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34, 35 Our study confirms that stopping motor neuron death may not be sufficient to slow disease, but that maintaining motor neuron function may be sufficient.
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Our findings suggest that disruption of LC noradrenergic neuron development and function may be a common pathobiological feature of CCHS.
One reason for the particular susceptibility of dopaminergic neurons toward loss of mortalin function may be because of a reduced mitochondrial mass of DA neurons in the substantia nigra compared with other neuronal populations as has been shown in mice.
This function may be interpreted as the mass action probability of neurons firing if their membrane potential is over the threshold, and can be derived from a stochastic neuron models [6, 36].
63 Cholinergic neurons that are implicated in cognitive functions may be regulated by oestrogens.
Moreover, these findings indicate that the processes involved in pathology include basal cellular functions that are not exclusive to neurons, although neurons may be more sensitive to alterations in these processes.
How this potential divergence in signaling may affect sensory neuron function is yet to be determined and ongoing research is further delineating the differential roles that insulin and IGF-1 may play in sensory nerve biology.
Our quantitative analysis of neuron morphology may be used to study various factors that could influence the development and functions of neurons that may be associated to brain disorders such as ASD.
A third assumption was that one function of workspace neurons may be to support related processing in more local systems [8] [10].
Therefore, the normal function of motor neurons may be particularly dependent on autophagy flux, making these cells more vulnerable to its disruption.
Finally, calpain activity could be important for the proper functioning of SMN in neurons or may be affected as a result of SMA.
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