Abstract
Long-term memory encoding is impaired in healthy aging but the underlying mechanisms in humans remain unclear. Here, we tested whether this relates to failures in associating information with previous memories to build multi-item representations. To gain insight into age-related differences in such neural mechanisms during online encoding, we employed the temporal precision of electroencephalography to examine how semantic integration during encoding is affected by healthy aging. As expected, we found that congruent matches improved subsequent recognition memory in younger adults (i.e. congruency effect) but this effect was reduced in the elderly. At the neural level, congruence caused changes in neural activity within ~1500 ms after stimulus presentation, and there were widespread differences in ERPs and alpha-beta oscillations (8-30 Hz), which are known to support semantic processing. Importantly, these ERP differences predicted increases in memory performance, especially for congruent items. Finally, age-related differences in memory were accompanied by an early positive ERP and a later decrease in theta-alpha and low beta power (5-13 Hz), during encoding, which were greater in the younger group. Our findings provide evidence that age-related memory impairments can be explained by deficits in online semantic integration, depending on theta-alpha and low beta oscillations.
Significance statement Memory impairments are a hallmark of healthy aging, but the underlying neural mechanisms in humans still remain unclear. We investigated how age-related memory deficits relate to failures during online encoding in associating information with previous memories. The results provide direct evidence that age-related memory impairments can be explained by deficits in online semantic integration within ~1500 ms after stimulus presentation, depending on theta-alpha and low beta neural oscillations (5-13 Hz). As such, our work gives new insights into the functional role of theta-alpha and low beta oscillations as well as into the physiological basis of memory impairments during healthy aging.
Footnotes
This work was supported by the German Research Foundation (Deutsche Forschungsgemeinschaft Grant BU 2670/7-1 to N.B.)
We are grateful to Maxi-Sophie Kuhlmey and Ramona Reineke for their help.
The authors declare no competing financial interests.