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We introduce a MEG dataset with 324 individuals: pa- mass model), we examined excitatory and inhibitory
tients with MCI and healthy controls. Their brain activity parameters of neuronal subpopulations and investi-
was recorded while resting with eyes closed, using a gated their specific associations to regional tau and
306-channel MEG scanner at one of two sites (Madrid Aβ, measured by positron emission tomography, in
or Cambridge), enabling tests of generalization across patients with AD.
sites. A T1-weighted MRI is provided to assist source
localisation. The MEG and MRI data are formatted ac- RESULTS Patients with AD showed abnormal excitatory
cording to international BIDS standards and analysed and inhibitory time-constants and neural gains com-
freely on the DPUK platform (https://portal.dementias- pared to age-matched controls. Increased excitatory
platform.uk/Apply). Here, we describe this dataset in time-constants distinctly correlated with higher tau
detail, report some example (benchmark) analyses, and depositions while increased inhibitory time-constants
consider its limitations and future directions. distinctly correlated with higher Aβ depositions.
NeuroImage (2022), Vol. 258 (35660461) (1 citation) CONCLUSIONS Our results provide critical insights
about potential mechanistic links between abnormal
neural oscillations and cellular correlates of impaired
Altered excitatory and inhibitory neuronal excitatory and inhibitory synaptic functions associated
subpopulation parameters are distinctly associated with tau and Aβ in patients with AD.
with tau and amyloid in Alzheimer's disease (2022)
FUNDING This study was supported by the National
Ranasinghe, Kamalini G; Verma, Parul; Cai, Chang; Xie, Institutes of Health grants: K08AG058749 (KGR),
Xihe; Kudo, Kiwamu; Gao, Xiao; Lerner, Hannah; Mizuiri, F32AG050434-01A1 (KGR), K23 AG038357 (KAV), P50
Danielle; Strom, Amelia; Iaccarino, Leonardo; La Joie, AG023501, P01 AG19724 (BLM), P50-AG023501 (BLM
Renaud; Miller, Bruce L; Gorno-Tempini, Maria Luisa; and GDR), R01 AG045611 (GDR); AG034570, AG062542
Rankin, Katherine P; Jagust, William J; Vossel, Keith; (WJ); NS100440 (SSN), DC176960 (SSN), DC017091
Rabinovici, Gil D; Raj, Ashish; Nagarajan, Srikantan S (SSN), AG062196 (SSN); a grant from John Douglas
French Alzheimer's Foundation (KAV); grants from Larry
Memory and Aging Center, Department of Neurology, L. Hillblom Foundation: 2015-A-034-FEL (KGR), 2019-A-
University of California, San Francisco, San Francisco, United 013-SUP (KGR); grants from the Alzheimer's Association:
States; Department of Radiology and Biomedical Imaging, AARG-21-849773 (KGR); PCTRB-13-288476 (KAV), and
University of California, San Francisco, San Francisco, United made possible by Part the CloudTM (ETAC-09-133596);
States; Medical Imaging Business Center, Ricoh Company, a grant from Tau Consortium (GDR and WJJ), and a gift
Kanazawa, Japan; Helen Wills Neuroscience Institute, Uni- from the S. D. Bechtel Jr. Foundation.
versity of California, Berkeley, Berkeley, United States; Mary S.
Easton Center for Alzheimer's Disease Research, Department Keywords: Alzheimer's disease, human, magnetoenceph-
of Neurology, David Geffen School of Medicine, University of alogrpahy, medicine, neural mass model, neuroscience,
California, Los Angeles, Los Angeles, United States tau-PET
BACKGROUND Neuronal- and circuit-level abnor- eLife (2022), Vol. 11 (35616532) (5 citations)
malities of excitation and inhibition are shown to be
associated with tau and amyloid-beta (Aβ) in preclinical
models of Alzheimer's disease (AD). These relationships
remain poorly understood in patients with AD.
METHODS Using empirical spectra from magnetoen-
cephalography and computational modeling (neural
ontents Index 58
C