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000277978 1001_ $$0P:(DE-2719)9001560$$aOeckl, Patrick$$b0$$eFirst author$$udzne
000277978 245__ $$aEarly increase of the synaptic blood marker β-synuclein in asymptomatic autosomal dominant Alzheimer's disease.
000277978 260__ $$aHoboken, NJ$$bWiley$$c2025
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000277978 520__ $$aβ-synuclein is a promising blood marker to track synaptic degeneration in Alzheimer's disease (AD) but changes in preclinical AD are unclear.We investigated serum β-synuclein in 69 cognitively unimpaired mutation non-carriers, 78 cognitively unimpaired AD mutation carriers (asymptomatic AD), and 31 symptomatic mutation carriers from the Dominantly Inherited Alzheimer Network.β-synuclein levels were already higher in asymptomatic AD mutation carriers compared to non-carriers and highest in symptomatic carriers. Longitudinal trajectories and correlation analyses indicated that β-synuclein levels start to rise after amyloid deposition preceding axonal degeneration, brain atrophy and hypometabolism, and cognitive decline. β-synuclein levels were associated with cognitive impairment and gradually increased with declining cognition.Our study supports the use of blood β-synuclein to track synaptic changes in preclinical AD and as a surrogate marker for cognitive impairment which might be used in early diagnosis and to support patient selection and monitoring of treatment effects in clinical trials.Blood β-synuclein levels were already higher in asymptomatic Alzheimer's disease (AD) mutation carriers. Blood β-synuclein levels were highest in symptomatic AD mutation carriers. Blood β-synuclein levels start to rise 11 years before symptom onset. Rise of β-synuclein precedes axonal degeneration, brain atrophy, and cognitive decline. β-synuclein levels gradually increased with declining cognition.
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000277978 650_7 $$2Other$$aasymptomatic mutation carriers
000277978 650_7 $$2Other$$aautosomal dominant Alzheimer´s disease
000277978 650_7 $$2Other$$ablood biomarker
000277978 650_7 $$2Other$$apreclinical Alzheimer´s disease
000277978 650_7 $$2Other$$asynaptic degeneration
000277978 650_7 $$2Other$$aβ‐synuclein
000277978 650_7 $$2NLM Chemicals$$aBiomarkers
000277978 650_7 $$2NLM Chemicals$$abeta-Synuclein
000277978 650_2 $$2MeSH$$aHumans
000277978 650_2 $$2MeSH$$aAlzheimer Disease: genetics
000277978 650_2 $$2MeSH$$aAlzheimer Disease: blood
000277978 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000277978 650_2 $$2MeSH$$aMale
000277978 650_2 $$2MeSH$$aFemale
000277978 650_2 $$2MeSH$$aBiomarkers: blood
000277978 650_2 $$2MeSH$$aMiddle Aged
000277978 650_2 $$2MeSH$$aMutation: genetics
000277978 650_2 $$2MeSH$$abeta-Synuclein: blood
000277978 650_2 $$2MeSH$$aAged
000277978 650_2 $$2MeSH$$aBrain: pathology
000277978 650_2 $$2MeSH$$aBrain: diagnostic imaging
000277978 650_2 $$2MeSH$$aSynapses
000277978 650_2 $$2MeSH$$aCognitive Dysfunction: blood
000277978 650_2 $$2MeSH$$aLongitudinal Studies
000277978 693__ $$0EXP:(DE-2719)DIAN-20090101$$5EXP:(DE-2719)DIAN-20090101$$eLongitudinal Study on Dominantly Inherited Alzheimer's Disease$$x0
000277978 7001_ $$aMayer, Benjamin$$b1
000277978 7001_ $$aBateman, Randall J$$b2
000277978 7001_ $$aDay, Gregory S$$b3
000277978 7001_ $$aFox, Nick C$$b4
000277978 7001_ $$aHuey, Edward D$$b5
000277978 7001_ $$aIbanez, Laura$$b6
000277978 7001_ $$aIkeuchi, Takeshi$$b7
000277978 7001_ $$0P:(DE-2719)2000010$$aJucker, Mathias$$b8$$udzne
000277978 7001_ $$0P:(DE-HGF)0$$aLee, Jae-Hong$$b9
000277978 7001_ $$0P:(DE-2719)2811659$$aLevin, Johannes$$b10$$udzne
000277978 7001_ $$aLlibre-Guerra, Jorge J$$b11
000277978 7001_ $$aLopera, Francisco$$b12
000277978 7001_ $$aMcDade, Eric$$b13
000277978 7001_ $$aMorris, John C$$b14
000277978 7001_ $$aNiimi, Yoshiki$$b15
000277978 7001_ $$aRoh, Jee Hoon$$b16
000277978 7001_ $$aSánchez-Valle, Raquel$$b17
000277978 7001_ $$aSchofield, Peter R$$b18
000277978 7001_ $$00000-0003-4273-4267$$aOtto, Markus$$b19
000277978 7001_ $$aNetwork, Dominantly Inherited Alzheimer$$b20$$eCollaboration Author
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