PH.D. Federal University of Minas Gerais
B.S.PH Federal University of Fluminense
Office: Robarts Research Institute
p. 519.931.5777 x. 24888
Visit: Dr. Prado at Robarts Research Institute
See Publications by Marco Prado on PubMed
My research is focused on understanding the cellular and molecular basis of neuronal communication and how this is changed in neurodegenerative diseases. Cellular communication is the foundation for nervous system function and is responsible for the ability of multi-cellular organisms to manage complex response patterns. We are interested to uncover how neuronal communication translates to complex behaviours. To achieve this goal we use a combination of molecular, cellular, pharmacological and behavioral approaches as well as genetically modified mice to understand neurochemical mechanisms in degenerative disorders. Of particular interest to us is the role of cholinergic synapses, that release the chemical mediator acetylcholine, in several diseases, such as Alzheimer's disease and Huntington's disease. We are also interested in how cholinergic neurotransmission in the peripheral nervous system may be targeted to ameliorate cardiac failure. Finally, we have a strong research program aimed to develop novel approaches to understand and treat transmissible spongiform encephalopathy, or prion diseases. These fatal diseases of mammals, that have "mad cow disease" as its more publicized example, are an important concern due to their unusual features. A long-term objective of my research program is to understand how we can manage distinct forms of neuronal communication to ameliorate the symptoms and provide novel pharmacological targets to treat these degenerative disorders.
Endocytosis of prion protein is required for ERK1/2 signaling induced by stress-inducible protein 1. Caetano FA, Lopes MH, Hajj GN, Machado CF, Pinto Arantes C, Magalhães AC, Vieira Mde P, Américo TA, Massensini AR, Priola SA, Vorberg I, Gomez MV, Linden R, Prado VF, Martins VR, Prado MA. J Neurosci. (2008) 28:6691-702.
Physiology of the prion protein. Linden R, Martins VR, Prado MA, Cammarota M, Izquierdo I, Brentani RR. Physiol Rev. (2008) 88:673-728.
Mice deficient for the vesicular acetylcholine transporter are myasthenic and have deficits in object and social recognition. Prado VF, Martins-Silva C, de Castro BM, Lima RF, Barros DM, Amaral E, Ramsey AJ, Sotnikova TD, Ramirez MR, Kim HG, Rossato JI, Koenen J, Quan H, Cota VR, Moraes MF, Gomez MV, Guatimosim C, Wetsel WC, Kushmerick C, Pereira GS, Gainetdinov RR, Izquierdo I, Caron MG, Prado MA. Neuron. (2006) 51:601-12.
The "ins" and "outs" of the high-affinity choline transporter CHT1. Ribeiro FM, Black SA, Prado VF, Rylett RJ, Ferguson SS, Prado MA. J Neurochem. (2006) 97:1-12
Structural requirements for steady-state localization of the vesicular acetylcholine transporter. Ferreira LT, Santos MS, Kolmakova NG, Koenen J, Barbosa J Jr, Gomez MV, Guatimosim C, Zhang X, Parsons SM, Prado VF, Prado MA. J Neurochem. (2005) 94:957-69.