Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
Higher plasma β-synuclein indicates early synaptic degeneration in Alzheimer's disease.
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Oeckl Patrick, Janelidze Shorena, Halbgebauer Steffen, Stomrud Erik, Palmqvist Sebastian, Otto Markus, Hansson Oskar
Аннотация
INTRODUCTION: β-Synuclein is an emerging synaptic blood biomarker for Alzheimer's disease (AD) but differences in β-synuclein levels in preclinical AD and its association with amyloid and tau pathology have not yet been studied.
METHODS: We measured plasma β-synuclein levels in cognitively unimpaired individuals with positive Aβ-PET (i.e., preclinical AD, N = 48) or negative Aβ-PET (N = 61), Aβ-positive patients with mild cognitive impairment (MCI, N = 36), and Aβ-positive AD dementia (N = 85). Amyloid (A) and tau (T) pathology were assessed by [18 F]flutemetamol and [18 F]RO948 PET.
RESULTS: Plasma β-synuclein levels were higher in preclinical AD and even higher in MCI and AD dementia. Stratification according to amyloid/tau pathology revealed higher β-synuclein in A+ T- and A+ T+ subjects compared with A- T- . Plasma β-synuclein levels were related to tau and Aβ pathology and associated with temporal cortical thinning and cognitive impairment.
DISCUSSION: Our data indicate that plasma β-synuclein might track synaptic dysfunction, even during the preclinical stages of AD.
HIGHLIGHTS: Plasma β-synuclein is already higher in preclinical AD. Plasma β-synuclein is higher in MCI and AD dementia than in preclinical AD. Aβ- and tau-PET SUVRs are associated with plasma β-synuclein levels. Plasma β-synuclein is already higher in tau-PET negative subjects. Plasma β-synuclein is related to temporal cortical atrophy and cognitive impairment.
METHODS: We measured plasma β-synuclein levels in cognitively unimpaired individuals with positive Aβ-PET (i.e., preclinical AD, N = 48) or negative Aβ-PET (N = 61), Aβ-positive patients with mild cognitive impairment (MCI, N = 36), and Aβ-positive AD dementia (N = 85). Amyloid (A) and tau (T) pathology were assessed by [18 F]flutemetamol and [18 F]RO948 PET.
RESULTS: Plasma β-synuclein levels were higher in preclinical AD and even higher in MCI and AD dementia. Stratification according to amyloid/tau pathology revealed higher β-synuclein in A+ T- and A+ T+ subjects compared with A- T- . Plasma β-synuclein levels were related to tau and Aβ pathology and associated with temporal cortical thinning and cognitive impairment.
DISCUSSION: Our data indicate that plasma β-synuclein might track synaptic dysfunction, even during the preclinical stages of AD.
HIGHLIGHTS: Plasma β-synuclein is already higher in preclinical AD. Plasma β-synuclein is higher in MCI and AD dementia than in preclinical AD. Aβ- and tau-PET SUVRs are associated with plasma β-synuclein levels. Plasma β-synuclein is already higher in tau-PET negative subjects. Plasma β-synuclein is related to temporal cortical atrophy and cognitive impairment.