scholarly journals Distinct white matter microstructural abnormalities and extracellular water increases relate to cognitive impairment in Alzheimer’s disease with and without cerebrovascular disease

2017 ◽  
Vol 9 (1) ◽  
Author(s):  
Fang Ji ◽  
Ofer Pasternak ◽  
Siwei Liu ◽  
Yng Miin Loke ◽  
Boon Linn Choo ◽  
...  
Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Jonathan Graff-Radford ◽  
Rosebud Roberts ◽  
Malini Madhavan ◽  
Alejandro Rabinstein ◽  
Ruth Cha ◽  
...  

The objective of this study was to investigate the cross-sectional associations of atrial fibrillation with neuroimaging measures of cerebrovascular disease and Alzheimer’s disease-related pathology, and their interaction with cognitive impairment. MRI scans of non-demented individuals (n=1044) from the population-based Mayo Clinic Study of Aging were analyzed for infarctions, total grey matter, hippocampal and white matter hyperintensity volumes. A subset of 496 individuals underwent FDG and C-11 Pittsburgh compound B (PiB) PET scans. We assessed the associations of atrial fibrillation with i) categorical MRI measures (cortical and subcortical infarctions) using multivariable logistic regression models, and with ii) continuous MRI measures ( hippocampal, total grey matter, and white matter hyperintensity volumes) and FDG-PET and PiB-PET measures using multivariable linear regression models, and adjusting for confounders. Among participants who underwent MRI (median age, 77.8, 51.6% male), 13.5% had atrial fibrillation. Presence of atrial fibrillation was associated with subcortical infarctions (odds ratio [OR], 1.83; p=0.002), cortical infarctions (OR, 1.91; p=0.03), total grey matter volume (Beta [β], -.025, p<.0001) after controlling for age, education, gender, APOE e4 carrier status, coronary artery disease, diabetes, history of clinical stroke, and hypertension. However, atrial fibrillation was not associated with white matter hyperintensity volume, hippocampal volume, Alzheimer’s pattern of FDG hypometabolism or PiB uptake. There was a significant interaction of cortical infarction (p for interaction=0.004) and subcortical infarction (p for interaction =0.015) with atrial fibrillation with regards to odds of mild cognitive impairment (MCI). Using subjects with no atrial fibrillation and no infarction as the reference, the OR (95% confidence intervals [CI]) for MCI was 2.98 (1.66, 5.35;p = 0.0002) among participants with atrial fibrillation and any infarction, 0.69 (0.36, 1.33;p= 0.27) for atrial fibrillation and no infarction, and 1.50 (0.96, 2.32;p = 0.07) for no atrial fibrillation and any infarction. These data highlight that atrial fibrillation is associated with MCI in the presence of infarctions.


2019 ◽  
Author(s):  
Karen Misquitta ◽  
Mahsa Dadar ◽  
D. Louis Collins ◽  
Maria Carmela Tartaglia ◽  

AbstractBackground and Purpose: Neuropsychiatric symptoms (NPS) are frequently encountered in patients with Alzheimer’s disease (AD). Focal grey matter atrophy has been linked to NPS development. Cerebrovascular disease can cause focal lesions and is common among AD patients. As cerebrovascular disease can be detected on MRI as white matter hyperintensities (WMH), this study evaluated WMH burden in mild cognitive impairment (MCI), AD and normal controls and determined their relationship with NPS. Methods: NPS were assessed using the Neuropsychiatric Inventory and grouped into subsyndromes. WMH were measured using an automatic segmentation technique and mean deformation-based morphometry was used to measure atrophy of grey matter regions. Results: WMHs and grey matter atrophy both contributed significantly to NPS subsyndromes in MCI and AD subjects, however, WMH burden played a greater role. Conclusions: This study could provide a better understanding of the pathophysiology of NPS in AD.


2019 ◽  
Author(s):  
Rannveig Sakshaug Eldholm ◽  
Maria Lage Barca ◽  
Karin Persson ◽  
Anne-Brita Knapskog ◽  
Knut Engedal ◽  
...  

Abstract Background: Diagnostic criteria of Alzheimer’s disease (AD) and vascular cognitive impairment (VCI) describe different cognitive profiles. AD patients often have concomitant cerebrovascular disease (CVD) and these patients could therefore be expected to display symptoms of both AD and VCI. AD patients with concomitant CVD display symptoms of cognitive impairment with less AD pathology than those without CVD. Medial temporal atrophy (MTA) on magnetic resonance imaging (MRI) is a biomarker of neurodegeneration in AD, and we would expect less MTA in AD patients with CVD. The first aim was to examine whether there were differences in the results of cognitive tests for memory, executive function, and processing speed, or in depressive symptoms, between AD patients with and without CVD. Secondly, to assess whether MTA on MRI is more pronounced among AD patients without CVD. Methods: A total of 192 AD patients with amnestic mild cognitive impairment or mild dementia underwent cognitive assessment and depression screening. Cerebral MRIs were assessed for MTA, white matter hyperintensities, and lacunar and cortical infarcts. CVD was defined as the presence of white matter hyperintensities Fazekas scale ≥2 or any infarct. To study the effect of CVD, several multiple linear regression analyses were carried out using CVD adjusted for age and sex as the independent variable, and cognitive test scores, depression scores, and MTA as dependent variables. Results: Mean age was 72.2 (SD 8.3) years. The number of AD patients with and without concomitant CVD was 121 and 71, respectively. The group with CVD scored significantly lower on tests of attention, executive function and immediate recall compared with the group without CVD. In analyses controlled for age and sex, concomitant CVD was not associated with significant differences in any cognitive test nor in depressive symptoms. A statistically significant association between AD with concomitant CVD and more pronounced MTA was identified. Conclusions: The results indicate that cognitive test profiles, depressive symptoms, and MTA scores cannot be used to distinguish AD patients with and without CVD.


Author(s):  
Francis Cambronero ◽  
Angela L. Jefferson

Hemodynamic impairment is a prominent feature in aging, vascular cognitive impairment and dementia, and Alzheimer’s disease, including patterned changes in cerebral blood flow (CBF) that can be detected prior to concomitant pathologies. These CBF abnormalities drive vascular dysfunction through a variety of biological pathways and ultimately contribute to cerebrovascular disease associated with cognitive impairment. Importantly, the co-existence of cerebrovascular disease and Alzheimer’s disease is exceedingly common and worsens the progression of clinical symptoms, likely through accelerating neurotoxic protein deposition and the loss of cerebrovascular integrity. Emerging evidence further suggests that the brain may be more susceptible to subclinical cardiovascular dysfunction in aging adults, particularly since the accumulation of cardiovascular risk factors over the lifespan creates a more vulnerable vascular system. Although age-associated CBF dysregulation has varied and complex origins, it undoubtedly serves a critical role in the early progression of neurodegenerative disease and may help explain the considerable overlap between the most common clinical dementias.


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