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000282473 037__ $$aDZNE-2025-01296
000282473 041__ $$aEnglish
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000282473 1001_ $$aKuzu, Taylan D$$b0
000282473 245__ $$aApraxic deficits in Alzheimer's disease are associated with altered dynamic connectivity in praxis-related networks.
000282473 260__ $$aAmsterdam [u.a.]$$bElsevier Science$$c2026
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000282473 520__ $$aApraxia is a common symptom in Alzheimer's disease (AD) that reduces autonomy and quality of life. However, the neural basis underlying apraxia in AD, for example, reflected by functional connectivity (FC) alterations, remains unexplored. We investigated static and dynamic FC using resting-state functional imaging in 14 patients with biomarker-confirmed AD pathology and 14 matched healthy participants. FC was estimated as average (static) and short-term (dynamic) connectivity strengths between motor- and praxis-related functional networks. Recurring connectivity patterns were clustered into dynamic states to compute temporal connectivity measures. Connectivity measures were used for correlations with apraxic deficits. In AD patients, static connectivity between visual and inferior parietal networks correlated with apraxic imitation (r = 0.762, PFDR = 0.043) and arm/hand gesture deficits (r = 0.848, PFDR = 0.020), while dynamic connectivity between these networks correlated with apraxic imitation deficits (r = 0.851, PFDR = 0.020). Dynamic FC analysis revealed a segregated and integrated state. AD patients spent more time overall (fraction time, PFDR < 0.001) and remained longer without switching (dwell time, PFDR = 0.004) in the segregated state. Both fraction (ρ = -0.858, PFDR = 0.015) and dwell time (ρ = -0.914, PFDR = 0.003) correlated with apraxic imitation deficits. Connectivity strengths between visual and inferior parietal networks and fraction time in the segregated state predicted apraxic imitation deficits (adjusted R2 = 0.782, P < 0.001). We conclude that apraxia in AD patients is associated with altered FC in praxis-related networks, suggesting FC as a potential clinical indicator for predicting motor-cognitive deficits.
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000282473 650_7 $$2Other$$aAging
000282473 650_7 $$2Other$$aAlzheimer’s disease
000282473 650_7 $$2Other$$aCologne apraxia screening (KAS)
000282473 650_7 $$2Other$$aFunctional magnetic resonance imaging
000282473 650_7 $$2Other$$aMotor system
000282473 650_7 $$2Other$$aPraxis
000282473 650_7 $$2Other$$aResting-state
000282473 650_2 $$2MeSH$$aHumans
000282473 650_2 $$2MeSH$$aAlzheimer Disease: complications
000282473 650_2 $$2MeSH$$aAlzheimer Disease: physiopathology
000282473 650_2 $$2MeSH$$aAlzheimer Disease: psychology
000282473 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000282473 650_2 $$2MeSH$$aMale
000282473 650_2 $$2MeSH$$aFemale
000282473 650_2 $$2MeSH$$aAged
000282473 650_2 $$2MeSH$$aApraxias: etiology
000282473 650_2 $$2MeSH$$aApraxias: physiopathology
000282473 650_2 $$2MeSH$$aApraxias: diagnostic imaging
000282473 650_2 $$2MeSH$$aNerve Net: physiopathology
000282473 650_2 $$2MeSH$$aAged, 80 and over
000282473 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000282473 650_2 $$2MeSH$$aMiddle Aged
000282473 650_2 $$2MeSH$$aBrain: physiopathology
000282473 7001_ $$aBrinkmann, Elena$$b1
000282473 7001_ $$aBonkhoff, Anna K$$b2
000282473 7001_ $$aWunderle, Veronika$$b3
000282473 7001_ $$aBischof, Gérard N$$b4
000282473 7001_ $$aGiehl, Kathrin$$b5
000282473 7001_ $$aSchmieschek, Maximilian H T$$b6
000282473 7001_ $$aOnur, Oezguer A$$b7
000282473 7001_ $$0P:(DE-2719)2000032$$aJessen, Frank$$b8$$udzne
000282473 7001_ $$aFink, Gereon R$$b9
000282473 7001_ $$0P:(DE-2719)2811239$$aDrzezga, Alexander$$b10$$udzne
000282473 7001_ $$aWeiss, Peter H$$b11
000282473 773__ $$0PERI:(DE-600)1498414-3$$a10.1016/j.neurobiolaging.2025.09.007$$gVol. 157, p. 36 - 47$$p36 - 47$$tNeurobiology of aging$$v157$$x0197-4580$$y2026
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