Alzheimers or temporal lobe epilepsy, the pathology in most cases is known to begin from or associate with temporal lobes. Could it mean that high activity dependent plasticity (leading to oxidative stress) at these structures including amygdala and hippocampus makes them more suitable for pathological insult or to be the pathological locus? If so could you please help me find labs working on this or point me the direction to look?

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