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We included 110 cognitively unimpaired individuals (67.9 \u00b1 5.7 years), who underwent [18F]flutemetamol (amyloid-\u03b2)-PET imaging and resting-state magnetoencephalography (MEG) recording at baseline and 4-year follow-up. We tested associations between baseline amyloid-\u03b2 deposition and MEG measures (oscillatory power and functional connectivity). Next, we examined the relationship between baseline amyloid-\u03b2 deposition and longitudinal MEG measures, as well as between baseline MEG measures and longitudinal amyloid-\u03b2 deposition. Finally, we assessed associations between longitudinal changes in both amyloid-\u03b2 deposition and MEG measures. Analyses were performed using linear mixed models corrected for age, sex and family. At baseline, amyloid-\u03b2 deposition in orbitofrontal-posterior cingulate regions (i.e. early Alzheimer\u2019s disease regions) was associated with higher theta (4\u20138\u2005Hz) power (\u03b2 = 0.17, P &amp;lt; 0.01) in- and lower functional connectivity [inverted Joint Permutation Entropy (JPEinv) theta, \u03b2 = \u22120.24, P &amp;lt; 0.001] of these regions, lower whole-brain beta (13\u201330\u2005Hz) power (\u03b2 = \u22120.13, P &amp;lt; 0.05) and lower whole-brain functional connectivity (JPEinv theta, \u03b2 = \u22120.18, P &amp;lt; 0.001). Whole-brain amyloid-\u03b2 deposition was associated with higher whole-brain theta power (\u03b2 = 0.17, P &amp;lt; 0.05), lower whole-brain beta power (\u03b2 = \u22120.13, P &amp;lt; 0.05) and lower whole-brain functional connectivity (JPEinv theta, \u03b2 = \u22120.21, P &amp;lt; 0.001). Baseline amyloid-\u03b2 deposition in early Alzheimer\u2019s disease regions also predicted future oscillatory slowing, reflected by increased theta power over time in early Alzheimer\u2019s disease regions and across the whole brain (\u03b2 = 0.11, \u03b2 = 0.08, P &amp;lt; 0.001), as well as decreased whole-brain beta power over time (\u03b2 = \u22120.04, P &amp;lt; 0.05). Baseline amyloid-\u03b2 deposition in early Alzheimer\u2019s disease regions also predicted a reduction in functional connectivity between these regions and the rest of the brain over time (JPEinv theta, \u03b2 = \u22120.07, P &amp;lt; 0.05). Baseline whole-brain amyloid-\u03b2 deposition was associated with increased whole-brain theta power over time (\u03b2 = 0.08, P &amp;lt; 0.01). Baseline MEG measures were not associated with longitudinal amyloid-\u03b2 deposition. Longitudinal changes in amyloid-\u03b2 deposition in early Alzheimer\u2019s disease regions were associated with longitudinal changes in functional connectivity of early Alzheimer\u2019s disease regions (JPEinv theta, \u03b2 = \u22120.19, P &amp;lt; 0.05) and the whole brain [corrected amplitude envelope correlations alpha (8\u201313\u2005Hz), \u03b2 = \u22120.22, P &amp;lt; 0.05]. Finally, longitudinal changes in whole-brain amyloid-\u03b2 deposition were associated with longitudinal changes in whole-brain relative theta power (\u03b2 = 0.21, P &amp;lt; 0.05). Disruptions of oscillatory power and functional connectivity appear to represent early functional consequences of emerging amyloid-\u03b2 deposition in cognitively unimpaired individuals. These findings suggest a role for neurophysiology in monitoring disease progression and potential treatment effects in pre-clinical Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.1093\/braincomms\/fcaf018","type":"journal-article","created":{"date-parts":[[2025,1,17]],"date-time":"2025-01-17T06:21:42Z","timestamp":1737094902000},"source":"Crossref","is-referenced-by-count":4,"title":["Amyloid-\u03b2 deposition predicts oscillatory slowing of magnetoencephalography signals and a reduction of functional connectivity over time in cognitively unimpaired adults"],"prefix":"10.1093","volume":"7","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4582-9563","authenticated-orcid":false,"given":"Elliz P","family":"Scheijbeler","sequence":"first","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology, Vrije Universiteit Amsterdam , Amsterdam UMC, 1081 HV Amsterdam, The Netherlands"},{"name":"Amsterdam Neuroscience, Neurodegeneration , 1081 HV Amsterdam, The 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HV Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anouk","family":"den Braber","sequence":"additional","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology, Vrije Universiteit Amsterdam , Amsterdam UMC, 1081 HV Amsterdam, The Netherlands"},{"name":"Amsterdam Neuroscience, Neurodegeneration , 1081 HV Amsterdam, The Netherlands"},{"name":"Department of Radiology and Nuclear Medicine, Vrije Universiteit Amsterdam , Amsterdam UMC, 1081 HV Amsterdam, The Netherlands"},{"name":"Amsterdam Neuroscience, Brain Imaging , 1081 HV Amsterdam, The Netherlands"},{"name":"Department of Biological Psychology, Vrije Universiteit Amsterdam , 1081 HV Amsterdam, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jori","family":"Tomassen","sequence":"additional","affiliation":[{"name":"Alzheimer Center Amsterdam, Department of Neurology, Vrije Universiteit Amsterdam , Amsterdam UMC, 1081 HV Amsterdam, The 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