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1.
Mariella Lauriola Roberto Esposito Stefano Delli Pizzi Massimiliano de Zambotti Francesco Londrillo Joel H. Kramer Gil D. Rabinovici Armando Tartaro 《Alzheimer's & dementia》2017,13(7):783-791
Introduction
Subjective cognitive decline (SCD) is a risk factor for mild cognitive impairment (MCI) and Alzheimer's disease (AD). Although sleep has been shown to be altered in MCI and AD, little is known about sleep in SCD.Methods
Seventy cognitively normal community-dwelling participants were classified as SCD (32) or controls (38) using the Subjective Cognitive Decline Questionnaire. Sleep was assessed using actigraphy and diaries. FreeSurfer was used for performing medial temporal lobes (MTLs) and brain cortical parcellation of 3T magnetic resonance images. Multiple regression models were used to assess the presence of sleep, MTL, or regional cortical differences between groups.Results
Objective sleep was disrupted in SCD participants, which showed increased nighttime wakefulness and reduced sleep efficiency. No group differences emerged in subjective sleep or magnetic resonance imaging outcomes.Discussion
Objective sleep resulted disrupted in community-dwelling SCD, without any subjective sleep or cortical change. Sleep assessment/intervention in SCD might help prevent/delay AD onset. 相似文献2.
Audrey Perrotin Renaud La Joie Vincent de La Sayette Louisa Barré Florence Mézenge Justine Mutlu Denis Guilloteau Stéphanie Egret Francis Eustache Gaël Chételat 《Alzheimer's & dementia》2017,13(5):550-560
Introduction
Subjective cognitive decline (SCD) could indicate preclinical Alzheimer's disease, but the existing literature is confounded by heterogeneous approaches to studying SCD. We assessed the differential cognitive, affective, and neuroimaging correlates of two aspects of SCD: reporting high cognitive difficulties on a self-rated questionnaire versus consulting at a memory clinic.Methods
We compared 28 patients from a memory clinic with isolated SCD, 35 community-recruited elders with similarly high levels of self-reported cognitive difficulties, and 35 community-recruited controls with low self-reported cognitive difficulties.Results
Increased anxiety and amyloid β deposition were observed in both groups with high self-reported difficulties, whereas subclinical depression and (hippocampal) atrophy were specifically associated with medical help seeking. Cognitive tests showed no group differences.Discussion
These results further validate the concept of SCD in both community- and clinic-based groups. Yet, recruitment methods influence associated biomarkers and affective symptomatology, highlighting the heterogeneous nature of SCD depending on study characteristics. 相似文献3.
Sean M. Nestor Bratislav Mišić Joel Ramirez Jiali Zhao Simon J. Graham Nicolaas P.L.G. Verhoeff Donald T. Stuss Mario Masellis Sandra E. Black 《Alzheimer's & dementia》2017,13(7):749-760
Introduction
Cerebral small vessel disease (SVD) is thought to contribute to Alzheimer's disease (AD) through abnormalities in white matter networks. Gray matter (GM) hub covariance networks share only partial overlap with white matter connectivity, and their relationship with SVD has not been examined in AD.Methods
We developed a multivariate analytical pipeline to elucidate the cortical GM thickness systems that covary with major network hubs and assessed whether SVD and neurodegenerative pathologic markers were associated with attenuated covariance network integrity in mild AD and normal elderly control subjects.Results
SVD burden was associated with reduced posterior cingulate corticocortical GM network integrity and subneocorticocortical hub network integrity in AD.Discussion
These findings provide evidence that SVD is linked to the selective disruption of cortical hub GM networks in AD brains and point to the need to consider GM hub covariance networks when assessing network disruption in mixed disease. 相似文献4.
Anna E. Leeuwis Marije R. Benedictus Joost P.A. Kuijer Maja A.A. Binnewijzend Astrid M. Hooghiemstra Sander C.J. Verfaillie Teddy Koene Philip Scheltens Frederik Barkhof Niels D. Prins Wiesje M. van der Flier 《Alzheimer's & dementia》2017,13(5):531-540
Introduction
We examined the association between decreased cerebral blood flow (CBF) and cognitive impairment in Alzheimer's disease (AD), mild cognitive impairment (MCI), and subjective cognitive decline (SCD).Methods
We included 161 AD, 95 MCI, and 143 SCD patients from the Amsterdam Dementia Cohort. We used 3-T pseudo-continuous arterial spin labeling to estimate whole-brain and regional partial volume–corrected CBF. Neuropsychological tests covered global cognition and five cognitive domains. Associations were investigated using linear regression analyses.Results
In the whole sample, reduced overall and regional CBF was associated with impairment in all cognitive domains. We found significant interactions between diagnosis and CBF for language and between diagnosis and parietal CBF for global cognition and executive functioning. Stratification showed that decreased CBF was associated with worse performance in AD patients but not in MCI or SCD.Discussion
Our results suggest that CBF may have potential as a functional marker of disease severity. 相似文献5.
