ArticleScientific reports2016
Common molecular mechanism of amyloid pore formation by Alzheimer's β-amyloid peptide and α-synuclein.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 1 of them a synthesis that pooled it.
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Who cites it
96 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.
- Effects of Higher Serum Lipid Levels on the Risk of Parkinson's Disease: A Systematic Review and Meta-Analysis.Frontiers in neurology · 2020Pooled it
- Membrane Complexity and Phase Behavior Dictate the Stability of Membrane-Inserted AβChemphyschem : a European journal of chemical physics and physical chemistry · 2026Article
- An Optimal Spray Device for the Nose-to-Brain Delivery of AmyP53, an Adaptive Therapeutic Peptide for Alzheimer's and Parkinson's Diseases.Pharmaceutics · 2026Article
- Epigenetic Evidence Implies Disturbed Proteostasis and Potentially Protein Aggregation in Suicidality.Biomolecules · 2026Review
- Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026Review
- Parallel in-register contact propensity predicts the Amyloidogenicity of ADan and ABri in familial dementias.International journal of biological macromolecules · 2026Article
- Lipid droplets in astrocytes: Key organelles for CNS homeostasis and disease (Review).International journal of molecular medicine · 2026Review
- The Influence of POPC as a Coaggregate in Amyloid-β Oligomer Formation.ACS chemical neuroscience · 2025Article
- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Uncovering Amyloid-β Interactions: Gray versus White Matter.ACS chemical neuroscience · 2025Article
- Emerging biophysical origins and pathogenic implications of amyloid oligomers.Nature communications · 2025Review
- Preclinical assessment of a ganglioside-targeted therapy for Parkinson's disease with the first-in-class adaptive peptide AmyP53.Scientific reports · 2025Article
- Interactions of alpha-synuclein with membranes in Parkinson's disease: Mechanisms and therapeutic strategies.Neurobiology of disease · 2024Review
- Review
- Consequences of Amyloid-β Deficiency for the Liver.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Polar lipids modify Alzheimer's Disease pathology by reducing astrocyte pro-inflammatory signaling through platelet-activating factor receptor (PTAFR) modulation.Lipids in health and disease · 2024Article
- What Is life? Rethinking Biology in Light of Fundamental Parameters.Life (Basel, Switzerland) · 2024Review
- Computational insights into the cross-talk between medin and Aβ: implications for age-related vascular risk factors in Alzheimer's disease.Briefings in bioinformatics · 2024Article
- Real-time monitoring of the amyloid βPNAS nexus · 2024Article
- Dissecting membrane interfacial cellular processes: an in vitro reconstitution approach.The European physical journal. Special topics · 2024Review
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Calcium-permeable pores formed by small oligomers of amyloid proteins are the primary pathologic species in Alzheimer's and Parkinson's diseases. However, the molecular mechanisms underlying the assembly of these toxic oligomers in the plasma membrane of brain cells remain unclear. Here we have analyzed and compared the pore-forming capability of a large panel of amyloid proteins including wild-type, variant and truncated forms, as well as synthetic peptides derived from specific domains of Aβ1-42 and α-synuclein. We show that amyloid pore formation involves two membrane lipids, ganglioside and cholesterol, that physically interact with amyloid proteins through specific structural motifs. Mutation or deletion of these motifs abolished pore formation. Moreover, α-synuclein (Parkinson) and Aβ peptide (Alzheimer) did no longer form Ca(2+)-permeable pores in presence of drugs that target either cholesterol or ganglioside or both membrane lipids. These results indicate that gangliosides and cholesterol cooperate to favor the formation of amyloid pores through a common molecular mechanism that can be jammed at two different steps, suggesting the possibility of a universal therapeutic approach for neurodegenerative diseases. Finally we present the first successful evaluation of such a new therapeutic approach (coined "membrane therapy") targeting amyloid pores formed by Aβ1-42 and α-synuclein.
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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.