Home > Publications Database > Florbetapir PET-assessed demyelination is associated with faster tau accumulation in an APOE ε4-dependent manner. > print

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037 _ _ |a DZNE-2024-00201
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Rubinski, Anna
|b 0
245 _ _ |a Florbetapir PET-assessed demyelination is associated with faster tau accumulation in an APOE ε4-dependent manner.
260 _ _ |a Heidelberg [u.a.]
|c 2024
|b Springer-Verl.
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520 _ _ |a The main objectives were to test whether (1) a decrease in myelin is associated with enhanced rate of fibrillar tau accumulation and cognitive decline in Alzheimer's disease, and (2) whether apolipoprotein E (APOE) ε4 genotype is associated with worse myelin decrease and thus tau accumulation.To address our objectives, we repurposed florbetapir-PET as a marker of myelin in the white matter (WM) based on previous validation studies showing that beta-amyloid (Aβ) PET tracers bind to WM myelin. We assessed 43 Aβ-biomarker negative (Aβ-) cognitively normal participants and 108 Aβ+ participants within the AD spectrum with florbetapir-PET at baseline and longitudinal flortaucipir-PET as a measure of fibrillar tau (tau-PET) over ~ 2 years. In linear regression analyses, we tested florbetapir-PET in the whole WM and major fiber tracts as predictors of tau-PET accumulation in a priori defined regions of interest (ROIs) and fiber-tract projection areas. In mediation analyses we tested whether tau-PET accumulation mediates the effect of florbetapir-PET in the whole WM on cognition. Finally, we assessed the role of myelin alteration on the association between APOE and tau-PET accumulation.Lower florbetapir-PET in the whole WM or at a given fiber tract was predictive of faster tau-PET accumulation in Braak stages or the connected grey matter areas in Aβ+ participants. Faster tau-PET accumulation in higher cortical brain areas mediated the association between a decrease in florbetapir-PET in the WM and a faster rate of decline in global cognition and episodic memory. APOE ε4 genotype was associated with a worse decrease in the whole WM florbetapir-PET and thus enhanced tau-PET accumulation.Myelin alterations are associated in an APOE ε4 dependent manner with faster tau progression and cognitive decline, and may therefore play a role in the etiology of AD.
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650 _ 7 |a APOE
|2 Other
650 _ 7 |a Florbetapir-PET
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650 _ 7 |a Myelin
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650 _ 7 |a Tau
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650 _ 7 |a Apolipoprotein E4
|2 NLM Chemicals
650 _ 7 |a florbetapir
|0 6867Q6IKOD
|2 NLM Chemicals
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Apolipoproteins E
|2 NLM Chemicals
650 _ 7 |a tau Proteins
|2 NLM Chemicals
650 _ 7 |a Aniline Compounds
|2 NLM Chemicals
650 _ 7 |a Ethylene Glycols
|2 NLM Chemicals
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Apolipoprotein E4: genetics
|2 MeSH
650 _ 2 |a Alzheimer Disease: diagnostic imaging
|2 MeSH
650 _ 2 |a Alzheimer Disease: genetics
|2 MeSH
650 _ 2 |a Alzheimer Disease: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Apolipoproteins E
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Cognitive Dysfunction: metabolism
|2 MeSH
650 _ 2 |a Demyelinating Diseases: metabolism
|2 MeSH
650 _ 2 |a tau Proteins: metabolism
|2 MeSH
650 _ 2 |a Positron-Emission Tomography
|2 MeSH
650 _ 2 |a Aniline Compounds
|2 MeSH
650 _ 2 |a Ethylene Glycols
|2 MeSH
700 1 _ |a Dewenter, Anna
|b 1
700 1 _ |a Zheng, Lukai
|b 2
700 1 _ |a Franzmeier, Nicolai
|b 3
700 1 _ |a Stephenson, Henry
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700 1 _ |a Deming, Yuetiva
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700 1 _ |a Duering, Marco
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700 1 _ |a Gesierich, Benno
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700 1 _ |a Denecke, Jannis
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700 1 _ |a Pham, An-Vi
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700 1 _ |a Bendlin, Barbara
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700 1 _ |a Ewers, Michael
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700 1 _ |a Initiative, Alzheimer’s Disease Neuroimaging
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773 _ _ |a 10.1007/s00259-023-06530-8
|g Vol. 51, no. 4, p. 1035 - 1049
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|t European journal of nuclear medicine and molecular imaging
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