Abstract

AbstractBackgroundSubjective cognitive decline (SCD) is a risk factor for cognitive decline and AD. SCD individuals display lower medial temporal lobe (MTL) volumes. Some features of SCD (SCDplus), such as specific worry and recent onset, have been proposed as more related to AD pathology. In this study we aimed to explore the differences in MTL volumes between SCD and control individuals and their associations with memory performance in a large sample of cognitively unimpaired subjects.Methods603 cognitively unimpaired individuals from a population‐based study (age: [47‐76], mean: 60.04∓6.57) underwent structural MRI, clinical and neuropsychological assessments. 184 were classified as SCD or 419 as Controls by their answers to the question “Do you perceive difficulties in memory or cognition as compared to how they used to be?”. A subgroup of 31 fulfilling two SCDplus criteria (Worry and Onset within last 5 years) was defined. Memory performance was assessed with the Free and Cued Selective Reminding Test (FCSRT).MTL and HS were segmented using ASHS using T1 and IR sequences. We compared regional volumes across SCD groups using linear models. Age, sex, education, APOE carriership and total intracranial volume were included as covariates. SCD group*memory scores interactions were assessed.ResultsSCD subjects showed lower volumes than Controls in right CA1 (p=0.031) and subiculum (p=0.026) (Figure 1). SCDplus subjects showed larger BA36 volumes in both hemispheres (Figure 2). In models comparing Controls and SCDplus we found a significant interaction (p=0.021) between SCDplus status and parahippocampal (PHC) bilateral volumes on FCSRT free recall score, with positive association in Controls and negative in SCDplus (poorer performance associated with larger PHC) (Figure 3).ConclusionAs previously reported in smaller and older samples (Schwarz et al, AAIC 2019) a reduction of CA1 and subiculum was found in SCD subjects. Moreover, PHC volume correlates negatively with memory performance in SCDplus: this may pinpoint a transitional phase in the AD continuum with increments of cortical volume, as described in (Gispert et al., 2015; Fortea et al., 2011). Further work including CSF biomarkers will assess how these associations may be mediated by AD pathology.

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