ArticleInternational journal of molecular sciences2024
Oxidative Stress Triggers a Pivotal Peptide Linked to Alzheimer's Disease.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Unraveling Hippocampal and Prefrontal Cortex Alterations in Experimental Type 1 and Type 2 Diabetes: A 100-Day Exploration of Biochemical and Behavioral-Cognitive Dysfunction.Molecular neurobiology · 2026Article
- Silymarin reverses post-traumatic stress-induced memory impairment in mice by containment of oxidative stress, cholinergic dysfunction, and modulation of neuronal caspase-3 expression.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- ZL006 Treatment Reduces Inflammation, Oxidative Stress, and Brain AβInternational journal of molecular sciences · 2026Article
- Evaluating the Efficacy of Monoclonal Antibodies Against a Bioactive Peptide Involved in Alzheimer's Disease: A Methodological Approach.Methods and protocols · 2026Article
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4 authors.
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Abstract
An aberrant recapitulation of a developmental mechanism driven by a 14 mer peptide ('T14') derived from acetylcholinesterase (AChE) has been implicated in Alzheimer's disease. T14 was suggested as an upstream driver of neurodegeneration due to its ability to stimulate the production of phosphorylated tau and amyloid beta. The activation of this mechanism in adulthood is thought to be brought upon by insult to the primarily vulnerable subcortical nuclei. Here, we show that oxidative stress, induced by high glucose and confirmed by an analysis of antioxidant enzyme mRNA expression, increased the levels of T14 peptide in PC12 cells. This increase in T14 corresponded with an increase in the mRNA expression of AChE and a decrease in the cell viability. The increase in T14 could be blocked by the cyclic form of T14, NBP14, which prevented any cytotoxic effects. These observations suggest that oxidative stress can directly trigger the inappropriate activation of T14 in the adult brain through the upregulation of
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