Page 79 - MEGIN Book Of Abstracts - 2023
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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







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