The structural and functional brain circuitries supporting episodic memory undergo profound reorganization in childhood and old age. We propose a two-component framework that combines and integrates evidence from child development and aging. It posits that episodic memory builds on two interacting components: (a) the strategic component, which refers to memory control operations, and (b) the associative component, which refers to mechanisms that bind different features of a memory episode into a compound representation. We hypothesize that: (a) children's difficulties in episodic memory primarily originate from low levels of strategic operations, and reflect the protracted development of the prefrontal cortex (PFC); (b) deficits in episodic memory performance among older adults originate from impairments in both strategic and associative components, reflecting senescent changes in the PFC and the medio-temporal lobes (MTL). Initial behavioral and neural evidence is consistent with both hypotheses. The two-component framework highlights the specificities of episodic memory in different age periods, helps to identify and dissociate its components, and contributes to understanding the interplay among maturation, learning, and senescence.

The authors investigated the strategic component (i.e., elaboration and organization of episodic features) and the associative component (i.e., binding processes) of episodic memory and their interactions in 4 age groups (10 -12, 13-15, 20 -25, and 70 -75 years of age). On the basis of behavioral and neural evidence, the authors hypothesized that the two components are functionally related but follow different life-span gradients. In a fully crossed design, age differences in recognition memory for single words versus word pairs (associative demand manipulation) were examined under instructions that emphasized item, pair, or elaborative-pair encoding (strategy manipulation). As predicted, the results showed that the strategic and associative components follow different life-span trajectories. Relative to younger adults, children's difficulties in episodic memory primarily reflected lower levels of strategic functioning. In contrast, older adults showed impairments in both strategic and associative components. The authors conclude that the comparison of strategic and associative components of episodic memory across the life span helps to delineate the two components' unique and interactive contributions to episodic memory performance.

Memory consolidation during sleep relies on the precisely timed interaction of rhythmic neural events. Here, we investigate differences in slow oscillations (SO; 0.5–1 Hz), sleep spindles (SP), and their coupling across the adult human lifespan and ask whether observed alterations relate to the ability to retain associative memories across sleep. We demonstrate that older adults do not show the fine-tuned coupling of fast SPs (12.5–16 Hz) to the SO peak present in younger adults but, instead, are characterized most by a slow SP power increase (9–12.5 Hz) at the end of the SO up-state. This slow SP power increase, typical for older adults, coincides with worse memory consolidation in young age already, whereas the tight precision of SO–fast SP coupling promotes memory consolidation across younger and older adults. Crucially, brain integrity in source regions of SO and SP generation, including the medial prefrontal cortex, thalamus, hippocampus and entorhinal cortex, reinforces this beneficial SO–SP coupling in old age. Our results reveal that cognitive functioning is not only determined by maintaining structural brain integrity across the adult lifespan, but also by the preservation of precisely timed neural interactions during sleep that enable the consolidation of declarative memories.