Abstract
BACKGROUND: Previous investigations into the impact of age on the Attentional Boost Effect (ABE) have produced inconsistent findings, primarily attributable to insufficient exploration of delay task duration as a critical variable. Current understanding of the neural bases underlying age-related effects in ABE remains incomplete, warranting further neurophysiological investigation. METHODS: Experiment 1 examined the effects of age and delay task duration on ABE with a mixed design of 2 (age: young adults, young-old adults) × 2 (delay task duration: 2 min, 10 min) × 2 (word type: target, distractor). Experiment 2 investigated the neural bases of age-related effects on ABE using fNIRS, with a mixed design of 2 (age: young adults, young-old adults) × 2 (word type: target, distractor). Young adults were college students and young-old adults were recruited from the community and university. Both experiments employed the study-test paradigm. RESULTS: Experiment 1 found that when the delay task duration was 2 min, both young and young-old adults exhibited ABE. When the delay task duration was 10 min, only young adults exhibited ABE. The effect size of ABE declined as delay task duration increased, with comparable magnitude of decline in two age groups. Experiment 2 found that individuals showed greater activation in the right Dorsolateral Prefrontal Cortex (DLPFC) and bilateral Pars Triangularis Areas (PTA) under the target condition relative to distractor condition. Young-old adults showed greater activation in the right DLPFC, right PTA and Primary Visual Cortex (V1) relative to young adults. CONCLUSIONS: Age influenced the formation of ABE in the encoding phase. Young-old adults showed greater activation in the right frontal lobe and occipital lobe to maintain ABE, which supported the Compensation-related Utilization of Neural Circuits Hypothesis. Young-old adults' ABE disappeared as delay task duration increased, and the magnitude of reduction in the effect size of ABE was comparable in both age groups, which partially contradicted the Vulnerable Boost Hypothesis. The frontal lobe played a pivotal role in ABE formation.