ArticleThe Journal of membrane biology2004
Architecture of the Alzheimer's A beta P ion channel pore.
Article in The Journal of membrane biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed.
- Serotonergic Regulation in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Aggregation dynamics of a 150 kDa Aβ42 oligomer: Insights from cryo electron microscopy and multimodal analysis.Computational and structural biotechnology journal · 2024Article
- A turn for the worse: Aβ β-hairpins in Alzheimer's disease.Bioorganic & medicinal chemistry · 2024Review
- The structure of tyrosine-10 favors ionic conductance of Alzheimer's disease-associated full-length amyloid-β channels.Nature communications · 2024Article
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- A novel apoE-mimetic increases brain apoE levels, reduces Aβ pathology and improves memory when treated before onset of pathology in male mice that express APOE3.Alzheimer's research & therapy · 2023Article
- Endogenous Amyloid-formed CaFunction (Oxford, England) · 2023Article
- Pharmacological sequestration of mitochondrial calcium uptake protects against dementia and β-amyloid neurotoxicity.Scientific reports · 2022Article
- Amyloids: The History of Toxicity and Functionality.Biology · 2021Review
- Boldine Attenuates Synaptic Failure and Mitochondrial Deregulation in Cellular Models of Alzheimer's Disease.Frontiers in neuroscience · 2021Article
- Endocytosis Is a Key Mode of Interaction between Extracellular β-Amyloid and the Cell Membrane.Biophysical journal · 2020Article
- Oligomerization and Conformational Change Turn Monomeric β-Amyloid and Tau Proteins Toxic: Their Role in Alzheimer's Pathogenesis.Molecules (Basel, Switzerland) · 2020Review
- Heat Shock Protein Inspired Nanochaperones Restore Amyloid-β Homeostasis for Preventative Therapy of Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019Article
- Insights into the Molecular Mechanisms of Alzheimer's and Parkinson's Diseases with Molecular Simulations: Understanding the Roles of Artificial and Pathological Missense Mutations in Intrinsically Disordered Proteins Related to Pathology.International journal of molecular sciences · 2018Review
- Effect of Cholesterol on Membrane Fluidity and Association of Aβ Oligomers and Subsequent Neuronal Damage: A Double-Edged Sword.Frontiers in aging neuroscience · 2018Article
- The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade.Journal of Alzheimer's disease : JAD · 2018Review
- Alzheimer's Toxic Amyloid Beta Oligomers: Unwelcome Visitors to the Na/K ATPase alpha3 Docking Station.The Yale journal of biology and medicine · 2017Article
- Ion Channel Formation by Amyloid-β42 Oligomers but Not Amyloid-β40 in Cellular Membranes.The Journal of biological chemistry · 2017Article
- Overview of Alzheimer's Disease and Some Therapeutic Approaches Targeting Aβ by Using Several Synthetic and Herbal Compounds.Oxidative medicine and cellular longevity · 2016Review
- Single-cell screening of cytosolic [Ca(2+)] reveals cell-selective action by the Alzheimer's Aβ peptide ion channel.Cell stress & chaperones · 2015Article
Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have proposed that the cytotoxic action of Alzheimer's amyloid beta protein might be initiated by the interaction with the neuronal cell membrane, and subsequent formation of toxic ion channels. Consequently, A beta P toxicity can be explained on the basis of harmful ion fluxes across A beta P channels. The conformation of A beta P in membranes is not known. However, several models suggests that a transmembrane annular polymeric structure is responsible for the ion channel properties of the membrane-bound A beta P. To identify that portion of the A beta P molecule making up the conducting pore we have hypothesized that the region of the A beta P sequence in the vicinity of the hypothetical pore might interact with complementary regions in the adjacent A beta P subunits. We have further hypothesized that an interaction by a peptide segment would block A beta P conductance. To test this hypothesis we synthesized peptides that encompass the histidine dyad (H-H) previously hypothesized to line the pore. We report here that peptides designed to most closely match the proposed pore are, in fact, the most effective at blocking ion currents through the membrane-incorporated A beta P channel. As previously shown for Zn(2+) blockade, peptide blockade is also asymmetric. The results also provide additional evidence for the asymmetric insertion of the A beta P molecules into lipid membranes, and give support to the concept that rings of histidines line the entry to one side of the A beta P pore.
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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.