Enfermedades De Las Motoneurons Pdf Download
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Esta publicación proporciona información general sobre las enfermedades de la neurona motora, incluyendo los síntomas comunes, el diagnóstico y los tratamientos. También se mencionan estudios de investigación que son financiados por el NINDS con el propósito de un mejor entendimiento de las enfermedades de la neurona motora. La publicación incluye una lista de recursos adicionales de información.
We found that, after intramuscular injection, bone marrow cells were able to engraft within the muscle. However, bone marrow cell intramuscular injection failed to promote a general therapeutic effect. In the second approach, we found that bone marrow cells had limited survival in the spinal cord, but this strategy significantly improved motor outcomes. Moreover, we also found that the dual cell therapy tended to preserve spinal motoneurons at late stages of the disease and to reduce microgliosis, although this did not prolong mice survival.
Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by a progressive and selective death of upper and lower motoneurons (MNs) . Resulting from neuronal loss, patients suffer progressive atrophy and eventual muscle paralysis that leads to their death a few years after the onset . As in other neurodegenerative disorders, most ALS cases are sporadic; however, several mutations have been identified in familial cases of ALS (fALS). The most prevalent forms include mutations encoded in the TARDBP (TDP43) gene, the hexanucleotide repeat expansions in chromosome-9 open reading frame 72 (C9ORF72) or in the superoxide dismutase gene (SOD1) . Indeed, the most used experimental model of ALS is a transgenic mouse that overexpresses a high-copy number of the mutated form of the human SOD1 gene . This transgenic ALS model mimics the human pathology, being the most used preclinical tool to study the disorder and test novel therapies . The pathogenic mechanisms underlying MN death involve alterations of multiple molecular mechanisms, including glutamate-mediated excitotoxicity, defective axonal transport, or activation of neighboring glial cells [6,7,8]. The simultaneous disruption of several molecular mechanisms and cell types raises the difficulty to find an effective treatment. In fact, novel therapies that only target a single factor have largely failed when translated into human clinical trials . These failures suggest that more effective therapeutic approaches should act simultaneously on several targets in order to mediate global neuroprotection. In this way, cell therapy has emerged as a promising way to target several cells and mechanisms involved in ALS. 2b1af7f3a8