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The most frequent genetic cause of frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) is the hexanucleotide repeat expansion in C9orf72. An important neuropathological hallmark associated with this mutation is the accumulation of the phosphorylated form of TAR (trans‐activation response element) DNA‐binding protein 43 (pTDP‐43). Glia plays a crucial role in the neurodegeneration...
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