ReviewNeurochemical research2004
Toxicity of amyloid beta peptide: tales of calcium, mitochondria, and oxidative stress.
Review in Neurochemical research, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 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
95 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Supplementation with Curcuma longa Reverses Neurotoxic and Behavioral Damage in Models of Alzheimer's Disease: A Systematic Review.Current neuropharmacology · 2019Pooled it
- Effect of tramiprosate in patients with mild-to-moderate Alzheimer's disease: exploratory analyses of the MRI sub-group of the Alphase study.The journal of nutrition, health & aging · 2009Trial
- Lessons learned in the use of volumetric MRI in therapeutic trials in Alzheimer's disease: the ALZHEMED (Tramiprosate) experience.The journal of nutrition, health & aging · 2009Trial
- Structural Assessment of Fibrillated Beta Amyloid to Reveal the Potential Epitopes for Alzheimer's Disease.Cell biochemistry and biophysics · 2026Article
- Article
- Preexisting Genetic Background Primes the Responses of Human Neurons to Amyloid β.International journal of molecular sciences · 2025Article
- Alzheimer's Disease Pathogenic Mechanisms: Linking Redox Homeostasis and Mitochondria-Associated Metabolic Pathways Through Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2).Antioxidants (Basel, Switzerland) · 2025Review
- Neurostimulation devices to treat Alzheimer's disease.Exploration of neuroscience · 2025Article
- The role of probiotics, prebiotics, and postbiotics: cellular and molecular pathways activated on glial cells in Alzheimer's disease.Frontiers in neuroscience · 2025Review
- The inter-organelle cross-talk finely orchestrated in the amyloidogenic processing of amyloid precursor protein in dendritic arborization neurons ofTheranostics · 2025Article
- Stabilization and Reduced Cytotoxicity of Amyloid Beta Aggregates in the Presence of Catechol Neurotransmitters.Neurochemical research · 2024Article
- Using Optogenetics to Model Cellular Effects of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Protein Interactome of Amyloid-β as a Therapeutic Target.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Alzheimer's disease: a mini-review for the clinician.Frontiers in neurology · 2023Review
- Protective effects ofNutrition research and practice · 2022Article
- Structural Plasticity of the Hippocampus in Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Chiral Linked Systems as a Model for Understanding D-Amino Acids Influence on the Structure and Properties of Amyloid Peptides.International journal of molecular sciences · 2022Review
- Comparison of the different isoforms of vitamin e against amyloid beta-induced neurodegeneration.Turkish journal of biology = Turk biyoloji dergisi · 2022Article
- Inorganic Polyphosphate, Mitochondria, and Neurodegeneration.Progress in molecular and subcellular biology · 2022Article
- Alzheimer's Disease Biomarkers Revisited From the Amyloid Cascade Hypothesis Standpoint.Frontiers in neuroscience · 2022Review
35 more citing papers are in PubMed but not listed here.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta (Abeta) peptides. Although the disease undoubtedly reflects the interaction of complex multifactorial processes, Abeta itself is toxic to neurons in vitro and the load of Abeta in vivo correlates well with the degree of cognitive impairment. There has therefore been considerable interest in the mechanism(s) of Abeta neurotoxicity. We here review the basic biology of Abeta processing and consider some of the major areas of focus of this research. It is clear that both AD and Abeta toxicity are characterized by oxidative stress, alterations in the activity of enzymes of intermediary metabolism, and mitochondrial dysfunction, especially impaired activity of cytochrome c oxidase. Studies in vitro also show alterations in cellular calcium signaling. We consider the mechanisms proposed to mediate cell injury and explore evidence to indicate which of these many changes in function are primary and which secondary.
Indexed as
Identifiers
15038611What 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.