ArticleInternational journal of Alzheimer's disease2012
Alterations in Lipid Levels of Mitochondrial Membranes Induced by Amyloid-β: A Protective Role of Melatonin.
Article in International journal of Alzheimer's disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 28 citations in OpenAlex.
- Physiological Implications of Pancreatic Amyloid Polypeptide Aggregation and Its Inhibition by Melatonin.International journal of molecular sciences · 2026Review
- Chromone derivatives suppress neuroinflammation and improve mitochondrial function in the sporadic form of Alzheimer's disease under experimental conditions.Iranian journal of basic medical sciences · 2022Article
- Inhalation of nebulized omega-3 fatty acids mitigate LPS-induced acute lung inflammation in rats: Implications for treatment of COPD and COVID-19.Prostaglandins, leukotrienes, and essential fatty acids · 2022Article
- Mitochondrially-Targeted Therapeutic Strategies for Alzheimer's Disease.Current Alzheimer research · 2021Review
- Antioxidants and Neuron-Astrocyte Interplay in Brain Physiology: Melatonin, a Neighbor to Rely on.Neurochemical research · 2021Review
- Mitochondria as Potential Targets in Alzheimer Disease Therapy: An Update.Frontiers in pharmacology · 2019Review
- Modulation of mitochondrial bioenergetics as a therapeutic strategy in Alzheimer's disease.Neural regeneration research · 2018Review
- Melatonin as a mitochondrial protector in neurodegenerative diseases.Cellular and molecular life sciences : CMLS · 2017Review
- Using an NMR metabolomics approach to investigate the pathogenicity of amyloid-beta and alpha-synuclein.Metabolomics : Official journal of the Metabolomic Society · 2017Article
- Oxidative Stress, Synaptic Dysfunction, and Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Review
- Melatonin as a Potential Agent in the Treatment of Sarcopenia.International journal of molecular sciences · 2016Review
- The Deleterious Effects of Oxidative and Nitrosative Stress on Palmitoylation, Membrane Lipid Rafts and Lipid-Based Cellular Signalling: New Drug Targets in Neuroimmune Disorders.Molecular neurobiology · 2016Review
- Therapeutic effects of melatonin receptor agonists on sleep and comorbid disorders.International journal of molecular sciences · 2014Review
- Identification of altered metabolic pathways in plasma and CSF in mild cognitive impairment and Alzheimer's disease using metabolomics.PloS one · 2013Article
- Current advances in the treatment of Alzheimer's disease: focused on considerations targeting Aβ and tau.Translational neurodegeneration · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer pathogenesis involves mitochondrial dysfunction, which is closely related to amyloid-β (Aβ) generation, abnormal tau phosphorylation, oxidative stress, and apoptosis. Alterations in membranal components, including cholesterol and fatty acids, their characteristics, disposition, and distribution along the membranes, have been studied as evidence of cell membrane alterations in AD brain. The majority of these studies have been focused on the cytoplasmic membrane; meanwhile the mitochondrial membranes have been less explored. In this work, we studied lipids and mitochondrial membranes in vivo, following intracerebral injection of fibrillar amyloid-β (Aβ). The purpose was to determine how Aβ may be responsible for beginning of a vicious cycle where oxidative stress and alterations in cholesterol, lipids and fatty acids, feed back on each other to cause mitochondrial dysfunction. We observed changes in mitochondrial membrane lipids, and fatty acids, following intracerebral injection of fibrillar Aβ in aged Wistar rats. Melatonin, a well-known antioxidant and neuroimmunomodulator indoleamine, reversed some of these alterations and protected mitochondrial membranes from obvious damage. Additionally, melatonin increased the levels of linolenic and n-3 eicosapentaenoic acid, in the same site where amyloid β was injected, favoring an endogenous anti-inflammatory pathway.
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.