Abstract
Late-life depression (LLD) may increase the risk of Alzheimer’s dementia (AD). While amyloidopathy accelerates AD progression, its role in such patients has not yet been elucidated. We hypothesized that cerebral amyloidopathy distinctly affects the alteration of brain network topology and may be associated with distinct cognitive symptoms. We recruited 26 and 27 depressed mild cognitive impairment (MCI) patients with (LLD-MCI-A(+)) and without amyloid accumulation (LLD-MCI-A(−)), respectively, and 21 normal controls. We extracted structural brain networks using their diffusion-weighted images. We aimed to compare the distinct network deterioration in LLD-MCI with and without amyloid accumulation and the relationship with their distinct cognitive decline. Thus, we performed a group comparison of the network topological measures and investigated any correlations with neurocognitive testing scores. Topological features of brain networks were different according to the presence of amyloid accumulation. Disrupted network connectivity was highly associated with impaired recall and recognition in LLD-MCI-A(+) patients. Inattention and dysexecutive function were more influenced by the altered networks involved in fronto-limbic circuitry dysfunction in LLD-MCI-A(−) patients. Our results show that alterations in brain network topology may reflect different cognitive dysfunction depending on amyloid accumulation in depressed older adults with MCI.
Highlights
Late-life depression (LLD) may increase the risk of Alzheimer’s dementia (AD)
Given that patients with LLD and mild cognitive impairment (MCI) present a broad spectrum of clinical symptoms related to cognitive dysfunction and emotional disturbances based on the pathophysiological mechanisms, it is postulated that they may be mediated by widespread network disconnectivity rather than by a single brain r egion[7,8]
We performed post-hoc tests for each score, which showed that the variations between healthy older adults (HOA) and depressed MCI patients without amyloid accumulation (LLD-MCIA(−)) and those between HOA and depressed MCI patients with amyloid accumulation (LLD-MCI-A(+)) were significant
Summary
Late-life depression (LLD) may increase the risk of Alzheimer’s dementia (AD). While amyloidopathy accelerates AD progression, its role in such patients has not yet been elucidated. Individuals without amyloid accumulation had cerebral glucose hypometabolism within the frontal region, which is responsible for executive function These results suggest that cerebral amyloid accumulation possibly determines distinguished cognitive impairment and altered brain metabolism in patients with LLD and MCI. A network analysis based on combining magneto-encephalography showed that dysfunctional communication between the brain modules resulted in cognitive impairment in patients with AD, indicating the significance of investigating the global network organization[9] In another recent study that investigated cognitively intact individuals with abnormal amyloid levels of cerebrospinal fluid (CSF), it was observed from cortical thickness data that cerebral amyloidopathy influenced the disruption of global connectivity across the brain network[10]. It is still unclear how different brain network regions interact with one another to produce cognitive and depressive symptoms and whether specific alterations in brain network topology reflect the presence or absence of underlying neuropathological changes
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