This protein is commonly used as a biomarker of neuronal damage.

Glutamate release occurs not only at excitatory synapses, but is also known to occur after neuronal damage or ischemic insult.

This can prevent the neuronal excitotoxic damage.

He is currently working to determine the sequence of events leading to neuronal oxidative damage and the source of the increased oxygen radicals.

Accumulation of minor neuronal damage that occurs during normal aging can transform microglia into enlarged and activated cells.

The hippocampus is a principal target site for GCs and therefore experiences a severity of neuronal damage that other areas of the brain do not.

Furthermore, these increased levels of quinolinic acid are great enough to produce excitotoxic neuronal damage.

Glial cells, including SGCs, have long been recognized for their roles in response to neuronal damage and injury.

After mercury changes in the environment to methylmercury, the most toxic form, it readily crosses the blood-brain barrier and can cause severe neuronal damage.

Similarly, the cognitive reserve hypothesis states that it is possible to develop the brain's resistance to neuronal damage and delay the onset of Alzheimer's.