Key result
Non-AD pathologic change is linked to faster cognitive decline and disease progression versus normal biomarkers.
Why the study?
The study aimed to evaluate long-term clinical and cognitive trajectories of older adults without dementia with non-Alzheimer's disease pathologic change compared to those with normal biomarkers and Alzheimer's disease pathophysiology.
Do older adults with non-AD pathologic change have faster cognitive decline compared to those with normal AD biomarkers?
Cohort
Do older adults with non-AD pathologic change have faster cognitive decline compared to those with normal AD biomarkers?
Older adults with non-AD pathologic change experience faster cognitive decline than those with normal biomarkers, though the presence of amyloid further accelerates this decline.
May inform prognosis via non-AD biomarkers; leaves open whether targeting tauopathy or neurodegeneration improves outcomes.
Based on the 'AT(N)' system, individuals with normal amyloid biomarkers but abnormal tauopathy or neurodegeneration biomarkers are classified as non-Alzheimer's disease (AD) pathologic change. This study aimed to assess the long-term clinical and cognitive trajectories of individuals with non-AD pathologic change among older adults without dementia, comparing them to those with normal AD biomarkers and AD pathophysiology. Analyzing Alzheimer's Disease Neuroimaging Initiative data, we evaluated clinical outcomes and conversion risk longitudinally using mixed effects models and multivariate Cox proportional hazard models. We found that compared to individuals with A-T-N-, those with abnormal tauopathy or neurodegeneration biomarkers (A-T + N-, A-T-N + , and A-T + N + ) had a faster rate of cognitive decline and disease progression. Individuals with A-T + N + had a faster rate of decline than those with A-T + N-. Additionally, in individuals with the same baseline tauopathy and neurodegeneration biomarker status, the presence of baseline amyloid could accelerate cognitive decline and clinical progression. These findings provide a foundation for future studies on non-AD pathologic change and its comparison with AD pathophysiology.
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Li et al. (2023) conducted a cohort in Non-AD pathologic change in older adults without dementia. Non-AD pathologic change (abnormal tauopathy or neurodegeneration) vs. Normal AD biomarkers (A-T-N-) was evaluated on Clinical outcomes and conversion risk (cognitive decline and disease progression). Older adults with non-AD pathologic change (abnormal tauopathy or neurodegeneration without amyloid) had faster cognitive decline and disease progression compared to those with normal biomarkers.
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