Frontiers in psychiatry · 2025
Longitudinal associations between amyloid and symptoms of depression and anxiety in subjective cognitive decline: the impact of personality characteristics.
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Trieu Calvin, van Leeuwenstijn Mardou S S A, Schlüter Lisa-Marie, Ebenau Jarith L, Verberk Inge M W, Sikkes Sietske A M, Verfaillie Sander C J, van de Giessen Elsmarieke, Teunissen Charlotte E, van der Flier Wiesje M, van Harten Argonde C
Аннотация
INTRODUCTION: Depressive/anxiety symptoms are common in subjective cognitive decline (SCD) and may relate to Alzheimer's pathology, potentially modulated by personality characteristics.
METHODS: Depressive/anxiety symptoms were assessed over 4 ± 2 years in 329 SCD (88 amyloid-positive/241 amyloid-negative) using Geriatric Depression Scale-15 (GDS), Center for Epidemiological Studies-Depression (CES-D), and Hospital Anxiety and Depression Scale-Anxiety (HADS-A). Mixed-effects models assessed associations between amyloid status and these symptoms, with neuroticism and somatization as effect-modifiers.
RESULTS: Amyloid status was not directly associated with GDS, CES-D or HADS-A. However, neuroticism modified the association between amyloid status and GDS (p<0.05). In lower neuroticism, amyloid positivity was associated with GDS increase (β:0.10 ± 0.08), but not in higher neuroticism (β:-0.04 ± 0.12). Somatization modified the association between amyloid status and CES-D (p<0.05). In lower somatization, amyloid positivity was associated with CES-D increase (β:0.65 ± 0.23), but not in higher somatization (β:-0.12 ± 0.29).
DISCUSSION: Amyloid-positive individuals with lower neuroticism/somatization increased more in depressive symptoms over time, suggesting a preclinical AD-related depressive phenotype.
METHODS: Depressive/anxiety symptoms were assessed over 4 ± 2 years in 329 SCD (88 amyloid-positive/241 amyloid-negative) using Geriatric Depression Scale-15 (GDS), Center for Epidemiological Studies-Depression (CES-D), and Hospital Anxiety and Depression Scale-Anxiety (HADS-A). Mixed-effects models assessed associations between amyloid status and these symptoms, with neuroticism and somatization as effect-modifiers.
RESULTS: Amyloid status was not directly associated with GDS, CES-D or HADS-A. However, neuroticism modified the association between amyloid status and GDS (p<0.05). In lower neuroticism, amyloid positivity was associated with GDS increase (β:0.10 ± 0.08), but not in higher neuroticism (β:-0.04 ± 0.12). Somatization modified the association between amyloid status and CES-D (p<0.05). In lower somatization, amyloid positivity was associated with CES-D increase (β:0.65 ± 0.23), but not in higher somatization (β:-0.12 ± 0.29).
DISCUSSION: Amyloid-positive individuals with lower neuroticism/somatization increased more in depressive symptoms over time, suggesting a preclinical AD-related depressive phenotype.