Sentence examples for motor neuron damage from inspiring English sources

Upper motor neuron damage will not lead to atrophy or fasciculations, but only weakness of the innervated muscles.

Our finding of Evans blue extravasion in early symptomatic G93A mice may suggest that large molecules such as IgG and other blood proteins appear in the spinal cord due to vascular leakage, one possible mechanism accelerating motor neuron damage.

In the spinal cord and brain of both ALS patients and animal models, infiltration of T-cell lymphocytes, monocyte-derived macrophages and dendritic cells, and IgG deposits have been observed that may have a critical role in motor neuron damage.

In the spinal cord and brain of both ALS patients and animal models, the presence of T-cell lymphocytes [25], [28], deposits of IgG [29] [32], complement components C3 and C4 [29], and monocyte/macrophage and dendritic cells [28], [33], [34] were observed that may have a critical role in motor neuron damage.

Thus, the dying-forward propagation of excitotoxin-induced motor neuron damage appears to be consistent between mice and rats.

Microvascular leakage and reduced tight junction protein expression are known to occur in ALS and could contribute to motor neuron damage.

Loss of astrocytic glutamate transport capacity in ALS spinal cord supports an excitotoxic contribution to motor neuron (MN) damage in the disease, and dominant gain of function mutations in Cu/Zn superoxide dismutase (SOD1) cause certain familial forms of ALS.

Further, the stimuli to which these mice are more susceptible are motor neuron axonal damage and glutamate toxicity, both closely related to ALS pathogenesis.

Growth factors such as glial cell line derived neurotrophic factor (GDNF) are known to protect motor neurons from damage in a range of models.

These results suggest that misfolded molecules containing mutant SOD1 may contribute to motor neuron-specific damage in ALS.

PEDF, a 50-kDa glycoprotein and a member of the serine protease inhibitor gene family, was initially confirmed as a potential neurotrophic and neuroprotective factor that promotes the survival of cerebellar granule cells as well as spinal motor neurons from damage caused by increased intraocular pressure of transient ischaemic reperfusion [ 23].