Linguistic Ability in Early Life and the Neuropathology of Alzheimer's Disease and Cerebrovascular Disease: Findings from the Nun Study

2000 ◽  
Vol 903 (1 VASCULAR FACT) ◽  
pp. 34-38 ◽  
Author(s):  
D. A. SNOWDON ◽  
L. H. GREINER ◽  
W. R. MARKESBERY
2009 ◽  
Vol 5 (4S_Part_4) ◽  
pp. P103-P104
Author(s):  
Suzanne L. Tyas ◽  
David A. Snowdon ◽  
Mark F. Desrosiers ◽  
Kathryn P. Riley ◽  
William R. Markesbery

2005 ◽  
Vol 11 (4) ◽  
pp. 499-501
Author(s):  
Bruce Reed

Vascular Dementia: Cerebrovascular Mechanisms and Clinical Management. Robert H. Paul, Ronald Cohen, Brian R. Ott, and Stephen Salloway (Eds.). 2004. Totowa, NJ: Humana Press, 356 pp., $145.00, £91.00 (HB).Interest in how vascular factors contribute to dementia is ascendant, propelled by a number of factors. One is the widespread use of MRI, which is a highly sensitive (if not always specific) test for cerebrovascular lesions. A second is a string of epidemiological reports revealing that Alzheimer's disease shares many of the well established risk factors for cardiovascular and cerebrovascular disease (Skoog & Gustafson, 2003). Recent autopsy studies using cohorts obtained outside of the potentially winnowing influence of the Alzheimer's disease centers have reminded us that vascular lesions are common in patients with dementia (Neuropathology Group of the Medical Research Council Cognitive Function and Ageing Study, 2001). The Nun study report suggesting that infarcts create an additive or greater effect on mental function in concert with AD pathology (Snowdon et al., 1997) received particularly wide exposure and helped revive interest in combined effects of AD and ischemic lesions. Finally, the discovery that polymorphisms of the apoE gene, long of interest in cardiovascular disease, strongly modify the risk of AD suggested the possibility of shared pathophysiological mechanisms between AD and vascular dementia (Panza et al., 2004; Strittmatter & Roses, 1995). The volumeVascular Dementia, edited by Paul, Cohen, Ott and Salloway, is thus a timely resource for those interested in the numerous issues surrounding the role of vascular factors in dementia.


2021 ◽  
Vol 337 ◽  
pp. 113552
Author(s):  
Tomoko Tanaka ◽  
Shinobu Hirai ◽  
Masato Hosokawa ◽  
Takashi Saito ◽  
Hiroshi Sakuma ◽  
...  

2002 ◽  
Vol 977 (1) ◽  
pp. 403-410 ◽  
Author(s):  
CHRISTINE C. WU ◽  
DAN MUNGAS ◽  
JAMIE L. EBERLING ◽  
BRUCE R. REED ◽  
WILLIAM J. JAGUST

2013 ◽  
Vol 1495 ◽  
pp. 61-75 ◽  
Author(s):  
Masatoshi Tomi ◽  
Yuanzi Zhao ◽  
Shanthie Thamotharan ◽  
Bo-Chul Shin ◽  
Sherin U. Devaskar

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.


2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Sang Joon Son ◽  
Bumhee Park ◽  
Hyung Woong Roh ◽  
Narae Kim ◽  
Yong Hyuk Jo ◽  
...  

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