Abstract

AbstractBackgroundAlzheimer’s disease (AD) affects nearly the entirety of the Down’s Syndrome population (DS) with a prevalence of 75% by the time they reach their 60s. The early symptoms of dementia in DS may reflect frontal lobe vulnerability to amyloid deposition. The Mismatch Negativity (MMN) is a frontocentral event‐related potential (ERP) component elicited by auditory violations. Predictive coding postulates that the brain creates neural predictions about future events by compiling statistical regularities from incoming stimuli. Within the MMN network, the MMN results from the failure of higher frontotemporal nodes to predict the incoming sensory input, which results in changes of coupling between the sensory and the frontotemporal cortices. In the typically developing (TD) population, the MMN response has been found to decrease with age. With a cross‐sectional and longitudinal study, we assessed whether the MMN reflects premature neurological aging in DS and whether it predicts cognitive decline one year later.MethodThe MMN ERP and the MMN Global‐Field Power (GFP) were elicited with an auditory global‐local task and recorded with high‐density EEG in 36 DS adults and in 39 age‐matched TD controls. Cognitive impairment was measured in DS with the neuropsychological battery CAMCOG‐DS. One year later, 34 adults with DS underwent a follow‐up administration of the CAMCOG‐DS. Linear models tested whether the MMN predicted age in the two groups. Linear and curvilinear models tested whether the MMN obtained at the first time‐point was predictive of cognitive decline one year later as measured by changes in CAMCOG‐DS scores.ResultIn the cross sectional phase, an interaction between the MMN amplitude, both expressed in ERP and GFP, and group was found. In particular, MMN amplitude predicted age in DS but not in TD. On the other hand, neither amplitude nor latency of the MMN predicted cognitive decline one year later.ConclusionOur study shows that in our cohort the MMN amplitude reflects accelerated aging in DS but not in TD, suggesting that MMN amplitude may be a sensitive marker of early onset AD in the DS population. On the other hand, neither MMN amplitude or latency predicts cognitive decline one year later.

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