Events during a day that we think important to remember are held in short term memory storage by an active hippocampus. Then, during deep, non-REM, slow brain wave sleep, enhanced connectivity between the hippocampus and frontal cortex cortex allow transfer of the information to long term storage in frontal and temporal lobes. It is also know that the duration of this deep sleep diminishes as our frontal lobes diminish in size (atrophy) with aging. Mandor et al., in worked pointed to in an article by Benedict Carey, have done an interesting study suggesting that the interaction of these factors represents a neuropatholgical pathway associated with cognitive decline in later life. Here is their abstract:
Aging has independently been associated with regional brain atrophy, reduced slow wave activity (SWA) during non–rapid eye movement (NREM) sleep and impaired long-term retention of episodic memories. However, whether the interaction of these factors represents a neuropatholgical pathway associated with cognitive decline in later life remains unknown. We found that age-related medial prefrontal cortex (mPFC) gray-matter atrophy was associated with reduced NREM SWA in older adults, the extent to which statistically mediated the impairment of overnight sleep–dependent memory retention. Moreover, this memory impairment was further associated with persistent hippocampal activation and reduced task-related hippocampal-prefrontal cortex functional connectivity, potentially representing impoverished hippocampal-neocortical memory transformation. Together, these data support a model in which age-related mPFC atrophy diminishes SWA, the functional consequence of which is impaired long-term memory. Such findings suggest that sleep disruption in the elderly, mediated by structural brain changes, represents a contributing factor to age-related cognitive decline in later life.