According to the most popular pathophysiological models of Alzheimer's disease, the amyloid hypothesis, amyloid deposition is the causative event triggering a chain of other downstream events which finally lead to Alzheimer's disease and dementia. In mouse models of Alzheimer's disease, 40 Hz multi-sensory (auditory and visual) stimulation was able to reduce the number and size of amyloid plaques throughout cortex and improve cognitive performance. The primary objective of this study is to assess whether an intervention consisting of 40 Hz multi-sensory (auditory and visual) stimulation is able to reduce the amyloid load in non-demented amyloid-positive individuals. As secondary objectives, the investigators will assess whether such intervention is able to: * improve the brain electrical activity, * improve or slow down the worsening of Alzheimer's blood-based biomarkers, * improve or slow down the worsening of cognition.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
TREATMENT
Masking
NONE
Enrollment
20
40 Hz multi-sensory (auditory + visual) stimulation and cognitive training (1 hour/day, per 5 days/week, for a total of 8 weeks)
Cognitive training (1 hour/day, per 5 days/week, for a total of 8 weeks)
Changes in amyloid load
Changes in amyloid load assessed by longitudinal amyloid-PET
Time frame: 8 weeks
Changes in brain electrical activity
Changes in brain electrical activity (e.g. gamma power spectral density) assessed by longitudinal EEG
Time frame: 8 weeks
Changes in Alzheimer's blood-based biomarkers
Changes in Alzheimer's blood-based biomarkers (e.g. plasma Aβ42/Aβ40 ratio, Aβ42, Aβ40, p-tau, and neurofilament light) assessed by longitudinal blood sample collection
Time frame: 8 weeks
Changes in cognition
Changes in cognition (using the Preclinical Alzheimer Cognitive Composite (PACC) score) assessed by longitudinal neuropsychological assessment
Time frame: 8 weeks
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