Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Souza da Silva 2020 Mol Neurobiol"

From Bioblast
(Created page with "{{Publication |title=da Silva JS, Nonose Y, Rohden F, Lukasewicz Ferreira PC, Fontella FU, Rocha A, Brochier AW, Apel RV, de Lima TM, Seminotti B, Amaral AU, Galina A, Souza D...")
 
Line 10: Line 10:
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration, Pharmacology;toxicology
|instruments=Oxygraph-2k
|diseases=Alzheimer's
|additional=2020-08
|organism=Mouse
|tissues=Nervous system
|preparations=Homogenate
|couplingstates=LEAK, OXPHOS, ET
|pathways=N, S, NS, ROX
|instruments=Oxygraph-2k, O2k-Fluorometer
|additional=2020-08, AmR
}}
}}

Revision as of 17:59, 21 August 2020

Publications in the MiPMap
da Silva JS, Nonose Y, Rohden F, Lukasewicz Ferreira PC, Fontella FU, Rocha A, Brochier AW, Apel RV, de Lima TM, Seminotti B, Amaral AU, Galina A, Souza DO (2020) Guanosine neuroprotection of presynaptic mitochondrial calcium homeostasis in a mouse study with amyloid-β oligomers. Mol Neurobiol [Epub ahead of print].

» PMID: 32789760

da Silva JS, Nonose Y, Rohden F, Lukasewicz Ferreira PC, Fontella FU, Rocha A, Brochier AW, Apel RV, de Lima TM, Seminotti B, Amaral AU, Galina A, Souza DO (2020) Mol Neurobiol

Abstract: Amyloid-β oligomers (AβOs) toxicity causes mitochondrial dysfunction, leading to synaptic failure in Alzheimer's disease (AD). Considering presynaptic high energy demand and tight Ca2+ regulation, impairment of mitochondrial function can lead to deteriorated neural activity and cell death. In this study, an AD mouse model induced by ICV (intracerebroventricular) injection of AβOs was used to investigate the toxicity of AβOs on presynaptic function. As a therapeutic approach, GUO (guanosine) was given by oral route to evaluate the neuroprotective effects on this AD model. Following 24 h and 48 h from the model induction, behavioral tasks and biochemical analyses were performed, respectively. AβOs impaired object recognition (OR) short-term memory and reduced glutamate uptake and oxidation in the hippocampus. Moreover, AβOs decreased spare respiratory capacity, reduced ATP levels, impaired Ca2+ handling, and caused mitochondrial swelling in hippocampal synaptosomes. Guanosine crossed the BBB, recovered OR short-term memory, reestablished glutamate uptake, recovered mitochondrial Ca2+ homeostasis, and partially prevented mitochondrial swelling. Therefore, this endogenous purine presented a neuroprotective effect on presynaptic mitochondria and should be considered for further studies in AD models. Keywords: Alzheimer’s disease, Amyloid-β oligomers, Guanosine, Neuroprotection, Presynaptic mitochondria Bioblast editor: Plangger M


Labels: MiParea: Respiration, Pharmacology;toxicology  Pathology: Alzheimer's 

Organism: Mouse  Tissue;cell: Nervous system  Preparation: Homogenate 


Coupling state: LEAK, OXPHOS, ET  Pathway: N, S, NS, ROX  HRR: Oxygraph-2k, O2k-Fluorometer 

2020-08, AmR