Unlike the degenerative disorders that cause dementias, which stem from a modest number of aberrant processes, aging-related cognitive changes reflect a host of mechanisms. These include mechanisms associated with a person’s condition, e.g., drugs, pain, depression, and sleep disorders. They include mechanistic changes linked to the aging process, e.g., enhanced neural network noise, increased neighborhood density, age of acquisition effects, degraded selective engagement of neural networks, alteration of the balance between volitional and reactive intention and attention, declines in neurotransmitter function, and brain ontogenesis over the life span. They include changes best characterized as senescent physiology and best demonstrated in decline in functions essential to episodic memory formation related to impaired encoding in the hippocampal cornu amonis (CA) fields and slowed neurogenesis in the hippocampal dentate gyrus. Finally, they include processes best characterized as senescent pathology, the best understood being degradation of myelin and associated reduction of central conduction velocities and slowing of processing speed. No longer should cognitive changes associated with aging be viewed as a simple manifestation of a unitary aging process. The large number of mechanisms at play and their complexity offer many opportunities for therapeutic intervention.