Molecular aging of the brain, neuroplasticity, and vulnerability to depression and other brain-related disorders.

摘要: The increased risk for neurodegenerative and neuropsychiatric disorders associated with extended lifespan has long suggested mechanistic links between chronological age brain-related disorders, including depression, Recent characterizations of age-dependent gene expression changes now show that aging the human brain engages a specific set biological pathways along continuous lifelong trajectory, same genes are normal also frequently similarly implicated in depression other disorders. These correlative observations suggest model age-by-disease molecular interactions, which promotes diseases, additional environmental factors genetic variability contribute to defining disease or resiliency trajectories. Here we review characteristic features terms function over time, then focus on evidence supporting accelerated depression. This proposed interaction addresses current gap research “normal” its connection late-life diseases. implications this profound, as it provides an investigational framework identifying critical moderating factors, outlines opportunities early interventions preventions, may form basis dimensional definition diseases goes beyond categorical system.