Caracterización morfológica y molecular de médula espinal y cerebro de cobayos deficientes en vitamina C como posible modelo animal de esclerosis lateral amiotrófica.
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Date
2024
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Universidad de Concepción
Abstract
La esclerosis lateral amiotrófica (ELA) es una enfermedad neurodegenerativa que afecta al sistema nervioso central (SNC). Se caracteriza por la degeneración y disfunción de las neuronas superiores e inferiores, lo que lleva a la debilidad progresiva de músculos esqueléticos voluntarios. Estudios han evaluado el efecto de la dieta en la progresión y desarrollo de enfermedades neurodegenerativas. En particular, la vitamina C se encuentra involucrada en varios procesos fisiológicos del SNC. EL rol de la vitamina C como un importante antioxidante a nivel cerebral nos sugiere que su deficiencia podría estar involucrada en el desarrollo y progresión de enfermedades neurodegenerativas como el ELA. Esta tesis postulaba que el cobayo con deficiencia de vitamina C reproducía características morfológicas y moleculares que se observan en ELA. A través de técnicas histológicas, inmunohistoquímica e inmunofluorescencia, se determinó que la deficiencia de vitamina C no induce degeneración neuronal ni activación de vías de muerte celular. Sin embargo, se observaron alteraciones en los procesos neuronales corticales, así como también alteraciones en el RE de las neuronas, activación de astrocitos en el tronco encefálico y la sustancia blanca de la médula espinal, y una disminución en la expresión del transportador SVCT2 en la vía corticoespinal. Este estudio se centra en la importancia de la Vitamina C, la cual es considerado el antioxidante más abundante del SNC, regulando una variedad de funciones y protegiendo a las distintas células neuronales.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that affects the central nervous system (CNS). It is characterized by the degeneration and dysfunction of both upper and lower motor neurons, leading to progressive weakness of voluntary skeletal muscles. Studies have evaluated the effect of diet on the progression and development of neurodegenerative diseases. Specifically, vitamin C is involved in various physiological processes of the CNS. The role of vitamin C as an important antioxidant in the brain suggests that its deficiency could be involved in the development and progression of neurodegenerative diseases such as ALS. This thesis postulated that guinea pigs with vitamin C deficiency would reproduce morphological and molecular characteristics observed in ALS. Through histological techniques, immunohistochemistry, and immunofluorescence, it was determined that vitamin C deficiency does not induce neuronal degeneration or activation of cell death pathways. However, alterations were observed in cortical neuronal processes, as well as alterations in the endoplasmic reticulum (ER) of neurons, activation of astrocytes in the brainstem and spinal cord white matter, and a decrease in the expression of the SVCT2 transporter in the corticospinal pathway. This study emphasizes the importance of vitamin C, which is considered the most abundant antioxidant in the CNS, regulating a variety of functions and protecting different neuronal cells.
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease that affects the central nervous system (CNS). It is characterized by the degeneration and dysfunction of both upper and lower motor neurons, leading to progressive weakness of voluntary skeletal muscles. Studies have evaluated the effect of diet on the progression and development of neurodegenerative diseases. Specifically, vitamin C is involved in various physiological processes of the CNS. The role of vitamin C as an important antioxidant in the brain suggests that its deficiency could be involved in the development and progression of neurodegenerative diseases such as ALS. This thesis postulated that guinea pigs with vitamin C deficiency would reproduce morphological and molecular characteristics observed in ALS. Through histological techniques, immunohistochemistry, and immunofluorescence, it was determined that vitamin C deficiency does not induce neuronal degeneration or activation of cell death pathways. However, alterations were observed in cortical neuronal processes, as well as alterations in the endoplasmic reticulum (ER) of neurons, activation of astrocytes in the brainstem and spinal cord white matter, and a decrease in the expression of the SVCT2 transporter in the corticospinal pathway. This study emphasizes the importance of vitamin C, which is considered the most abundant antioxidant in the CNS, regulating a variety of functions and protecting different neuronal cells.
Description
Tesis presentada para optar al título de Bioquímico/a.
Keywords
Médula Espinal, Cerebro, Avitaminosis, Esclerosis Amiotrófica Lateral, Cobayas, Ácido Ascórbico