ReviewCellular and molecular neurobiology1995
Ion channel hypothesis for Alzheimer amyloid peptide neurotoxicity.
Review in Cellular and molecular neurobiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- The Framework for an Integrative Theory of Alzheimer's Disease.Current Alzheimer research · 2025Review
- Ribonuclease 4 functions as an intestinal antimicrobial protein to maintain gut microbiota and metabolite homeostasis.Nature communications · 2024Article
- Altered Extracellular Vesicle miRNA Profile in Prodromal Alzheimer's Disease.International journal of molecular sciences · 2023Article
- Rational design of stapled antimicrobial peptides.Amino acids · 2023Review
- Intracellular Injection of Brain Extracts from Alzheimer's Disease Patients Triggers Unregulated CaCells · 2022Article
- Article
- Alzheimer's Disease as a Membrane Disorder: Spatial Cross-Talk Among Beta-Amyloid Peptides, Nicotinic Acetylcholine Receptors and Lipid Rafts.Frontiers in cellular neuroscience · 2019Review
- Dietary Modulation of Oxidative Stress in Alzheimer's Disease.International journal of molecular sciences · 2017Review
- The mechanism of membrane disruption by cytotoxic amyloid oligomers formed by prion protein(106-126) is dependent on bilayer composition.The Journal of biological chemistry · 2014Article
- The glaucoma-associated olfactomedin domain of myocilin forms polymorphic fibrils that are constrained by partial unfolding and peptide sequence.Journal of molecular biology · 2014Article
- Bilayer measurement of endoplasmic reticulum Ca2+ channels.Cold Spring Harbor protocols · 2013Article
- Two-step mechanism of membrane disruption by Aβ through membrane fragmentation and pore formation.Biophysical journal · 2012Article
- Modes of Aβ toxicity in Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2011Review
- Antimicrobial protegrin-1 forms ion channels: molecular dynamic simulation, atomic force microscopy, and electrical conductance studies.Biophysical journal · 2010Article
- Kinetic study of beta-amyloid residue accessibility using reductive alkylation and mass spectrometry.Biotechnology and bioengineering · 2009Article
- Activation of group III metabotropic glutamate receptor reduces intracellular calcium in beta-amyloid peptide [31-35]-treated cortical neurons.Neurotoxicity research · 2009Article
- An update on the toxicity of Abeta in Alzheimer's disease.Neuropsychiatric disease and treatment · 2008Article
- Do amyloid oligomers act as traps for misfolded proteins? A hypothesis.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2008Review
- Neurosteroids block the increase in intracellular calcium level induced by Alzheimer’s β-amyloid protein in long-term cultured rat hippocampal neurons.Neuropsychiatric disease and treatment · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Alzheimer's disease (AD) is a chronic dementia and neurodegenerative disorder affecting the oldest portions of the population. Brains of AD patients accumulate large amount of the A beta P peptide in amyloid plaques. 2. The A beta P[1-40] peptide is derived by proteolytic processing from a much larger amyloid precursor protein (APP), and has been circumstantially identified as the toxic principle causing cell damage in the disease. 4. The A beta P[1-40] peptide is able to form quite characteristic calcium channels in planar lipid bilayers. These channels have conductances in the nS range, and can dissipate ion gradients quickly. The peptide can also cause equivalent cation conductances in cells. 5. We suggest that amyloid channel blocking agents might be therapeutically useful in Alzheimer's Disease, and have constructed molecular models of the channels to aid in the design of such compounds.
Indexed as
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.