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• W1969523250 abstract "TAR DNA binding protein 43 (TDP-43) has been considered a signature protein in frontotemporal dementia and amyotrophic lateral sclerosis (ALS), but not in ALS associated with the superoxide dismutase 1 (SOD1) gene mutations (ALS1). To clarify how TDP may be involved in ALS pathogenesis, clinical and pathological features in cases of sporadic ALS ([SALS] n = 18) and ALS1 (n = 6) were analyzed. In SALS patients with rapid clinical courses, TDP mislocalization (i.e. cytoplasmic staining and TDP-positive cytoplasmic inclusions) in anterior horn cells was frequent. In SALS patients with slow clinical courses, TDP-43 mislocalization was rare. In an ALS1 patient with the SOD1 gene mutation C111Y, there were numerous TDP-positive inclusions and colocalization of SOD1 and TDP. In mutant SOD1 transgenic (G93A) mice at the end stage (median, 256 days), TDP-positive inclusions and TDP colocalization with SOD1 were also observed; nuclear TDP-43 immunoreactivity was highly correlated with life span in these mice. In both humans and mice, nuclei that stained strongly for TDP were large and circular; weakly stained nuclei were atrophic or deformed. In conclusion, low levels of TDP expression in the nucleus cor relate with a rapid clinical course in SALS and in ALS1 model mice, suggesting that nuclear TDP may play a protective role against motor neuron death resulting from different underlying etiologies." @default.
• W1969523250 created "2016-06-24" @default.
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• W1969523250 date "2009-01-01" @default.
• W1969523250 modified "2023-09-27" @default.
• W1969523250 title "Nuclear TAR DNA Binding Protein 43 Expression in Spinal Cord Neurons Correlates With the Clinical Course in Amyotrophic Lateral Sclerosis" @default.
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• W1969523250 doi "https://doi.org/10.1097/nen.0b013e3181919cb5" @default.
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