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000276276 1001_ $$0P:(DE-2719)9001307$$aGrazia, Alice$$b0$$udzne
000276276 245__ $$aBasal forebrain global functional connectivity is preserved in asymptomatic presenilin-1 E280A mutation carriers: Results from the Colombia cohort.
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000276276 520__ $$aImaging studies showed early atrophy of the cholinergic basal forebrain in prodromal sporadic Alzheimer's disease and reduced posterior basal forebrain functional connectivity in amyloid positive individuals with subjective cognitive decline. Similar investigations in familial cases of Alzheimer's disease are still lacking.To test whether presenilin-1 E280A mutation carriers have reduced basal forebrain functional connectivity and whether this is linked to amyloid pathology.This is a cross-sectional study that analyzes baseline functional imaging data.We obtained data from the Colombia cohort Alzheimer's Prevention Initiative Autosomal-Dominant Alzheimer's Disease Trial.We analyzed data from 215 asymptomatic subjects carrying the presenilin-1 E280A mutation [64% female; 147 carriers (M = 35 years), 68 noncarriers (M = 40 years)].We extracted functional magnetic resonance imaging data using seed-based connectivity analysis to examine the anterior and posterior subdivisions of the basal forebrain. Subsequently, we performed a Bayesian Analysis of Covariance to assess the impact of carrier status on functional connectivity in relation to amyloid positivity. For comparison, we also investigated hippocampus connectivity.We found no effect of carrier status on anterior (Bayesian Factor10 = 1.167) and posterior basal forebrain connectivity (Bayesian Factor10 = 0.033). In carriers, we found no association of amyloid positivity with basal forebrain connectivity.We falsified the hypothesis of basal forebrain connectivity reduction in preclinical mutation carriers with amyloid pathology. If replicated, these findings may not only confirm a discrepancy between familial and sporadic Alzheimer's disease, but also suggest new potential targets for future treatments.
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000276276 650_7 $$2Other$$aBasal forebrain
000276276 650_7 $$2Other$$aBayesian analysis
000276276 650_7 $$2Other$$aColombia cohort
000276276 650_7 $$2Other$$aPSEN1 E280A
000276276 650_7 $$2Other$$aResting-state fMRI
000276276 650_7 $$2NLM Chemicals$$aPresenilin-1
000276276 650_7 $$2NLM Chemicals$$aPSEN1 protein, human
000276276 650_2 $$2MeSH$$aHumans
000276276 650_2 $$2MeSH$$aPresenilin-1: genetics
000276276 650_2 $$2MeSH$$aFemale
000276276 650_2 $$2MeSH$$aColombia
000276276 650_2 $$2MeSH$$aMale
000276276 650_2 $$2MeSH$$aCross-Sectional Studies
000276276 650_2 $$2MeSH$$aAdult
000276276 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000276276 650_2 $$2MeSH$$aMutation
000276276 650_2 $$2MeSH$$aBasal Forebrain: diagnostic imaging
000276276 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000276276 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000276276 650_2 $$2MeSH$$aAlzheimer Disease: physiopathology
000276276 650_2 $$2MeSH$$aHeterozygote
000276276 650_2 $$2MeSH$$aCohort Studies
000276276 650_2 $$2MeSH$$aMiddle Aged
000276276 7001_ $$0P:(DE-2719)2810283$$aDyrba, Martin$$b1$$udzne
000276276 7001_ $$aPomara, Nunzio$$b2
000276276 7001_ $$0P:(DE-2719)2814291$$aTemp, Anna G$$b3
000276276 7001_ $$0P:(DE-2719)2810708$$aGrothe, Michel J$$b4
000276276 7001_ $$0P:(DE-2719)2000026$$aTeipel, Stefan J$$b5$$eLast author$$udzne
000276276 7001_ $$aInitiative, Alzheimer's Prevention$$b6$$eCollaboration Author
000276276 773__ $$0PERI:(DE-600)2782183-3$$a10.1016/j.tjpad.2024.100030$$gVol. 12, no. 2, p. 100030 -$$n2$$p100030$$tThe journal of prevention of Alzheimer's disease$$v12$$x2274-5807$$y2025
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