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When significantly reduced, the compound motor action potential (CMAP) – correlating with the number of functional axons – is an indicator for axonal damage.
At the lesion edge 32%% of the axons showed accumulation of APP, but only 12%% revealed the presence of axonal end bulbs as an indicator for axonal transection.
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Therapeutic approaches to promote axonal regeneration and synapse formation after spinal chord injury use a MLR marker, cholera toxin B, as a direct indicator of axonal regeneration and de novo synapse formation [53], [54].
Based on these findings, axonal ovoid formation may be regarded as an early indicator of axonal degeneration.
Another non-conventional MRI approach utilized to study axonal degeneration is the magnetization transfer ratio, which has been demonstrated to show strong correlations with the degree of myelin content, therefore serving as an indicator of axonal degeneration [ 22].
CSF NFL can serve as an indicator of axonal injury in a wide variety of neurodegenerative conditions [ 65- 72], including HIV infection [ 26].
Our results indicate no change in CMAP duration but a decrease in amplitude and observable prolongation of the latency which is regarded as an indicator of axonal degeneration.
However, reduced NAA levels in RRMS without signs of progression might be a strong indicator for clinically still undetectable progressive axonal degeneration.
Our data show a role for HDAC6 during the initial development of axons, where HDAC6 is necessary for axonal elongation and the development of the axonal initial segment.
This mutant promoted axonal elongation similar to wild-type JIP1, indicating that JNK binding to JIP1 is not essential for axonal growth.
Oligodendrocyte axonal interaction may be disturbed and constitute a primary trigger for axonal degeneration, oxidative stress and mitochondrial dysfunction in the axons of AMN patients.
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