Affiliations: [a] Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA
| [b] Department of Neuroscience, University of Pittsburgh, Pittsburgh, PA, USA
| [c] Department of Radiology, University of Pittsburgh, Pittsburgh, PA, USA
| [d] Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA, USA
| [e] Department of Neurology, University of Pittsburgh, Pittsburgh, PA, USA
Correspondence:
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Correspondence to: Akiko Mizuno, PhD, Department of Psychiatry, University of Pittsburgh, 3811 O’Hara St, Pittsburgh, PA 15213, USA. E-mail: [email protected].
Abstract: Background:Subjective cognitive decline (SCD) may be an early manifestation of pre-clinical Alzheimer’s disease. Elevated amyloid-β (Aβ) is a correlate of SCD symptoms in some individuals. The underlying neural correlates of SCD symptoms and their association with Aβ is unknown. SCD is a heterogeneous condition, and cognitive reserve may explain individual differences in its neural correlates. Objective:We investigated the association between brain activation during memory encoding and SCD symptoms, as well as with Aβ, among older individuals. We also tested the moderating role of education (an index of cognitive reserve) on the associations. Methods:We measured brain activation during the “face-name” memory-encoding fMRI task and Aβ deposition with Pittsburgh Compound-B (PiB)-PET among cognitively normal older individuals (n = 63, mean age 73.1 ± 7.4 years). We tested associations between activation and SCD symptoms by self-report measures, Aβ, and interactions with education. Results:Activation was not directly associated with SCD symptoms or Aβ. However, education moderated the association between activation and SCD symptoms in the executive control network, salience network, and subcortical regions. Greater SCD symptoms were associated with greater activation in those with higher education, but with lower activation in those with lower education. Conclusion:SCD symptoms were associated with different patterns of brain activation in the extended memory system depending on level of cognitive reserve. Greater SCD symptoms may represent a saturation of neural compensation in individuals with greater cognitive reserve, while it may reflect diminishing neural resources in individuals with lower cognitive reserve.
