International journal of molecular sciences · 2022Article
- Innovative treatment targeting gangliosides aimed at blocking the formation of neurotoxic α-synuclein oligomers in Parkinson's disease.Glycoconjugate journal · 2022Review
- Cholesterol as a key player in amyloid β-mediated toxicity in Alzheimer's disease.Frontiers in molecular neuroscience · 2022Review
- Virtual reality-based monitoring test for MCI: A multicenter feasibility study.Frontiers in psychiatry · 2022Article
- Molecular dynamics simulations of amyloid-β peptides in heterogeneous environments.Biophysics and physicobiology · 2022Article
10 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer, Parkinson and other neurodegenerative diseases involve a series of brain proteins, referred to as 'amyloidogenic proteins', with exceptional conformational plasticity and a high propensity for self-aggregation. Although the mechanisms by which amyloidogenic proteins kill neural cells are not fully understood, a common feature is the concentration of unstructured amyloidogenic monomers on bidimensional membrane lattices. Membrane-bound monomers undergo a series of lipid-dependent conformational changes, leading to the formation of oligomers of varying toxicity rich in beta-sheet structures (annular pores, amyloid fibrils) or in alpha-helix structures (transmembrane channels). Condensed membrane nano- or microdomains formed by sphingolipids and cholesterol are privileged sites for the binding and oligomerisation of amyloidogenic proteins. By controlling the balance between unstructured monomers and alpha or beta conformers (the chaperone effect), sphingolipids can either inhibit or stimulate the oligomerisation of amyloidogenic proteins. Cholesterol has a dual role: regulation of protein-sphingolipid interactions through a fine tuning of sphingolipid conformation (indirect effect), and facilitation of pore (or channel) formation through direct binding to amyloidogenic proteins. Deciphering this complex network of molecular interactions in the context of age- and disease-related evolution of brain lipid expression will help understanding of how amyloidogenic proteins induce neural toxicity and will stimulate the development of innovative therapies for neurodegenerative diseases.
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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.