Examples of neurotoxicity

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During simulated ischemia, severe neurotoxicity occurs and is diminished by enzymatic degeneration of extracellular glutamate or by blockade of glutamate release.
Taken together, these observations suggest that formation of fibrillar inclusions may protect neurons against protofibril-induced neurotoxicity.
These results suggest that simulated ischemia enhances glutamate-mediated neurotoxicity in par t by depressing glutamate uptake.
An intact interchain disulfide bond is required for the neurotoxicity of tetanus toxin.
Under such conditions, exogenous glutamate typically causes glia swelling and requires very high concentrations to produce neurotoxicity.
Therefore, some patients did not benefit from the response of their tumor to treatment because their function was rapidly compromised by neurotoxicity.
However, the combination with radiotherapy resulted in high rates of neurotoxicity, which eventually developed in 30% of patients.
Mitochondrial dysfunction is a primary event in glutamate neurotoxicity.
Genetic influences on glucose neurotoxicity, aging, and diabetes: a possible role for glucose hysteresis.
One example of such processes is the glutamate-induced neurotoxicity in glaucomatous retinal ganglion cells.
We demonstrated that the first 2 years are critical, with all first relapses and the majority of neurotoxicity occurring within that period.
Minocycline prevents neurotoxicity induced by cerebrospinal fluid from patients with motor neurone disease.
The mechanisms underlying the development of neurotoxicity are poorly understood.
Patients over 60 years are at significant risk of neurotoxicity and, therefore, should probably receive chemotherapy alone as initial treatment.
Hypercortisolism and insensitivity to feedback suppression is a common phenomenon in major depression, rendering the hypothesis of hippocampal neurotoxicity in depressive individuals likely.
As yet, the relative contribution of activated microglia toward neurotoxicity versus neuroprotection is a subject of high debate.
However, we also observed that the development of neurotoxicity was not a "latedelayed" event, since the onset can be as early as 4 months.

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