Synergistic association of A$β$ and tau pathology with cortical neurophysiology and cognitive decline in asymptomatic older adults. Gallego-Rudolf, J., Wiesman, A. I, Pichet Binette, A., Villeneuve, S., Baillet, S., & PREVENT-AD Research Group Nat. Neurosci., 27(11):2130–2137, Springer Science and Business Media LLC, November, 2024.
abstract   bibtex   
Animal and computational models of Alzheimer's disease (AD) indicate that early amyloid-$β$ (A$β$) deposits drive neurons into a hyperactive regime, and that subsequent tau depositions manifest an opposite, suppressive effect as behavioral deficits emerge. Here we report analogous changes in macroscopic oscillatory neurophysiology in the human brain. We used positron emission tomography and task-free magnetoencephalography to test the effects of A$β$ and tau deposition on cortical neurophysiology in 104 cognitively unimpaired older adults with a family history of sporadic AD. In these asymptomatic individuals, we found that A$β$ depositions colocalize with accelerated neurophysiological activity. In those also presenting medial-temporal tau pathology, linear mixed effects of A$β$ and tau depositions indicate a shift toward slower neurophysiological activity, which was also linked to cognitive decline. We conclude that early A$β$ and tau depositions relate synergistically to human cortical neurophysiology and subsequent cognitive decline. Our findings provide insight into the multifaceted neurophysiological mechanisms engaged in the preclinical phases of AD.
@ARTICLE{Gallego-Rudolf2024-jp,
  title     = "Synergistic association of {A$\beta$} and tau pathology with
               cortical neurophysiology and cognitive decline in asymptomatic
               older adults",
  author    = "Gallego-Rudolf, Jonathan and Wiesman, Alex I and Pichet Binette,
               Alexa and Villeneuve, Sylvia and Baillet, Sylvain and
               {PREVENT-AD Research Group}",
  abstract  = "Animal and computational models of Alzheimer's disease (AD)
               indicate that early amyloid-$\beta$ (A$\beta$) deposits drive
               neurons into a hyperactive regime, and that subsequent tau
               depositions manifest an opposite, suppressive effect as
               behavioral deficits emerge. Here we report analogous changes in
               macroscopic oscillatory neurophysiology in the human brain. We
               used positron emission tomography and task-free
               magnetoencephalography to test the effects of A$\beta$ and tau
               deposition on cortical neurophysiology in 104 cognitively
               unimpaired older adults with a family history of sporadic AD. In
               these asymptomatic individuals, we found that A$\beta$
               depositions colocalize with accelerated neurophysiological
               activity. In those also presenting medial-temporal tau
               pathology, linear mixed effects of A$\beta$ and tau depositions
               indicate a shift toward slower neurophysiological activity,
               which was also linked to cognitive decline. We conclude that
               early A$\beta$ and tau depositions relate synergistically to
               human cortical neurophysiology and subsequent cognitive decline.
               Our findings provide insight into the multifaceted
               neurophysiological mechanisms engaged in the preclinical phases
               of AD.",
  journal   = "Nat. Neurosci.",
  publisher = "Springer Science and Business Media LLC",
  volume    =  27,
  number    =  11,
  pages     = "2130--2137",
  month     =  nov,
  year      =  2024,
  copyright = "https://creativecommons.org/licenses/by-nc-nd/4.0",
  language  = "en"
}

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