ArticleFrontiers in neuroscience2015
Soluble beta amyloid evokes alteration in brain norepinephrine levels: role of nitric oxide and interleukin-1.
Article in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
- Glucoraphanin Triggers Rapid Antidepressant Responses in a Rat Model of Beta Amyloid-Induced Depressive-like Behaviour.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Distribution and inter-regional relationship of amyloid-beta plaque deposition in a 5xFAD mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Sublingual AKBA Exerts Antidepressant Effects in the Aβ-Treated Mouse Model.Biomolecules · 2021Article
- N-3 PUFA Prevent Oxidative Stress in a Rat Model of Beta-Amyloid-Induced Toxicity.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Precision Medicine in Alzheimer's Disease: Investigating Comorbid Common Biological Substrates in the Rat Model of Amyloid Beta-Induced Toxicity.Frontiers in pharmacology · 2021Article
- Memory-Enhancing Effects ofAntioxidants (Basel, Switzerland) · 2020Article
- Pathways Connecting Late-Life Depression and Dementia.Frontiers in pharmacology · 2020Review
- Mesenchymal stem cell-derived exosomes promote neurogenesis and cognitive function recovery in a mouse model of Alzheimer's disease.Neural regeneration research · 2019Article
- Monoaminergic System Modulation in Depression and Alzheimer's Disease: A New Standpoint?Frontiers in pharmacology · 2019Review
- Ferulic Acid Improves Cognitive Skills Through the Activation of the Heme Oxygenase System in the Rat.Molecular neurobiology · 2018Article
- Amyloid-β Homeostasis Bridges Inflammation, Synaptic Plasticity Deficits and Cognitive Dysfunction in Multiple Sclerosis.Frontiers in molecular neuroscience · 2017Article
- Maternal Malnutrition in the Etiopathogenesis of Psychiatric Diseases: Role of Polyunsaturated Fatty Acids.Brain sciences · 2016Review
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Strong evidence showed neurotoxic properties of beta amyloid (Aβ) and its pivotal role in the Alzheimer's disease (AD) pathogenesis. Beside, experimental data suggest that Aβ may have physiological roles considering that such soluble peptide is produced and secreted during normal cellular activity. There is now suggestive evidence that neurodegenerative conditions, like AD, involve nitric oxide (NO) in their pathogenesis. Nitric oxide also possess potent neuromodulatory actions in brain regions, such as prefrontal cortex (PFC), hippocampus (HIPP), and nucleus accumbens (NAC). In the present study, we evaluated the effect of acute Aβ injection on norepinephrine (NE) content before and after pharmacological manipulations of nitrergic system in above mentioned areas. Moreover, effects of the peptide on NOS activity were evaluated. Our data showed that 2 h after i.c.v. soluble Aβ administration, NE concentrations were significantly increased in the considered areas along with increased iNOS activity. Pre-treatment with NOS inhibitors, 7-Nitroindazole (7-NI), and N6-(1-iminoethyl)-L-lysine-dihydrochloride (L-NIL), reversed Aβ-induced changes. Ultimately, pharmacological block of interleukin1 (IL-1) receptors prevented NE increase in all brain regions. Taken together our findings suggest that NO and IL-1 are critically involved in regional noradrenergic alterations induced by soluble Aβ injection.
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