Abstract
Antemortem tau positron emission tomography imaging suggests elevated tau pathology in autosomal dominant versus late‐onset Alzheimer’s disease at equivalent clinical stages, but does not implicate the specific tau pathologies responsible. Here we made stereological measurements of tau neurofibrillary tangles, neuritic plaques, and neuropil threads and found compared to late‐onset Alzheimer’s disease, autosomal dominant Alzheimer’s disease showed even greater tangle and thread burdens. Regional tau burden resembled that observed in tau imaging of a separate cohort at earlier clinical stages. Finally, our results suggest tau imaging measures total tau burden in Alzheimer’s disease, composed predominantly of tangle and thread pathology.
Highlights
Antemortem tau positron emission tomography (PET) imaging suggests elevated tau pathology in autosomal dominant (ADAD) versus late-onset Alzheimer’s disease (LOAD) at equivalent clinical stages
Previous work quantitatively comparing AD tau pathology with PET imaging has typically been performed in a single individual,[4,5] and it is not known whether these results generalize, given the disease heterogeneity of both ADAD6 and LOAD7
To investigate which tau pathologies contribute to elevated 18F-flortaucipir binding in ADAD versus LOAD cohorts, we made stereological measurements of three major features of AD tau pathology: neurofibrillary tangles, neuritic plaques, and neuropil threads
Summary
Antemortem tau positron emission tomography (PET) imaging suggests elevated tau pathology in autosomal dominant (ADAD) versus late-onset Alzheimer’s disease (LOAD) at equivalent clinical stages. Compared to LOAD, ADAD has shown elevated 18F-flortaucipir[1] radioligand binding in prefrontal, premotor, and inferior parietal cortices,[2] as well as precuneus and lateral parietal cortices.[3] PET imaging does not implicate specific tau pathologies responsible. Previous work quantitatively comparing AD tau pathology with PET imaging has typically been performed in a single individual,[4,5] and it is not known whether these results generalize, given the disease heterogeneity of both ADAD6 and LOAD7. To investigate which tau pathologies contribute to elevated 18F-flortaucipir binding in ADAD versus LOAD cohorts, we made stereological measurements of three major features of AD tau pathology: neurofibrillary tangles, neuritic plaques, and neuropil threads
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