Neuroscience of aging

[3] Exercising has frequently increased the reproduction of neuronal precursor cells and helped with age-related declines in neurogenesis.

[4] However, one review found that the amygdala and ventromedial prefrontal cortex remained relatively free of atrophy, consistent with the finding of emotional stability occurring with non-pathological aging.

[7] Increased hyperpolarization, possibly due to dysfunctional calcium regulation, decreases neuron firing rate and plasticity.

In aged neurons, the medium and slow hyperpolarization phases involve the prolonged opening of calcium-dependent potassium channels.

The prolonging of this phase has been hypothesized to result from deregulated calcium and hypoactivity of cholinergic, dopaminergic, serotonergic and glutaminergic pathways.

[9] Older adults can exhibit reduced activity in specific brain regions during cognitive tasks, particularly in medial temporal areas related to memory processing.

[10] Older adults also tend to engage their prefrontal cortex more often during working memory tasks, possibly to compensate for executive functions.

[28] Treatments with anticancer chemotherapeutic agents often are toxic to the cells of the brain, leading to memory loss and cognitive dysfunction that can persist long after the period of exposure.

[36] Physical exercise significantly lowers the risk of cognitive decline in old age[37] and is an effective treatment for those with dementia[38][39] and Parkinson's disease.