scholarly journals Cerebral microbleeds on 7 Tesla MRI in preclinical Alzheimer’s disease: The Medea‐7T study

2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Maarten H.T. Zwartbol ◽  
Rashid Ghaznawi ◽  
Kim Blom ◽  
Hugo J. Kuijf ◽  
Theo Witkamp ◽  
...  
2011 ◽  
Vol 7 ◽  
pp. S719-S719
Author(s):  
Geoffrey Kerchner ◽  
Gayle Deutsch ◽  
Michael Zeineh ◽  
Brian Rutt

2011 ◽  
Vol 7 ◽  
pp. S60-S61
Author(s):  
Geoffrey Kerchner ◽  
Gayle Deutsch ◽  
Michael Zeineh ◽  
Brian Rutt

2015 ◽  
Vol 45 (4) ◽  
pp. 1247-1256 ◽  
Author(s):  
Laura E.M. Wisse ◽  
Yael D. Reijmer ◽  
Annemieke ter Telgte ◽  
Hugo J. Kuijf ◽  
Alexander Leemans ◽  
...  

2012 ◽  
Author(s):  
Jennifer A. Eastman ◽  
Kristy S. Hwang ◽  
Sona Babakchanian ◽  
Nicole Chow ◽  
Leslie Ramirez ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Soo Hyun Cho ◽  
Sookyoung Woo ◽  
Changsoo Kim ◽  
Hee Jin Kim ◽  
Hyemin Jang ◽  
...  

AbstractTo characterize the course of Alzheimer’s disease (AD) over a longer time interval, we aimed to construct a disease course model for the entire span of the disease using two separate cohorts ranging from preclinical AD to AD dementia. We modelled the progression course of 436 patients with AD continuum and investigated the effects of apolipoprotein E ε4 (APOE ε4) and sex on disease progression. To develop a model of progression from preclinical AD to AD dementia, we estimated Alzheimer’s Disease Assessment Scale-Cognitive Subscale 13 (ADAS-cog 13) scores. When calculated as the median of ADAS-cog 13 scores for each cohort, the estimated time from preclinical AD to MCI due to AD was 7.8 years and preclinical AD to AD dementia was 15.2 years. ADAS-cog 13 scores deteriorated most rapidly in women APOE ε4 carriers and most slowly in men APOE ε4 non-carriers (p < 0.001). Our results suggest that disease progression modelling from preclinical AD to AD dementia may help clinicians to estimate where patients are in the disease course and provide information on variation in the disease course by sex and APOE ε4 status.


2021 ◽  
Vol 79 (1) ◽  
pp. 225-235
Author(s):  
Maya Arvidsson Rådestig ◽  
Johan Skoog ◽  
Henrik Zetterberg ◽  
Jürgen Kern ◽  
Anna Zettergren ◽  
...  

Background: We have previously shown that older adults with preclinical Alzheimer’s disease (AD) pathology in cerebrospinal fluid (CSF) had slightly worse performance in Mini-Mental State Examination (MMSE) than participants without preclinical AD pathology. Objective: We therefore aimed to compare performance on neurocognitive tests in a population-based sample of 70-year-olds with and without CSF AD pathology. Methods: The sample was derived from the population-based Gothenburg H70 Birth Cohort Studies in Sweden. Participants (n = 316, 70 years old) underwent comprehensive cognitive examinations, and CSF Aβ-42, Aβ-40, T-tau, and P-tau concentrations were measured. Participants were classified according to the ATN system, and according to their Clinical Dementia Rating (CDR) score. Cognitive performance was examined in the CSF amyloid, tau, and neurodegeneration (ATN) categories. Results: Among participants with CDR 0 (n = 259), those with amyloid (A+) and/or tau pathology (T+, N+) showed similar performance on most cognitive tests compared to participants with A-T-N-. Participants with A-T-N+ performed worse in memory (Supra span (p = 0.003), object Delayed (p = 0.042) and Immediate recall (p = 0.033)). Among participants with CDR 0.5 (n = 57), those with amyloid pathology (A+) scored worse in category fluency (p = 0.003). Conclusion: Cognitively normal participants with amyloid and/or tau pathology performed similarly to those without any biomarker evidence of preclinical AD in most cognitive domains, with the exception of slightly poorer memory performance in A-T-N+. Our study suggests that preclinical AD biomarkers are altered before cognitive decline.


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