Carly Oboudiyat Tamar Gefen Eleni Varelas Sandra Weintraub Emily Rogalski Eileen H. Bigio M.-Marsel Mesulam 《Alzheimer's & dementia》2017,13(5):598-601
Introduction
The accuracy of cerebrospinal fluid (CSF) biomarkers for detecting Alzheimer's disease (AD) pathology has not been fully validated in autopsied nonamnestic dementias.Methods
We retrospectively evaluated CSF amyloid β 1–42, phosphorylated-tau, and amyloid-tau index as predictors of Alzheimer pathology in patients with primary progressive aphasia, frontotemporal dementia, and progressive supranuclear palsy.Results
Nineteen nonamnestic autopsied cases with relevant CSF values were included. At autopsy, nine had AD and 10 had non-AD pathologies. All six patients whose combined CSF phosphorylated-tau and amyloid β levels were “consistent with AD” had postmortem Alzheimer pathology. The two patients whose biomarker values were “not consistent with AD” had non-AD pathologies. The CSF values of the remaining eight non-AD cases were in conflicting or borderline ranges.Discussion
CSF biomarkers reliably identified Alzheimer pathology in nonamnestic dementias and may be useful as a screening measure for inclusion of nonamnestic cases into Alzheimer's trials. 相似文献6.
Stephanie Kielb Emily Rogalski Sandra Weintraub Alfred Rademaker 《Alzheimer's & dementia》2017,13(12):1337-1344
Introduction
Functional and cognitive features of subjective cognitive decline (SCD) were identified in a longitudinal database from the National Alzheimer's Coordinating Center.Methods
Cognitively normal older adults with (SCD+) and without (SCD?) self-reported memory complaints (N = 3915) were compared on (1) baseline Functional Assessment Questionnaire ratings, (2) baseline scores and longitudinal rate of change estimates from nine neuropsychological tests, and (3) final clinical diagnoses.Results
SCD+ had higher baseline ratings of functional impairment, reduced episodic memory practice effects and poorer performance on neuropsychological tests of psychomotor speed and language, and higher frequencies of mild cognitive impairment and dementia diagnoses at the end of follow-up compared with the SCD-group.Discussion
Subtle clinical features of SCD identified in this large cohort are difficult to detect at the individual level. More sensitive tests are needed to identify those with SCD who are vulnerable to cognitive decline and dementia. 相似文献7.
8.
Juliane Schelle Lisa M. Häsler Jens C. Göpfert Thomas O. Joos Hugo Vanderstichele Erik Stoops Eva-Maria Mandelkow Ulf Neumann Derya R. Shimshek Matthias Staufenbiel Mathias Jucker Stephan A. Kaeser 《Alzheimer's & dementia》2017,13(6):701-709
Introduction
The inhibition of the β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) is a main therapeutic approach for the treatment of Alzheimer's disease (AD). We previously reported an age-related increase of tau protein in the cerebrospinal fluid (CSF) of amyloid β (Aβ) precursor protein (APP) transgenic mice.Methods
APP transgenic mice were treated with a potent BACE1 inhibitor. CSF tau and CSF Aβ levels were assessed. A novel high-sensitivity tau sandwich immunoassay was developed.Results
We demonstrate that long-term BACE1 inhibition prevents CSF tau increase both in early-depositing APP transgenic mice and APP transgenic mice with moderate Aβ pathology.Discussion
Our results demonstrate that BACE1 inhibition not only reduces Aβ generation but also downstream AD pathophysiology. The tight correlation between Aβ aggregation in brain and CSF tau levels renders CSF tau a valuable marker to predict the effectiveness of BACE1 inhibitors in current clinical trials. 相似文献9.
Diego Mastroeni Omar M. Khdour Elaine Delvaux Jennifer Nolz Gary Olsen Nicole Berchtold Carl Cotman Sidney M. Hecht Paul D. Coleman 《Alzheimer's & dementia》2017,13(5):510-519
Introduction
We have comprehensively described the expression profiles of mitochondrial DNA and nuclear DNA genes that encode subunits of the respiratory oxidative phosphorylation (OXPHOS) complexes (I–V) in the hippocampus from young controls, age matched, mild cognitively impaired (MCI), and Alzheimer's disease (AD) subjects.Methods
Hippocampal tissues from 44 non-AD controls (NC), 10 amnestic MCI, and 18 AD cases were analyzed on Affymetrix Hg-U133 plus 2.0 arrays.Results
The microarray data revealed significant down regulation in OXPHOS genes in AD, particularly those encoded in the nucleus. In contrast, there was up regulation of the same gene(s) in MCI subjects compared to AD and ND cases. No significant differences were observed in mtDNA genes identified in the array between AD, ND, and MCI subjects except one mt-ND6.Discussion
Our findings suggest that restoration of the expression of nuclear-encoded OXPHOS genes in aging could be a viable strategy for blunting AD progression. 相似文献10.
Tharick A. Pascoal Sulantha Mathotaarachchi Monica Shin Andrea L. Benedet Sara Mohades Seqian Wang Tom Beaudry Min Su Kang Jean-Paul Soucy Aurelie Labbe Serge Gauthier Pedro Rosa-Neto 《Alzheimer's & dementia》2017,13(6):644-653