ArticleOxidative medicine and cellular longevity2012
Accumulation of exogenous amyloid-beta peptide in hippocampal mitochondria causes their dysfunction: a protective role for melatonin.
Article in Oxidative medicine and cellular longevity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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
25 citing papers in PubMed, 61 citations in OpenAlex.
- Mitochondrial calcium cycling in neuronal function and neurodegeneration.Frontiers in cell and developmental biology · 2023Review
- Melatonin: A Neurotrophic Factor?Molecules (Basel, Switzerland) · 2022Review
- Article
- Melatonin Enhances the Mitochondrial Functionality of Brown Adipose Tissue in Obese-Diabetic Rats.Antioxidants (Basel, Switzerland) · 2021Article
- Inhibition of Amyloid β-Induced Lipid Membrane Permeation and Amyloid β Aggregation by K162.ACS chemical neuroscience · 2021Article
- Lupeol, a Plant-Derived Triterpenoid, Protects Mice Brains against Aβ-Induced Oxidative Stress and Neurodegeneration.Biomedicines · 2020Article
- Alzheimer's disease-related amyloid β peptide causes structural disordering of lipids and changes the electric properties of a floating bilayer lipid membrane.Nanoscale advances · 2020Article
- Melatonin regulates mitochondrial dynamics and alleviates neuron damage in prion diseases.Aging · 2020Article
- Noxious Iron-Calcium Connections in Neurodegeneration.Frontiers in neuroscience · 2019Review
- Mitochondria as Potential Targets in Alzheimer Disease Therapy: An Update.Frontiers in pharmacology · 2019Review
- Mitochondrial Molecular Abnormalities Revealed by Proteomic Analysis of Hippocampal Organelles of Mice Triple Transgenic for Alzheimer Disease.Frontiers in molecular neuroscience · 2018Article
- The Function of the Mitochondrial Calcium Uniporter in Neurodegenerative Disorders.International journal of molecular sciences · 2017Review
- The Case for Abandoning Therapeutic Chelation of Copper Ions in Alzheimer's Disease.Frontiers in neuroscience · 2017Review
- Amyloid-β and α-Synuclein Decrease the Level of Metal-Catalyzed Reactive Oxygen Species by Radical Scavenging and Redox Silencing.Journal of the American Chemical Society · 2016Article
- The Protective Effect of Icariin on Mitochondrial Transport and Distribution in Primary Hippocampal Neurons from 3× Tg-AD Mice.International journal of molecular sciences · 2016Article
- AP39, a Mitochondria-Targeted Hydrogen Sulfide Donor, Supports Cellular Bioenergetics and Protects against Alzheimer's Disease by Preserving Mitochondrial Function in APP/PS1 Mice and Neurons.Oxidative medicine and cellular longevity · 2016Article
- Neuroprotective Effects of Icariin on Brain Metabolism, Mitochondrial Functions, and Cognition in Triple-Transgenic Alzheimer's Disease Mice.CNS neuroscience & therapeutics · 2016Article
- Prophylactic melatonin significantly reduces Alzheimer's neuropathology and associated cognitive deficits independent of antioxidant pathways in AβPP(swe)/PS1 mice.Molecular neurodegeneration · 2015Article
- Ceramides in Alzheimer's Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and Aβ Accumulation.Oxidative medicine and cellular longevity · 2015Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid-beta (Aβ) pathology is related to mitochondrial dysfunction accompanied by energy reduction and an elevated production of reactive oxygen species (ROS). Monomers and oligomers of Aβ have been found inside mitochondria where they accumulate in a time-dependent manner as demonstrated in transgenic mice and in Alzheimer's disease (AD) brain. We hypothesize that the internalization of extracellular Aβ aggregates is the major cause of mitochondrial damage and here we report that following the injection of fibrillar Aβ into the hippocampus, there is severe axonal damage which is accompanied by the entrance of Aβ into the cell. Thereafter, Aβ appears in mitochondria where it is linked to alterations in the ionic gradient across the inner mitochondrial membrane. This effect is accompanied by disruption of subcellular structure, oxidative stress, and a significant reduction in both the respiratory control ratio and in the hydrolytic activity of ATPase. Orally administrated melatonin reduced oxidative stress, improved the mitochondrial respiratory control ratio, and ameliorated the energy imbalance.
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.