ArticlePloS one2013
CNF1 increases brain energy level, counteracts neuroinflammatory markers and rescues cognitive deficits in a murine model of Alzheimer's disease.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Effects of theInternational journal of molecular sciences · 2021Pooled it
- Sex differences in cognition, anxiety-phenotype and therapeutic effect of metformin in the aged apoE-TR mice.Biology of sex differences · 2025Article
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- Some Examples of Bacterial Toxins as Tools.Toxins · 2024Review
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- Effects of the Rho GTPase-activating toxin CNF1 on fibroblasts derived from Rett syndrome patients: A pilot study.Journal of cellular and molecular medicine · 2023Article
- Immunomodulatory properties of CNF1 toxin fromAmerican journal of cancer research · 2022Review
- The Cytotoxic Necrotizing Factors (CNFs)-A Family of Rho GTPase-Activating Bacterial Exotoxins.Toxins · 2021Review
- Treatment with the Bacterial Toxin CNF1 Selectively Rescues Cognitive and Brain Mitochondrial Deficits in a Female Mouse Model of Rett Syndrome Carrying a MeCP2-Null Mutation.International journal of molecular sciences · 2021Article
- Aggregate Trends of Apolipoprotein E on Cognition in Transgenic Alzheimer's Disease Mice.Journal of Alzheimer's disease : JAD · 2021Article
- The Bacterial Toxin CNF1 Protects Human Neuroblastoma SH-SY5Y Cells against 6-Hydroxydopamine-Induced Cell Damage: The Hypothesis of CNF1-Promoted Autophagy as an Antioxidant Strategy.International journal of molecular sciences · 2020Article
- Article
- The bacterial protein CNF1 as a new strategy against Plasmodium falciparum cytoadherence.PloS one · 2019Article
- The Bacterial Protein CNF1 as a Potential Therapeutic Strategy against Mitochondrial Diseases: A Pilot Study.International journal of molecular sciences · 2018Article
- Bacterial Toxins and Targeted Brain Therapy: New Insights from Cytotoxic Necrotizing Factor 1 (CNF1).International journal of molecular sciences · 2018Review
- Rho GTPases as therapeutic targets in Alzheimer's disease.Alzheimer's research & therapy · 2017Review
- Electrophysiology of glioma: a Rho GTPase-activating protein reduces tumor growth and spares neuron structure and function.Neuro-oncology · 2016Article
- Article
- Long-lasting beneficial effects of central serotonin receptor 7 stimulation in female mice modeling Rett syndrome.Frontiers in behavioral neuroscience · 2015Article
- CNF1 Enhances Brain Energy Content and Counteracts Spontaneous Epileptiform Phenomena in Aged DBA/2J Mice.PloS one · 2015Article
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of pro-inflammatory cytokines and cellular energy failure are associated with neuroinflammatory disorders, such as Alzheimer's disease. Transgenic mice homozygous for human ApoE4 gene, a well known AD and atherosclerosis animal model, show decreased levels of ATP, increased inflammatory cytokines level and accumulation of beta amyloid in the brain. All these findings are considered responsible for triggering cognitive decline. We have demonstrated that a single administration of the bacterial E. coli protein toxin CNF1 to aged apoE4 mice, beside inducing a strong amelioration of both spatial and emotional memory deficits, favored the cell energy restore through an increment of ATP content. This was accompanied by a modulation of cerebral Rho and Rac1 activity. Furthermore, CNF1 decreased the levels of beta amyloid accumulation and interleukin-1β expression in the hippocampus. Altogether, these data suggest that the pharmacological modulation of Rho GTPases by CNF1 can improve memory performances in an animal model of Alzheimer's disease via a control of neuroinflammation and a rescue of systemic energy homeostasis.
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