Studies on metals in motor neuron disease

作者: Per M. Roos

DOI:

关键词: NeurodegenerationParalysisSpinal cordAmyotrophic lateral sclerosisParkinson's diseaseMetal toxicityMotor neuronPathologyMedicineNervous system

摘要: A slow but steady increase in neurodegenerative disorders has been noted recent decades. Degenerations the nervous system are found Alzheimer s disease, Parkinson disease and motor neuron diseases. Amyotrophic lateral sclerosis (ALS) is most common of It often considered a model disorder neurodegeneration. Early symptoms ALS limb weakness or muscles speech swallowing. Muscle atrophy follow slowly progressing paralysis spreads to respiratory invariably leading death failure. Neurophysiological investigations necessary for proper diagnosis, it important rule out treatable diagnostic alternatives such as myopathies polyneuropathies. The cause unknown. Prevailing theories include genetic, viral, inflammatory, oxidative toxic mechanisms. Some indications point toward metallotoxic etiologies. Clusters have observed regions where geological conditions elevated metal concentrations water soil. Several studies show increased frequency certain occupations. ALS-like animals, notably horses, exposure can be suspected. In addition animal experiments accumulations metals spinal cord. aim this thesis project clarify role ALS. hypothesis tested that neurotoxic contribute significantly pathogenesis To study we measured 22 cerebrospinal fluid (CSF) plasma from patients with controls, correlated findings literature data suggest pathogenesis. Increased were manganese, aluminum, cadmium, cobalt, copper, zinc, lead, vanadium uranium CSF compared controls. Manganese showed prominent correlation. Simultaneous sampling did not these concentrations, indicating CSF. Most detected neurotoxicants. Studies mercury distribution monkey cord after mercury. Motor neurons seem more vulnerable toxicity then surrounding cells, they lack protection metal-binding protein metallothionein. Patient metals, by bloodstream, penetration protective barriers direct effects on suggested causative concluded reach affect anterior horn cells thereby ISBN 978-91-7549-046-5

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