| Objective: Subsyndromal symptomatic depression(SSD)is very common among older individuals.Nevertheless,it is still confusing whether there are effects of SSD on brain aging outcomes(cognition and brain structures),particularly in the presence of abnormal Alzheimer’s Disease(AD)pathology.Methods: In present analysis,a total of 1,188 non-demented individuals were contained from the Alzheimer’s Disease Neuroimaging Initiative(ADNI)database.The 15-item Geriatric Depression Scale(GDS-15)was used to estimate participants’ depressive symptoms.The cross-sectional and longitudinal associations of SSD with brain aging outcomes were explored among all multivariable models.We further evaluated whether baseline amyloid-β(Aβ)load modifies the relations between SSD and brain aging outcomes.Results: SSD at baseline was associated with significantly longitudinal decline in cognition(p < 0.001)and displayed significantly accelerated atrophy in hippocampus(p = 0.001)and middle temporal(p = 0.006)among non-demented elderly.When analyzed in subgroups,these significant associations were consistently observed among Aβ-Positive individuals.In secondary analyses,there were interactions between SSD and baseline Aβ load in prognosticating longitudinal decline in Mini Mental State Examination(MMSE)(p = 0.023),episodic memory(p = 0.004)and increase in Alzheimer’s Disease Assessment Scale Cognition 13-item scale(ADAS-cog13)(p = 0.026).Conclusions: Our findings suggested that the non-demented elderly with both SSD and a high level of Aβ load may have higher risk of cognitive deterioration and brain atrophy.Therapeutic mitigation of depressive symptoms,especially in those with abnormal Aβ levels,may help delay or slow progressive decline in cognition. |