Alzheimerʼs Disease biomarkers and cortical thickness in persons reporting subjective cognitive decline and healthy controls: Data derived from the DZNE DELCDODE-Study

Introduction Subjective cognitive decline (SCD) without objective performance deficits reflects in some individuals the earliest symptomatic manifestation of Alzheimerʼs Disease (AD) at the late preclinical stage1, 2. It is crucial to delineate the relationship between this syndrome, AD- specific biomarkers and the localization of early neurodegeneration.

Methods We investigated data from 293 individuals from the baseline-dataset of the DZNE-DELCODE-study3. In this subset, 39 AD-patients, 74 patients with mild cognitive impairment (MCI), 104 participants with SCD, and 76 healthy controls (CO) received biomarker assessment (Aβ-42, total-tau, phosphorylated-tau) through lumbar puncture as well as structural MRI. The cortical thickness values were estimated via FreeSurferV.6.0 in 135 subjects. Statistical analyses included one-way-ANCOVAs with a between-subject factor of diagnosis (covariates: age, sex and scanner-site) for the bilateral entorhinal cortices and bilateral parahippocampi defined as regions of Interest (ROI) reflecting regions of early AD pathology. Subsequently we calculated two-way-ANCOVAs for these ROIS with between-subject factors of diagnosis and CSF-biomarkers with the same covariates.

Results Our data show decreased bilateral entorhinal thickness in amyloid-positive persons reporting SCD compared to controls.

Conclusion This finding supports the assumption that SCD mirrors a late preclinical stage of AD in persons with amyloid pathology and is associated with mild neurodegeneration in brain regions affected early in AD. Our data confirm initial findings in independent samples4.