Options to treat amyotrophic
lateral sclerosis (ALS) are limited. Recent studies show that ALS and
tau-negative frontotemporal dementia (FTD) have the same neuropathology
associated with TDP-43 positive inclusions. Basically, TDP-43 can recruit ALS
pathogenesis. Incorrect localization, misfolding or phosphorylation of TDP-43
can lead to disease. In a study where by Walker et al. (2015), when compared to
normal TDP-43, they found that phosphorylated TDP-43 leads to a definite ALS
diagnosis. The biggest discovery in their new mouse model they developed to
further understand TDP-43 phosphorylation, it was shown that even after
degeneration of neurons and motor abilities, the removal of cytoplasmic TDP-43
and return of nuclear TDP-43 led to neuron preservation and recovery of
function. 

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