Temporal stability of the ventral attention network and general cognition along the Alzheimer's disease spectrum.
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ABSTRACT:
SUBMITTER: Chumin EJ
PROVIDER: S-EPMC8220588 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:BackgroundAffective symptoms in Alzheimer's disease (AD) can be rated with both informant- and self-ratings. Information from these two modalities may not converge. We estimated network structures of affective symptoms in AD with both rating modalities and assessed the longitudinal stability of the networks.MethodsNetwork analyses combining self-rated and informant-rated affective symptoms were conducted in 3198 individuals with AD at two time points (mean follow-up 387 days), drawn from the NACC database. Self-rated symptoms were assessed by Geriatric Depression Scale, and informant-rated symptoms included depression, apathy and anxiety questions from Neuropsychiatric Inventory Questionnaire.ResultsInformant-rated symptoms were mainly connected to symptoms expressing lack of positive affect, but not to the more central symptoms of self-rated worthlessness and helplessness. Networks did not differ in structure (p = .71), or connectivity (p = .92) between visits. Symptoms formed four clinically meaningful clusters of depressive symptoms and decline, lack of positive affect, informant-rated apathy and anxiety and informant-rated depression.LimitationsThe symptom dynamics in our study could have been present before AD diagnosis. The lack of positive affect cluster may represent a methodological artefact rather than a theoretically meaningful subgroup. Requiring follow-up lead to a selection of patients with less cognitive decline.ConclusionsInformant rating may only capture the more visible affective symptoms, such as not being in good spirits, instead of more central and severe symptoms, such as hopelessness and worthlessness. Future research should continue to be mindful of differences between self- and informant-rated symptoms even in earlier stages of AD.
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Project description:INTRODUCTION:Several characteristics associated with increased risk for Parkinson's disease (PD) have been identified, including specific genotypes and various non-motor symptoms. Characterizing non-motor features, such as cognitive abilities, among individuals considered at-risk for PD is essential to improving prediction of future neurodegeneration. METHODS:Participants belonging to the following cohorts of the Parkinson Progression Markers Initiative (PPMI) study were included: de novo PD with dopamine transporter binding deficit (n = 423), idiopathic REM sleep behavior disorder (RBD, n = 39), hyposmia (n = 26) and non-PD mutation carrier (NMC; Leucine-rich repeat kinase 2 (LRRK2) G2019S (n = 88) and glucocerebrosidase (GBA) gene (n = 38) mutations)). Inclusion criteria enriched the RBD and hyposmia cohorts, but not the NMC cohort, with individuals with dopamine transporter binding deficit. Baseline neuropsychological performance was compared, and analyses were adjusted for age, sex, education, and depression. RESULTS:The RBD cohort performed significantly worse than the hyposmia and NMC cohorts on Symbol Digit Modality Test (mean (SD) 32.4 (9.16) vs. 41.8 (9.98), p = 0.002 and vs. 45.2 (10.9), p<0.001) and Judgment of Line Orientation (11.3 (2.36) vs.12.9 (1.87), p = 0.004 and vs. 12.9 (1.87), p<0.001). The RBD cohort also performed worse than the hyposmia cohort on the Montreal Cognitive Assessment (25.5 (4.13) vs. 27.3 (1.71), p = 0.02). Hyposmics did not differ from PD or NMC cohorts on any cognitive test score. CONCLUSION:Among individuals across a spectrum of risk for PD, cognitive function is worse among those with the characteristic most strongly associated with future risk of PD or dementia with Lewy bodies, namely RBD.
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Project description:Human episodic memory critically depends on subregions of the medial temporal lobe, which are part of functional brain systems such as the anterior-temporal and the posterior-medial system. Here we analysed how Alzheimer's pathology affects functional connectivity within these systems. Data from 256 amyloid-β-negative cognitively unimpaired, 103 amyloid-β-positive cognitively unimpaired, and 83 amyloid-β-positive individuals with mild cognitive impairment were analysed. Amyloid-β and tau pathology were measured using the CSF amyloid-β42/40 ratio and phosphorylated tau, respectively. We found that amyloid-β-positive cognitively unimpaired individuals were mainly characterized by decreased functional connectivity between the medial temporal lobe and regions in the anterior-temporal system, most prominently between left perirhinal/entorhinal cortices and medial prefrontal cortex. Furthermore, correlation analysis in this group revealed decreasing functional connectivity between bilateral perirhinal/entorhinal cortices, anterior hippocampus and posterior-medial regions with increasing levels of phosphorylated tau. The amyloid-β-positive individuals with mild cognitive impairment mostly exhibited reduced connectivity between the medial temporal lobe and posterior-medial regions, predominantly between the anterior hippocampus and posterior cingulate cortex. In addition, they showed hyperconnectivity within the medial temporal lobe and its immediate proximity. Lower medial temporal-cortical functional connectivity networks resulting from the group comparisons of cognitively unimpaired individuals were associated with reduced memory performance and more rapid longitudinal memory decline as shown by linear mixed-effects regression analysis. Finally, we found that reduced medial temporal-cortical connectivity in mildly cognitively impaired individuals was related to reduced entorhinal thickness and white matter integrity of the parahippocampal cingulum and the fornix. No such relationships were found in cognitively unimpaired individuals. In conclusion, our findings show that the earliest changes in preclinical Alzheimer's disease might involve decreased connectivity within the anterior-temporal system, and early changes in connectivity might be related to memory impairment, but not to structural changes. With disease progression and increased tau pathology, medial temporal functional connectivity with posterior-medial regions seems to be increasingly impaired. In individuals with mild cognitive impairment, reduced functional connectivity is associated with structural brain changes as well as the emergence of locally increased connectivity patterns. Thus, functional connectivity between the medial temporal lobe and the anterior-temporal and posterior-medial system could serve as stage-specific functional markers in early Alzheimer's disease.
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