Abstract
Alzheimer’s disease (AD) has a long preclinical stage that can last for decades prior to progressing toward amnestic mild cognitive impairment (aMCI) and/or dementia. Subjective cognitive decline (SCD) is characterized by self-experienced memory decline without any evidence of objective cognitive decline and is regarded as the later stage of preclinical AD. It has been reported that the changes in structural covariance patterns are affected by AD pathology in the patients with AD and aMCI within the specific large-scale brain networks. However, the changes in structural covariance patterns including normal control (NC), SCD, aMCI, and AD are still poorly understood. In this study, we recruited 42 NCs, 35 individuals with SCD, 43 patients with aMCI, and 41 patients with AD. Gray matter (GM) volumes were extracted from 10 readily identifiable regions of interest involved in high-order cognitive function and AD-related dysfunctional structures. The volume values were used to predict the regional densities in the whole brain by using voxel-based statistical and multiple linear regression models. Decreased structural covariance and weakened connectivity strength were observed in individuals with SCD compared with NCs. Structural covariance networks (SCNs) seeding from the default mode network (DMN), salience network, subfields of the hippocampus, and cholinergic basal forebrain showed increased structural covariance at the early stage of AD (referring to aMCI) and decreased structural covariance at the dementia stage (referring to AD). Moreover, the SCN seeding from the executive control network (ECN) showed a linearly increased extent of the structural covariance during the early and dementia stages. The results suggest that changes in structural covariance patterns as the order of NC-SCD-aMCI-AD are divergent and dynamic, and support the structural disconnection hypothesis in individuals with SCD.
Highlights
Alzheimer’s disease (AD), beginning with cognitive impairment, is the most common type of dementia, characterized by progressive and irreversible pathology with a long preclinical phase (Masters et al, 2015)
The pattern changes of Structural covariance networks (SCNs) seeding from the anterior hippocampus, posterior hippocampus, Ch4p, and Ch1/2 as the order of normal control (NC)-Subjective cognitive decline (SCD)-amnestic mild cognitive impairment (aMCI)-AD showed similar trends to the SCNs anchored to the default mode network (DMN)
We investigated the connectivity changes of Gray matter (GM) SCNs in individuals with SCD, aMCI, and AD
Summary
Alzheimer’s disease (AD), beginning with cognitive impairment, is the most common type of dementia, characterized by progressive and irreversible pathology with a long preclinical phase (Masters et al, 2015). Mild cognitive impairment (MCI) is the early symptomatic stage of AD, characterized by objective cognitive impairment, but largely preserves the daily functioning of individuals compared with dementia (Albert et al, 2011; Jack et al, 2018). Subjective cognitive decline (SCD) refers to the self-perceived worsening of cognitive ability, which is defined at the preclinical stage of AD and is independent of the neuropsychological tests (Jessen et al, 2014, 2020). The majority of individuals with SCD will not show sustained cognitive decline or progress to AD (Jessen et al, 2020) because the associations between self-perceived cognitive decline and objective cognitive impairment are complex. Diagnosis and intervention to preserve cognitive function is an important way to combat AD (Livingston et al, 2017); it is critical to investigate the associations among biomarkers of SCD, MCI, and AD to provide a better opportunity for an early therapy (Jessen et al, 2020)
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