Articles by Mário F. Neto in JoVE
Investigating the Spreading and Toxicity of Prion-like Proteins Using the Metazoan Model Organism C. elegans Carmen I. Nussbaum-Krammer1, Mário F. Neto1, Renée M. Brielmann1, Jesper S. Pedersen1, Richard I. Morimoto1 1Department of Molecular Biosciences, Rice Institute for Biomedical Research, Northwestern University Prion-like propagation of protein aggregates has recently emerged as being implicated in many neurodegenerative diseases. The goal of this protocol is to describe, how to use the nematode C. elegans as a model system to monitor protein spreading and to investigate prion-like phenomena.
Filtration Isolation of Nucleic Acids: A Simple and Rapid DNA Extraction Method Sally M. McFall1, Mário F. Neto1, Jennifer L. Reed1, Robin L. Wagner2 1Center for Innovation in Global Health Technologies (CIGHT), Department of Biomedical Engineering, Northwestern University, 2Pritzker School of Medicine, The University of Chicago We describe here a simple and rapid paper-based DNA extraction method of HIV proviral DNA from whole blood detected by quantitative PCR. This protocol can be extended for use in detecting other genetic markers or using alternative amplification methods.
Other articles by Mário F. Neto on PubMed
Serotonergic Signalling Suppresses Ataxin 3 Aggregation and Neurotoxicity in Animal Models of Machado-Joseph Disease Brain : a Journal of Neurology. Nov, 2015 | Pubmed ID: 26373603 Polyglutamine diseases are a class of dominantly inherited neurodegenerative disorders for which there is no effective treatment. Here we provide evidence that activation of serotonergic signalling is beneficial in animal models of Machado-Joseph disease. We identified citalopram, a selective serotonin reuptake inhibitor, in a small molecule screen of FDA-approved drugs that rescued neuronal dysfunction and reduced aggregation using a Caenorhabditis elegans model of mutant ataxin 3-induced neurotoxicity. MOD-5, the C. elegans orthologue of the serotonin transporter and cellular target of citalopram, and the serotonin receptors SER-1 and SER-4 were strong genetic modifiers of ataxin 3 neurotoxicity and necessary for therapeutic efficacy. Moreover, chronic treatment of CMVMJD135 mice with citalopram significantly reduced ataxin 3 neuronal inclusions and astrogliosis, rescued diminished body weight and strikingly ameliorated motor symptoms. These results suggest that small molecule modulation of serotonergic signalling represents a promising therapeutic target for Machado-Joseph disease.