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000285017 037__ $$aDZNE-2026-00143
000285017 041__ $$aEnglish
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000285017 1001_ $$0P:(DE-2719)9002484$$aHoenig, Merle C$$b0
000285017 245__ $$aModifiable Factors Associated with the Longitudinal Increase and Spatial Extent of Tau Pathology in Alzheimer Disease.
000285017 260__ $$aNew York, NY$$bSoc.$$c2026
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000285017 520__ $$aThere are 14 modifiable factors that are associated with a significantly lower risk of dementia. We tested the interactive effect of modifiable factors, genetic determinants, and initial pathologic burden on the spatial progression and local amplification of tau pathology. Methods: In total, 162 amyloid-positive individuals were included, for whom longitudinal [18F]AV-1451 PET scans, baseline information on global amyloid burden, ApoE4 status, body mass index (BMI), hypertension, education, neuropsychiatric symptom severity, and demographic information were available in the Alzheimer Disease Neuroimaging Initiative. All [18F]AV-1451 scans were intensity-standardized (reference: inferior cerebellum), z-transformed (control sample: 147 amyloid-negative subjects), thresholded (z score, >1.96), and converted to volume maps. Longitudinal tau changes were then assessed in terms of tau spatial extent (i.e., newly affected volume at follow-up) and tau level rise (i.e., tau increase in previously affected volume). These 2 measures were entered as dependent variables in linear mixed-effects models, including baseline modifiable risk factors (BMI, education, hypertension, neuropsychiatric symptom severity), global amyloid, tau volume or tau burden, ApoE4 status, clinical stage, sex, and age as predictors. Next, we tested the interactive effects between baseline amyloid or tau burden with the 4 modifiable factors on tau extent or tau level rise, respectively. Results: Greater tau extent was linked to higher BMI (β = 0.002; 95% CI, 0.0003-0.003), ApoE4 status (β = 0.024; 95% CI, 0.001-0.046), and baseline tau volume (β = 0.207; 95% CI, 0.107-0.308) across groups. In terms of tau level rise, we observed that absence of hypertension (β = 0.295; 95% CI, -0.477 to -0.114), dementia group (β = 0.305; 95% CI, 0.088-0.522), and BMI (β = 0.011; 95% CI, 0.00004-0.022) were linked to increased tau burden. A load-dependent effect of baseline amyloid and tau volume/burden was found for both tau extent (β = -0.005; 95% CI, -0.008 to -0.002) and tau level rise (β = -0.003; 95% CI, -0.005 to -0.001). Higher amyloid and BMI (β = 0.001; 95% CI, 0.0004-0.001) and lower education and higher tau burden (β = -0.035; 95% CI, -0.064 to -0.006) were linked to greater tau level rise. Conclusion: Education, BMI, and hypertension differentially influence tau's spatial extent and increase by its interaction with initial pathologic burden. Timely modification of these factors may overall slow tau progression.
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000285017 650_7 $$2Other$$a(non-)modifiable risk factors
000285017 650_7 $$2Other$$aspatial extent
000285017 650_7 $$2Other$$atau pathology
000285017 650_7 $$2NLM Chemicals$$atau Proteins
000285017 650_7 $$0J09QS3Z3WB$$2NLM Chemicals$$a7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole
000285017 650_7 $$2NLM Chemicals$$aCarbolines
000285017 650_2 $$2MeSH$$aHumans
000285017 650_2 $$2MeSH$$atau Proteins: metabolism
000285017 650_2 $$2MeSH$$aMale
000285017 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000285017 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000285017 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000285017 650_2 $$2MeSH$$aFemale
000285017 650_2 $$2MeSH$$aAged
000285017 650_2 $$2MeSH$$aLongitudinal Studies
000285017 650_2 $$2MeSH$$aPositron-Emission Tomography
000285017 650_2 $$2MeSH$$aCarbolines
000285017 650_2 $$2MeSH$$aAged, 80 and over
000285017 650_2 $$2MeSH$$aMiddle Aged
000285017 650_2 $$2MeSH$$aBody Mass Index
000285017 650_2 $$2MeSH$$aRisk Factors
000285017 7001_ $$aDzialas, Verena$$b1
000285017 7001_ $$0P:(DE-2719)9000532$$aDoering, Elena$$b2$$udzne
000285017 7001_ $$0P:(DE-2719)9002485$$aBischof, Gérard N$$b3
000285017 7001_ $$0P:(DE-2719)2812285$$aEimeren, Thilo$$b4$$udzne
000285017 7001_ $$0P:(DE-2719)2811239$$aDrzezga, Alexander$$b5$$eLast author$$udzne
000285017 7001_ $$aInitiative, Alzheimer’s Disease Neuroimaging$$b6$$eCollaboration Author
000285017 773__ $$0PERI:(DE-600)2040222-3$$a10.2967/jnumed.125.270593$$gVol. 67, no. 2, p. jnumed.125.270593 -$$n2$$p291-296$$tJournal of nuclear medicine$$v67$$x0097-9058$$y2026
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