scholarly journals Tau pathology in posterior DMN is related to aberrant SN‐DMN network connectivity in atypical Alzheimer’s disease

2020 ◽  
Vol 16 (S1) ◽  
Author(s):  
Deepti Putcha ◽  
Ryan Eckbo ◽  
Alexandra Touroutoglou ◽  
Brad C. Dickerson ◽  
Jessica A. Collins
2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Ryan Eckbo ◽  
Brad C. Dickerson ◽  
Nikos Makris ◽  
Jessica A. Collins

2021 ◽  
Author(s):  
Sophie Dautricourt ◽  
Robin Flores ◽  
Brigitte Landeau ◽  
Géraldine Poisnel ◽  
Matthieu Vanhoutte ◽  
...  

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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