The effects of cerebral amyloidopathy on regional glucose metabolism in older adults with depression and mild cognitive impairment while performing memory tasks.

Co-occurring depression and mild cognitive impairment (MCI) in older adults are important because they have a high risk of conversion to dementia. In the present study, task-related F-18 fluorodeoxyglucose positron emission tomography (FDG-PET) was used to analyse older adults with concomitant depression and MCI. We recruited 20 older adults with simultaneous depression and MCI and 10 older adults with normal cognition (NC). The Verbal Paired Associates test and digit span test were used for the task-related FDG-PET. The 20 older adults with depression and MCI were classified into two groups based on the F-18 florbetaben PET results: depressed MCI patients with (LLD-MCI-A[+]; n = 11) and without amyloid accumulation (LLD-MCI-A[-]; n = 9). Reduced regional cerebral glucose metabolism (rCMglc) in the left superior frontal region was observed in the LLD-MCI-A(-) group compared with the NC group. Analyses of the NC and LLD-MCI-A(+) groups showed significantly decreased rCMglc in the right inferior parietal and left middle frontal regions in the LLD-MCI-A(+) group. rCMglc in the left precuneus was lower in the LLD-MCI-A(+) group than in the LLD-MCI-A(-) group. Significant correlations between the rCMglc in the right inferior parietal/left precuneus regions and memory task scores were observed based on correlation analyses of NC and LLD-MCI-A(+) groups. The findings in the present study indicate the presence of amyloid accumulation influences glucose metabolism in depressed elderly subjects with MCI while performing cognitive tasks. Task-related FDG-PET examinations may help differentiate MCI associated with depression from comorbid depression in patients with prodromal Alzheimer's disease.

Brain amyloid accumulation possibly exacerbates concurrent mild cognitive impairment with subthreshold depression in older adults: A 1-year follow-up study.

BACKGROUND: This study aimed to investigate the 1-year changes in neuropsychological test results in older adults with concomitant late-life depression (LLD) and mild cognitive impairment (MCI) according to the presence or absence of brain amyloidopathy. METHODS: All subjects underwent 18F-florbetaben-positron emission tomography and a standardized neuropsychological battery. The subjects were divided based on brain amyloidopathy and severity of depressive symptoms into the following groups: LLD-MCI-A(+), subthreshold depression (STD)-MCI-A(+), major depressive disorder (MDD)-MCI-A(+), LLD-MCI-A(-), STD-MCI-A(-), and MDD-MCI-A(-). After one year, follow-up neurocognitive tests were conducted. Fifty-nine participants completed both the baseline and 1-year follow-up neurocognitive tests. RESULTS: In the LLD-MCI-A(+) group, the word list recall and word list recognition scores decreased during the follow-up period. The STD-MCI-A(+) group also showed a significant decrease in word list recall score and the score/Z-score of word list recognition. On the other hand, the word list recall Z-score improved at the 1-year follow-up in the LLD-MCI-A(-) group. In particular, the MDD-MCI-A(-) group showed significant increases in word list memory score/Z-score and word list recall Z-score during the follow-up period. LIMITATIONS: Considering that AD progresses slowly, a longer follow-up period may be required. CONCLUSIONS: Our findings showed differences in the extent of change of neuropsychological test results depending on the severity of depressive symptoms and presence or absence of brain amyloidopathy. Our results suggest that clinicians might explore the underlying neuropathology when assessing older adults with concomitant depression and cognitive impairment, even if the symptoms of depression are not severe.

Brain network analysis reveals that amyloidopathy affects comorbid cognitive dysfunction in older adults with depression.

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.

Cerebral amyloid accumulation is associated with distinct structural and functional alterations in the brain of depressed elders with mild cognitive impairment.

BACKGROUND: Elderly patients with late-life depression (LLD) often report mild cognitive impairment (MCI), so Alzheimer's disease (AD) is hard to identify in these patients. We aimed to identify the structural and functional differences between prodromal AD and LLD-related MCI. METHODS: We performed voxel-based morphometry and functional connectivity (FC) analyses in elderly patients with both LLD and MCI to compare alterations between those with cerebral amyloidopathy and those without. We subdivided patients into subthreshold depression (STD) and major depressive disorder (MDD) groups. Using florbetaben positron emission tomography (PET), we compared volume and connectivity between healthy controls and four STD and MDD groups with or without amyloid deposition(A): STD-MCI-A(+), MDD-MCI-A(+), STD-MCI-A(-), and MDD-MCI-A(-). RESULTS: Subjects with MDD or amyloid deposition showed greater volume reduction in the left middle temporal gyrus. MDD groups had lower FC than STD groups in the frontal, cortical, and limbic areas. The STD-MCI-A(+) group showed greater FC reduction than the MDD-MCI-A(-) and STD-MCI-A(-) groups, particularly in the hippocampus, parahippocampus, and frontal and temporal cortices. The functional differences associated with amyloid plaques were more evident in the STD group than in the MDD group. LIMITATIONS: Limitations include disproportional sex ratios, inability to determine the longitudinal effects of amyloidopathy in large populations. CONCLUSIONS: Regional gray matter loss and alterations in brain networks may reflect impairments caused by amyloid deposition and depression. Such changes may facilitate the detection of prodromal AD in elderly patients with both depression and cognitive dysfunction, allowing earlier intervention and more appropriate treatment.