By Dr. Gustavo Pigino, from IMMF-CONICET-UNC
Aberrant signals, altered axonal transport and retrograde progressive neuropathies
Neurodegenerative diseases that occur in adulthood (ENEA), They comprise a heterogeneous group of neuropathic characterized by a progressive deterioration of neuronal functions dependent on age, followed by a loss of specific neuronal populations. Alterations in synaptic function and axonal connectivity represent critical early pathogenic events and Aeneas, however the molecular mechanisms underlying these disorders are not fully known. The extreme length axonal, its complex functional architecture and the lack of an effective protein synthesis in said compartment, leaves very vulnerable neurons to alterations in axonal transport (TA). Even more, TA defects have been documented in many Aeneas, suggesting the existence of a common acquired different mechanism pathogenic pathways travez. These observations suggest that many Aeneas can be categorized as disferopatías, diseases in which changes in the TA represents a critical component in their pathology. This presentation will mention various molecular mechanisms underlying the alterations in the TA in several Aeneas. The molecular understanding of these mechanisms, You could set the stage for the development of new therapeutic strategies to prevent both axonal synaptic dysfunction as in various Aeneas.
For the seventh “CIQUIBIC Open Doors” Lecture, CIQUIBIC is pleased to welcome Dr. Gustavo Pigino, CONICET Independent Researcher at the Institute for Medical Research and Mercedes Martin Ferreyra and Adjunct Assistant Professor at the University of Illinois in Chicago.
The conference will be held on Tuesday October 13, at 11 pm in the Auditorium of the Scientific Technological Center CONICET (CCT-Córdoba)
Aberrant signals, altered axonal transport and retrograde progressive neuropathies
Adult-onset neurodegenerative diseases (AoND) comprise a heterogeneous group of neuropathic characterized by a age-dependent progressive deterioration of neuronal functions, followed by a loss of specific neuronal populations. Alterations in synaptic function and axonal connectivity represent critical early pathogenic events in AoND. However, the molecular mechanisms underlying these disorders are not fully known. The extreme axonal length, complex functional architecture and the lack of an effective protein synthesis in such compartment, make neurons vulnerable to alterations in axonal transport (AT). Furthermore, AT defects have been documented in many AoND, suggesting the existence of a common mechanism underlying different pathogenic pathways. These observations suggest that many AoND can be categorized as disferopathies, diseases in which changes in AT represents a critical component in their pathology. In this presentation I will mention various molecular mechanisms underlying the alterations in AT in several AoND. The understanding of these molecular mechanisms could provide the basis for the development of new therapeutic strategies to prevent both axonal and synaptic dysfunctions in various AoND.
Design: Jeremías Di Pietro / Graphic design CCT CONICET CORDOBA