Chronic kidney disease (CKD) has emerged as a possible new risk factor of cognitive impairment and dementia, but results of studies remain conflicting.
A systematic literature research of electronic ...databases (MEDLINE, Cochrane Library and Goggle Scholar covering the period from 1980 to January 2012) and meta-analysis of relevant cross-sectional and longitudinal studies were conducted to assess the association of CKD and cognitive decline.
Most cross-sectional and longitudinal studies suggest an association between cognitive impairment and CKD. Meta-analysis of cross-sectional and longitudinal studies comprising 54,779 participants yielded an association of cognitive decline in patients with CKD compared with patients without CKD (OR 1.65, 95% CI 1.32-2.05; p < 0.001, and OR 1.39, 95% CI 1.15-1.68; p < 0.001, respectively).
This is the first meta-analysis assessing the impact of CKD on cognitive decline. Our results suggest CKD being a significant and independent somatic risk factor in the development of cognitive decline.
Alzheimer's disease (AD) is a neurodegenerative disorder that prominently affects cerebral connectivity. Assessing the functional connectivity at rest, recent functional MRI (fMRI) studies reported ...on the existence of resting-state networks (RSNs). RSNs are characterized by spatially coherent, spontaneous fluctuations in the blood oxygen level-dependent signal and are made up of regional patterns commonly involved in functions such as sensory, attention, or default mode processing. In AD, the default mode network (DMN) is affected by reduced functional connectivity and atrophy. In this work, we analyzed functional and structural MRI data from healthy elderly (n = 16) and patients with amnestic mild cognitive impairment (aMCI) (n = 24), a syndrome of high risk for developing AD. Two questions were addressed: (i) Are any RSNs altered in aMCI? (ii) Do changes in functional connectivity relate to possible structural changes? Independent component analysis of restingstate fMRI data identified eight spatially consistent RSNs. Only selected areas of the DMN and the executive attention network demonstrated reduced network-related activity in the patient group. Voxel-based morphometry revealed atrophy in both medial temporal lobes (MTL) of the patients. The functional connectivity between both hippocampi in the MTLs and the posterior cingulate of the DMN was present in healthy controls but absent in patients. We conclude that in individuals at risk for AD, a specific subset of RSNs is altered, likely representing effects of ongoing early neurodegeneration. We interpret our finding as a proof of principle, demonstrating that functional brain disorders can be characterized by functional-disconnectivity profiles of RSNs.
Socially-induced cognitive emotion regulation (Social-Reg) is crucial for emotional well-being and social functioning; however, its brain mechanisms remain poorly understood. Given that both social ...cognition and cognitive emotion regulation engage key regions of the default-mode network (DMN), we hypothesized that Social-Reg would rely on the DMN, and that its effectiveness would be associated with social functioning. During functional MRI, negative emotions were elicited by pictures, and – via short instructions – a psychotherapist either down-regulated participants' emotions by employing reappraisal (Reg), or asked them to simply look at the pictures (Look). Adult Attachment Scale was used to measure social functioning. Contrasting Reg versus Look, aversive emotions were successfully reduced during Social-Reg, with increased activations in the prefrontal and parietal cortices, precuneus and the left temporo-parietal junction. These activations covered key nodes of the DMN and were associated with Social-Reg success. Furthermore, participants' attachment security was positively correlated with both Social-Reg success and orbitofrontal cortex involvement during Social-Reg. In addition, specificity of the neural correlates of Social-Reg was confirmed by comparisons with participants' DMN activity at rest and their brain activations during a typical emotional self-regulation task based on the same experimental paradigm without a psychotherapist. Our results provide first evidence for the specific involvement of the DMN in Social-Reg, and the association of Social-Reg with individual differences in attachment security. The findings suggest that DMN dysfunction, found in many neuropsychiatric disorders, may impair the ability to benefit from Social-Reg.
•Neural correlates of social cognitive emotion regulation were investigated.•Social cognitive emotion regulation successfully down-regulated negative emotions.•Social cognitive emotion regulation recruited key regions of the DMN.•Reliance on social–DMN nodes was specific for the social (and not self) regulation.•Effectiveness of social regulation was linked to attachment security.
Background A decreased concentration of beta amyloid (1-42) (Aβ42) has consistently been found in the cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD) and is considered a ...diagnostic biomarker. However, it is not clear to which extent CSF Aβ42 levels are reflective of cerebral pathology in AD. The aim of the study was to determine the association between cerebral amyloid plaque load, as measured by means of the positron emission tomography (PET) tracer carbon-11-labeled Pittsburgh Compound B (11 CPiB) and CSF Aβ42 in AD. Methods A group of 30 patients with probable AD, as defined by established clinical criteria and by an AD-typical pattern of tracer uptake in fluorine-18-labeled fluorodeoxyglucose (18 FFDG) PET, were included. In all patients, 11 CPiB PET and CSF analysis were performed. The association between amyloid load and CSF Aβ42 levels was examined in three different ways: by linear regression analysis using an overall 11 CPiB value for the entire cerebrum, by correlation analyses using 11 CPiB measurements in anatomically defined regions of interest, and by voxel-based regression analyses. Results All patients showed a positive 11 CPiB scan demonstrating amyloid deposition. Linear regression analysis revealed a significant inverse correlation between the overall 11 CPiB uptake and CSF Aβ42 levels. Voxel-based regression and regional correlation analyses did not attain statistical significance after correction for multiple comparisons. Numerically, correlation coefficients were higher in brain regions adjacent to CSF spaces. Conclusions The study demonstrates a moderate linear negative association between cerebral amyloid plaque load and CSF Aβ42 levels in AD patients in vivo and suggests possible regional differences of the association.
Neuroimaging studies of major depressive disorder (MDD) have consistently observed functional and structural changes of the hippocampus (HP) and amygdale (AY). Thus, these brain regions appear to be ...critical elements of the pathophysiology of MDD. The HP and AY directly interact and show broad and overlapping intrinsic functional connectivity (iFC) to other brain regions. Therefore, we hypothesized the HP and AY would show a corresponding pattern of aberrant intrinsic connectivity in MDD. Resting-state functional MRI was acquired from 21 patients with MDD and 20 healthy controls. ß-Maps of region-of-interest-based FC for bilateral body of the HP and basolateral AY were used as surrogates for iFC of the HP and AY. Analysis of variance was used to compare ß-maps between MDD and healthy control groups, and included covariates for age and gender as well as gray matter volume of the HP and AY. The HP and AY of MDD patient's showed an overlapping pattern of reduced FC to the dorsomedial-prefrontal cortex and fronto-insular operculum. Both of these regions are known to regulate the interactions among intrinsic networks (i.e., default mode, central executive, and salience networks) that are disrupted in MDD. These results provide the first evidence of overlapping aberrant HP and AY intrinsic connectivity in MDD. Our findings suggest that aberrant HP and AY connectivity may interact with dysfunctional intrinsic network activity in MDD.
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