Abstract
Early detection of patients with late-life depression (LLD) with a high risk of developing dementia contributes to early intervention. Odor identification (OI) dysfunction serves as a marker for predicting dementia, but whether OI dysfunction increases the risk of dementia in LLD patients remains unclear. The present study aimed to explore the interactive effect of LLD and OI dysfunction on the risk of dementia and its underlying neuroimaging changes. One hundred and fifty-seven LLD patients and 101 normal controls were recruited, and data on their OI, cognition, activity of daily living (ADL), and resting-state functional magnetic resonance imaging were collected. Two × two factorial analyses were used to analyze the interactive effects of LLD and OI dysfunction on neuropsychological and neuroimaging abnormalities. Mediation analyses were used to explore whether abnormalities detected by neuroimaging mediated the the associations between OI and cognition/ADL. The results suggested that LLD and OI dysfunction exhibited additive effects on reduced ADL, global cognition and memory scores, as well as neuroimaging variables including (i) increased fractional amplitude of low-frequency fluctuation (fALFF) in the right orbitofrontal cortex and right precentral cortex, and (ii) increased regional homogeneity (ReHo) in the left hippocampus/fusiform gyrus, etc. In addition, these increased fALFF and ReHo values were associated with reduced neuropsychological scores (ADL, global cognition, memory, and language). Moreover, ReHo of the left hippocampus/fusiform gyrus completely mediated the relationship between OI and ADL, and partially mediated the relationship between OI and global cognition. Overall, mediated by the hypersynchronization of the left hippocampus/fusiform gyrus, OI dysfunction may increase the risk of dementia in LLD patients.
Highlights
Late-life depression (LLD), which affects 3.5–7.5% of the geriatric population, is a risk factor for dementia[1,2]
Our results suggested that there were additive effects between LLD and Odor identification (OI) dysfunction that resulted in (1) reduced scores of activity of daily living (ADL), global cognition, and memory; (2) increased fractional amplitude of low-frequency fluctuation (fALFF) in the right orbitofrontal cortex and right precentral cortex; and (3) increased regional homogeneity (ReHo) in the right rectus/olfactory cortex, left hippocampus/fusiform gyrus, right calcarine/lingual/ parahippocampal gyrus, and right superior frontal gyrus
The present results suggest that there were additive effects between LLD and OI dysfunction that resulted in reduced scores of ADL, global cognition, and memory, suggesting that LLD patients with OI dysfunction exhibited more severe impairment of cognitive performance and ADL
Summary
Late-life depression (LLD), which affects 3.5–7.5% of the geriatric population (over age 60 years), is a risk factor for dementia[1,2]. The risk of developing dementia in patients with LLD was 1.71–6.75 times higher than that in healthy elderly[3,4]. Chen et al Translational Psychiatry (2021)11:172 shares many common mechanisms with Alzheimer’s disease (AD), such as metabolic disturbance in glucocorticoid steroids[5], hippocampal dysfunction[6], dysfunctions of brain-derived neurotrophic factors[7], and neuroinflammatory changes[8]. These common mechanisms may accelerate neurodegeneration in patients with LLD and, as a result, increase their risk of conversion to AD. The assessment of amyloid β (Aβ) and tau by cerebrospinal fluid (CSF) or positron emission tomography–computed tomography (PET-CT) may contribute to the early detection of neurodegeneration in patients with LLD9–11
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