It has been suggested that age-related cognitive decline is due in part not to neuronal death but to synaptic alterations.

In animal models, melatonin has been shown to ameliorate glutamate-induced neuronal death, it is presumed due to its antioxidant effects.

The buildup of these aggregates in the brain leads to progressive neuronal death, and eventually death of the entire organism.

This disease is associated with neuronal death.

However more general ageing considers loss of synaptic strength over neuronal death.

This increase in mediators contributes to neuronal death.

There are also multiple brain regions, 200 types of neurons, even large-scale neuronal deaths.

It may be related to oxidative stress, protein aggregation and neuronal death, but the mechanisms are not fully understood.

Now, another group of researchers has used modeling to shine some light on physical mechanisms to explain brain signals that occur during and after neuronal death.

Protective effect of gamma-glutamylethylamide (theanine) on ischemic delayed neuronal death in gerbils.