scholarly journals “End-Stage” Neurofibrillary Tangle Pathology in Preclinical Alzheimer's Disease: Fact or Fiction?

2011 ◽  
Vol 25 (3) ◽  
pp. 445-453 ◽  
Author(s):  
Erin L. Abner ◽  
Richard J. Kryscio ◽  
Frederick A. Schmitt ◽  
Karen S. SantaCruz ◽  
Gregory A. Jicha ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangle ◽  
Preclinical Alzheimer’S Disease ◽  
Tangle Pathology ◽  
End Stage

scholarly journals Amyloid and tau imaging biomarkers explain cognitive decline from late middle-age

Brain ◽  
2019 ◽  
Vol 143 (1) ◽  
pp. 320-335 ◽  
Author(s):  
Tobey J Betthauser ◽  
Rebecca L Koscik ◽  
Erin M Jonaitis ◽  
Samantha L Allison ◽  
Karly A Cody ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Middle Age ◽  
Neurofibrillary Tangle ◽  
Imaging Biomarkers ◽  
Cognitive Tests ◽  
Preclinical Alzheimer’S Disease ◽  
Significant Group ◽  
Health Factors

Abstract This study investigated differences in retrospective cognitive trajectories between amyloid and tau PET biomarker stratified groups in initially cognitively unimpaired participants sampled from the Wisconsin Registry for Alzheimer’s Prevention. One hundred and sixty-seven initially unimpaired individuals (baseline age 59 ± 6 years; 115 females) were stratified by elevated amyloid-β and tau status based on 11C-Pittsburgh compound B (PiB) and 18F-MK-6240 PET imaging. Mixed effects models were used to determine if longitudinal cognitive trajectories based on a composite of cognitive tests including memory and executive function differed between biomarker groups. Secondary analyses investigated group differences for a variety of cross-sectional health and cognitive tests, and associations between 18F-MK-6240, 11C-PiB, and age. A significant group × age interaction was observed with post hoc comparisons indicating that the group with both elevated amyloid and tau pathophysiology were declining approximately three times faster in retrospective cognition compared to those with just one or no elevated biomarkers. This result was robust against various thresholds and medial temporal lobe regions defining elevated tau. Participants were relatively healthy and mostly did not differ between biomarker groups in health factors at the beginning or end of study, or most cognitive measures at study entry. Analyses investigating association between age, MK-6240 and PiB indicated weak associations between age and 18F-MK-6240 in tangle-associated regions, which were negligible after adjusting for 11C-PiB. Strong associations, particularly in entorhinal cortex, hippocampus and amygdala, were observed between 18F-MK-6240 and global 11C-PiB in regions associated with Braak neurofibrillary tangle stages I–VI. These results suggest that the combination of pathological amyloid and tau is detrimental to cognitive decline in preclinical Alzheimer’s disease during late middle-age. Within the Alzheimer’s disease continuum, middle-age health factors likely do not greatly influence preclinical cognitive decline. Future studies in a larger preclinical sample are needed to determine if and to what extent individual contributions of amyloid and tau affect cognitive decline. 18F-MK-6240 shows promise as a sensitive biomarker for detecting neurofibrillary tangles in preclinical Alzheimer’s disease.

scholarly journals Bridging Integrator 1 (BIN1) Protein Expression Increases in the Alzheimer's Disease Brain and Correlates with Neurofibrillary Tangle Pathology

2014 ◽  
Vol 42 (4) ◽  
pp. 1221-1227 ◽  
Author(s):  
Christopher J. Holler ◽  
Paulina R. Davis ◽  
Tina L. Beckett ◽  
Thomas L. Platt ◽  
Robin L. Webb ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Protein Expression ◽  
Neurofibrillary Tangle ◽  
Tangle Pathology

P3-407: PATTERN OF CORTICAL THINNING AND SHAPE VARIABILITY RELATED TO ALZHEIMER'S DISEASE IN REGIONS AFFECTED BY EARLIEST NEUROFIBRILLARY TANGLE PATHOLOGY

2006 ◽  
Vol 14 (7S_Part_23) ◽  
pp. P1259-P1260
Author(s):  
Long Xie ◽  
Laura Wisse ◽  
Sandhitsu R. Das ◽  
Ranjit Ittyerah ◽  
Paul A. Yushkevich ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangle ◽  
Cortical Thinning ◽  
Tangle Pathology

scholarly journals Amyloid Plaque and Neurofibrillary Tangle Pathology in a Regulatable Mouse Model of Alzheimer's Disease

2008 ◽  
Vol 173 (3) ◽  
pp. 762-772 ◽  
Author(s):  
Jennifer B. Paulson ◽  
Martin Ramsden ◽  
Colleen Forster ◽  
Mathew A. Sherman ◽  
Eileen McGowan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Neurofibrillary Tangle ◽  
Amyloid Plaque ◽  
Model Of Alzheimer’S Disease ◽  
Tangle Pathology

IC-P-173: PATTERN OF CORTICAL THINNING AND SHAPE VARIABILITY RELATED TO ALZHEIMER'S DISEASE IN REGIONS AFFECTED BY EARLIEST NEUROFIBRILLARY TANGLE PATHOLOGY

2006 ◽  
Vol 14 (7S_Part_2) ◽  
pp. P146-P148 ◽  
Author(s):  
Long Xie ◽  
Laura Wisse ◽  
Sandhitsu R. Das ◽  
Ranjit Ittyerah ◽  
Paul A. Yushkevich ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangle ◽  
Cortical Thinning ◽  
Tangle Pathology

3D Mapping of Verbal Memory in Clinical and Preclinical Alzheimer's Disease

2012 ◽  
Author(s):  
Jennifer A. Eastman ◽  
Kristy S. Hwang ◽  
Sona Babakchanian ◽  
Nicole Chow ◽  
Leslie Ramirez ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Verbal Memory ◽  
3D Mapping ◽  
Preclinical Alzheimer’S Disease

scholarly journals Disease progression modelling from preclinical Alzheimer’s disease (AD) to AD dementia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Soo Hyun Cho ◽  
Sookyoung Woo ◽  
Changsoo Kim ◽  
Hee Jin Kim ◽  
Hyemin Jang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Disease Progression ◽  
Disease Assessment ◽  
Time Interval ◽  
Disease Course ◽  
Preclinical Alzheimer’S Disease ◽  
Apoe Ε4 ◽  
Preclinical Ad ◽  
Cognitive Subscale

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.

scholarly journals Cognitive Performance and Cerebrospinal Fluid Markers in Preclinical Alzheimer’s Disease: Results from the Gothenburg H70 Birth Cohort Studies

2021 ◽  
Vol 79 (1) ◽  
pp. 225-235
Author(s):  
Maya Arvidsson Rådestig ◽  
Johan Skoog ◽  
Henrik Zetterberg ◽  
Jürgen Kern ◽  
Anna Zettergren ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cerebrospinal Fluid ◽  
Cohort Studies ◽  
Cognitive Performance ◽  
Birth Cohort ◽  
Population Based ◽  
Tau Pathology ◽  
Preclinical Alzheimer’S Disease ◽  
Preclinical Ad

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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