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Cited by 151Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeural dynamics and brain function

Electromagnetic signatures of the preclinical and prodromal stages of Alzheimer’s disease

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Nakamura, Akinori, Cuesta, Pablo, Fernández, Alberto, Arahata, Yutaka, Iwata, Kaori, Kuratsubo, Izumi, Bundo, Masahiko, Hattori, Hideyuki +10 more·2018·Brain
DOI 10.1093/brain/awy044PMC PMC5920328
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Abstract

Biomarkers useful for the predementia stages of Alzheimer's disease are needed. Electroencephalography and magnetoencephalography (MEG) are expected to provide potential biomarker candidates for evaluating the predementia stages of Alzheimer's disease. However, the physiological relevance of EEG/MEG signal changes and their role in pathophysiological processes such as amyloid-β deposition and neurodegeneration need to be elucidated. We evaluated 28 individuals with mild cognitive impairment and 38 cognitively normal individuals, all of whom were further classified into amyloid-β-positive mild cognitive impairment (n = 17, mean age 74.7 ± 5.4 years, nine males), amyloid-β-negative mild cognitive impairment (n = 11, mean age 73.8 ± 8.8 years, eight males), amyloid-β-positive cognitively normal (n = 13, mean age 71.8 ± 4.4 years, seven males), and amyloid-β-negative cognitively normal (n = 25, mean age 72.5 ± 3.4 years, 11 males) individuals using Pittsburgh compound B-PET. We measured resting state MEG for 5 min with the eyes closed, and investigated regional spectral patterns of MEG signals using atlas-based region of interest analysis. Then, the relevance of the regional spectral patterns and their associations with pathophysiological backgrounds were analysed by integrating information from Pittsburgh compound B-PET, fluorodeoxyglucose-PET, structural MRI, and cognitive tests. The results demonstrated that regional spectral patterns of resting state activity could be separated into several types of MEG signatures as follows: (i) the effects of amyloid-β deposition were expressed as the alpha band power augmentation in medial frontal areas; (ii) the delta band power increase in the same region was associated with disease progression within the Alzheimer's disease continuum and was correlated with entorhinal atrophy and an Alzheimer's disease-like regional decrease in glucose metabolism; and (iii) the global theta power augmentation, which was previously considered to be an Alzheimer's disease-related EEG/MEG signature, was associated with general cognitive decline and hippocampal atrophy, but was not specific to Alzheimer's disease because these changes could be observed in the absence of amyloid-β deposition. The results suggest that these MEG signatures may be useful as unique biomarkers for the predementia stages of Alzheimer's disease.

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  • Tau pathology can interfere with neuronal circuits, resulting in theta and gamma oscillation deficits long before neurons die.

    “Previous studies have shown that tau pathology can interfere with neuronal circuits, resulting in theta and gamma oscillation deficits long before neurons die16,20–23.”

    From The R136S mutation in the APOE3 gene confers resilience against tau pathology via inhibition of the cGAS-STING-IFN pathway (2025) · cites this paper as [23]

    The Results (General profile of the regional power spectra; page unavailable) report altered theta-band power in mild cognitive impairment, supporting only the broad point that oscillations change. The paper does not link those changes to tau pathology, report gamma deficits, or establish that they occur before neuronal death; its Results instead relate theta power to hippocampal grey-matter volume. (LLM, conf=0.84)

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Authors
Nakamura, A., Cuesta, P., Fernández, A., Arahata, Y., Iwata, K., Kuratsubo, I., Bundo, M., Hattori, H., Sakurai, T., Fukuda, K., Washimi, Y., Endo, H., Takeda, A., Diers, K., Bajo, R., Maestú, F., Ito, K., & Kato, T.
Affiliations
  • National Center for Geriatrics and Gerontology (JP)
  • Universidad Complutense de Madrid (ES)
  • National Hospital for Geriatric Medicine, National Center for Geriatrics and Gerontology (JP)
  • Technische Universität Dresden (DE)
Corresponding author
Nakamura, Akinori
ORCID
Venue
Brain
Publisher
Oxford University Press (OUP)
Published
2018-03-07
Volume
141
Issue
5
Pages
1470-1485
ISSN
  • 0006-8950 (ISSN-L)
  • 1460-2156
DOI
10.1093/brain/awy044
PMC
PMC5920328
OpenAlex
W2790598060
Cited by
151
References
7
Citations by year
2026: 8 · 2025: 17 · 2024: 22 · 2023: 30 · 2022: 23 · 2021: 22 · 2020: 12 · 2019: 15 · 2018: 2
FWCI
10.03
Type
journal article
Language
en
Open access
Licence
Locations
  • Brain (publishedVersion, cc-by-nc)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
NCGG
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
Keywords
Alzheimer's disease, prodromal Alzheimer's disease, mild cognitive impairment, resting-state MEG, EEG biomarkers, amyloid-beta deposition, Pittsburgh compound B PET, alpha power, delta power, theta power, hippocampal atrophy, glucose metabolism, disease progression, cognitive decline
MeSH terms
Aged, Aged, 80 and over, Alzheimer Disease, Analysis of Variance, Aniline Compounds, Brain, Brain Mapping, Female, Humans, Magnetic Resonance Imaging, Male, Neuropsychological Tests, Psychiatric Status Rating Scales, Thiazoles, Magnetoencephalography, Amyloid beta-Peptides, Disease Progression, Positron-Emission Tomography, Cognitive Dysfunction, Prodromal Symptoms

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