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Gonzalo Emiliano Aranda Abreu

Universidad Veracruzana

Professor Dr. Gonzalo Emiliano Aranda Abreu who works at the Brain Research Institute for Universidad Veracruzana, Xalapa, Veracruz, México, was born in 1968 in Ciudad del Carmen Campeche, México. He received his BSc (Experimental Biology) degree from the Universidad Autónoma Metropolitana, Iztalapa, México, in 1992. His MSc degree in Molecular Biology and Genetics from the Centro de Investigación y Estudios Avanzados, IPN, México in 1996, and his Ph.D. degree in Neurobiology from Weizmann Institute of Science, Rehovot, Israel, in 2001. He is an expert in Alzheimer’s disease research, principally analyzing tau protein transport in the neural axon and in relation to Alzheimer’s disease. Also, he has book chapters in relation to brain rehabilitation and is president and member of the Southeastern Mexican chapter of the Society for Neuroscience, USA. He is involved in the training of doctoral students and teaches molecular and cellular neurobiology and bioinformatics to Ph.D. students.

2books edited

2chapters authored

Latest work with IntechOpen by Gonzalo Emiliano Aranda Abreu

The brain is the most complex structure that exists in the universe, consisting of neurons whose function is to receive information through dendrites and transmit information through the axon. In neurosciences one of the main problems that exists are neurodegenerative diseases for which until now there has been no cure. This book is mainly focused on updating the information on the signaling process carried out in the development of axons. Topics such as axon guidance and its interaction with the extracellular matrix are discussed. Other important topics are semaphorins and their relationship with neurodegenerative diseases, and the neurobiology of the gap junction in the dorsal root ganglion. Finally, the topic of bioelectrical interfaces destined to regenerate damaged nerves is covered. The information in this book will be very important both for researchers who work with these issues and doctoral students who are involved in neuroscience.

Neurons

Neurons

Edited by Gonzalo Emiliano Aranda Abreu

Books edited

Mechanisms of Neuroinflammation

Mechanisms of Neuroinflammation

Edited by Gonzalo Emiliano Aranda Abreu

Chapters authored

Therapeutics of Alzheimer’s Disease

By Marisol Herrera-Rivero and Gonzalo Emiliano Aranda-Abreu

Part of the book: Advanced Understanding of Neurodegenerative Diseases

Alternative Splicing and Alzheimer’s Disease

By Gonzalo Emiliano Aranda Abreu, Sonia Lilia Mestizo Gutiérrez, María Elena Hernández Aguilar and Fausto Rojas Durán

Alzheimer’s disease is a neurodegenerative process whose origin is unknown. It has been associated with this process at least two important proteins: the first is the β-amyloid forming amyloid plaques and the second protein is Tau, which has been determined to precipitates inside the neuron because hyperphosphorylation, causing instability in the axon. Tau microtubule-associated protein (MAP) is essential for the development of neuronal cell polarity. Tau protein is preferentially localized in the axons, whereas MAP2, another neuronal specific microtubule-associated protein, is localized in the somatodendritic domain. Previous studies have demonstrated that the localization of these proteins depends, at least in part, on messenger RNA (mRNA) subcellular localization, that is, Tau mRNA into the axon and MAP2 mRNA into the dendrite. Tau protein has an essential role in the pathology of Alzheimer’s disease, and hyperphosphorylated Tau promotes destabilization of microtubules. Tau alternative splicing generates six isoforms in the adult human brain due to the inclusion or exclusion of exons 2, 3, and 10. The failure in the splicing process of exon 10 generates a tauopathy, which can be carried out by the amyloid peptide; however, the splicing of other exons is less studied. The impact of amyloid peptide on the alternative splicing of exons 2, 3, and 6 caused formed cell processes to retract in differentiated cells and altered the expression of exons 2/3 in cell culture. Expression of exon 6 was repressed under β-amyloid treatment. The molecular mechanism for this amyloid-Tau interaction remains to be determined, but may have potential implications for the understanding of the underlying neuropathological processes in Alzheimer’s disease.

Part of the book: Update on Dementia

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