ArticleEC pharmacology and toxicology2019
Alzheimer's Pathogenesis, Metal-Mediated Redox Stress, and Potential Nanotheranostics.
Article in EC pharmacology and toxicology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 4 citations in OpenAlex.
- Oxidative/Nitrosative Stress, Apoptosis, and Redox Signaling: Key Players in Neurodegenerative Diseases.Journal of biochemical and molecular toxicology · 2025Review
- Redox dysregulation as a driver for DNA damage and its relationship to neurodegenerative diseases.Translational neurodegeneration · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) characterized by insoluble amyloid-β (Aβ) deposits, neurofibrillary tangles (NFTs), and neuronal demise. The influence of environmental and genetic factors on AD progression remains elusive, however evidence suggests biometal dyshomeostasis elicits neuronal death, neuroinflammation, and accumulated oxidative damages in AD brain. As such, three pathways have been identified that result from abnormal biometal accumulation and increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in AD brain parenchyma: (1) the damage caused by direct oxidation of cellular components such as DNA and proteins; (2) the oligomerization of Aβ and NFTs, and (3) the promotion of apoptosis through NF-κB signaling pathway. Finally, given recent developments in nanotechnology, we have briefly reviewed potential nanotheranostic agents as potential AD theranostics.
Indexed as
Identifiers
31565701PMC6764777W2990816195What 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.