Abstract
Late-onset depression (LOD) is regarded as a risk factor or a prodrome of Alzheimer’s disease (AD). Moreover, LOD patients with cognitive deficits have the higher risk of subsequent AD. Thus, it is necessary to understand the neural underpinnings of cognitive deficits and its pathological implications in LOD. Consistent findings show that the default mode network (DMN) is an important and potentially useful brain network for the cognitive deficits in LOD patients. In recent years, genetics has been actively researched as a possible risk factor in the pathogenesis of LOD. So, in this review, we discuss the current research progress on the cognitive deficits and DMN in LOD through a combined view of brain network and genetics. We find that different structural and functional impairments of the DMN might be involved in the etiological mechanisms of different cognitive impairments in LOD patients.
Highlights
Late-onset depression (LOD) is defined as a depression occurring for the first time after the age of 50, 55, 60 or 65 years and the age of 55 is the most commonly used cutoff age (Unützer and Park, 2012; Wang et al, 2016; Geerlings and Gerritsen, 2017)
To improve early identification of LOD which may convert to Alzheimer’s disease (AD) and to achieve further advances in the LOD treatments, we review the progress of neuroimaging and genetic investigations as well as the current clinical status on the cognitive deficits in LOD
A recent study provided the risk factors associated with cognitions for LOD patients based on the anterior default mode network (DMN) and posterior DMN and revealed that visual perception function impairment was associated with a lower functional connectivity (FC) of ventral mPFC (vmPFC)- left PCu and a higher vmPFC- right middle temporal gyrus (MTG) and PCC- left PCu
Summary
Late-onset depression (LOD) is defined as a depression occurring for the first time after the age of 50, 55, 60 or 65 years and the age of 55 is the most commonly used cutoff age (Unützer and Park, 2012; Wang et al, 2016; Geerlings and Gerritsen, 2017). Late-life depression (LLD) contains LOD and early-onset depression (EOD) that recurs or continues into old age. Late-onset depression (LOD) is associated with a high disability, high recurrence rate, and high family caregiving burden as well as high risk for cognition deficits (Andreescu et al, 2013; Diniz et al, 2014; Kaup et al, 2016). Another study followed up for 5 to 7 years revealed that the conversion rate of dementia in depressed elderly patients with reversible cognitive impairments was 71.4% (Sáez-Fonseca et al, 2007). Genetics has been actively researched as a possible risk factor for the cognitive deficits of LOD (Hou et al, 2010; Wang et al, 2012; Yin et al, 2015b). To improve early identification of LOD which may convert to AD and to achieve further advances in the LOD treatments, we review the progress of neuroimaging and genetic investigations as well as the current clinical status on the cognitive deficits in LOD
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