scholarly journals Cardiorespiratory fitness mitigates brain atrophy and cognitive decline in preclinical Alzheimer’s disease

2021 ◽  
Vol 17 (S10) ◽  
Author(s):  
Ryan J Dougherty ◽  
Erin M Jonaitis ◽  
Sterling C Johnson ◽  
Ozioma C Okonkwo ◽  
Dane B Cook
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Cardiorespiratory Fitness ◽  
Brain Atrophy ◽  
Preclinical Alzheimer’S Disease

scholarly journals Cardiorespiratory fitness mitigates brain atrophy and cognitive decline in adults at risk for Alzheimer's disease

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Ryan J. Dougherty ◽  
Erin M. Jonaitis ◽  
Julian M. Gaitán ◽  
Sarah R. Lose ◽  
Brandon M. Mergen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
At Risk ◽  
Cognitive Decline ◽  
Cardiorespiratory Fitness ◽  
Brain Atrophy

IC-P-134: Differentiating Preclinical Alzheimer’s Disease from Normal Aging: The Effects of Age and Amyloid on Cognitive Decline Over 3.5 Years

2016 ◽  
Vol 12 ◽  
pp. P100-P100
Author(s):  
Michelle E. Farrell ◽  
Kristen M. Kennedy ◽  
Karen M. Rodrigue ◽  
Gagan S. Wig ◽  
Gérard N. Bischof ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Normal Aging ◽  
Preclinical Alzheimer’S Disease

Preclinical Alzheimer's disease

2014 ◽  
Vol 24 (2) ◽  
pp. 117-121
Author(s):  
P Gil-Gregorio ◽  
R Yubero-Pancorbo
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Diagnostic Criteria ◽  
Stage I ◽  
Disease Stage ◽  
Synaptic Dysfunction ◽  
Preclinical Alzheimer’S Disease ◽  
Cerebral Amyloidosis ◽  
Three Stages

SummaryRecently, diagnostic criteria for preclinical Alzheimer's disease have been proposed. These describe and define three stages of disease. Stage I is focused on asymptomatic cerebral amyloidosis. Stage II includes evidence of synaptic dysfunction and/or early degeneration. Finally, stage III of the disease is characterized by the beginning of cognitive decline.

scholarly journals Concentration-Dependent Activity of Hydromethylthionine on Cognitive Decline and Brain Atrophy in Mild to Moderate Alzheimer’s Disease

2019 ◽  
Vol 72 (3) ◽  
pp. 931-946 ◽  
Author(s):  
Bjoern O. Schelter ◽  
Helen Shiells ◽  
Thomas C. Baddeley ◽  
Christopher M. Rubino ◽  
Harish Ganesan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Brain Atrophy ◽  
Dependent Activity

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.

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