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Current hypotheses for the biology underlying sporadic and familial ALS forms in humans represent non-competing mechanisms that are likely to converge in various unfortunate patterns to mediate selective motor neuron degeneration [3].
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Under overstimulation, they mediate glutamate-excitotoxicity, which results in selective motor neuron degeneration and death [153 155].
It is this central channel and the FG Nups that seem sufficient to mediate selective receptor-mediated transport [refs 6, 7].
Sharma, A. et al. ALS-associated mutant FUS induces selective motor neuron degeneration through toxic gain of function.
Cleveland, D. W. & Rothstein, J. D. From Charcot to Lou Gehrig: Deciphering Selective Motor Neuron Death in ALS.
Therefore, unlike chemotherapeutic agents, these receptors can potentially mediate selective killing of tumor cells.
Motor branch of the rectus femoris: anatomic location for selective motor branch block in stiff-legged gait.
Patients with patterns of 5 and 6 (reciprocal electromyographic activities) had more selective motor control.
The mechanisms underlying the selective motor neuron degeneration in ALS remain elusive.
Recent studies have shown that motor neurons derived from iPS cells from patients with spinal muscular atrophy have been shown to have selective motor neuron death [26].
Retrograde axonal degeneration, initiated by abrupt distal pruning of selective motor neuron axons, is assumed to be critical in the development of motor neuron degeneration [16].
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