The aim of our study was to use functional magnetic resonance imaging to investigate how spontaneous activity interacts with evoked activity, as well as how the temporal structure of spontaneous activity, that is, long-range temporal correlations, relate to this interaction. Using an extremely sparse event-related design (intertrial intervals: 52-60 s), a novel blood oxygen level-dependent signal correction approach (accounting for spontaneous fluctuations using pseudotrials) and phase analysis, we provided direct evidence for a nonadditive interaction between spontaneous and evoked activity. We demonstrated the discrepancy between the present and previous observations on why a linear superposition between spontaneous and evoked activity can be seen by using co-occurring signals from homologous brain regions. Importantly, we further demonstrated that the nonadditive interaction can be characterized by phase-dependent effects of spontaneous activity, which is closely related to the degree of long-range temporal correlations in spontaneous activity as indexed by both power-law exponent and phase-amplitude coupling. Our findings not only contribute to the understanding of spontaneous brain activity and its scale-free properties, but also bear important implications for our understanding of neural activity in general.
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http://dx.doi.org/10.1093/cercor/bhv288 | DOI Listing |
J Mol Model
January 2025
Laboratorio de Química Teórica Computacional (QTC), Facultad de Química y de Farmacia, Pontificia Universidad Católica de Chile, Avenida Vicuña Mackenna 4860, 7820436, Santiago de Chile, Chile.
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December 2024
Ivane Beritashvili Center of Experimental Biomedicine, Tbilisi, Georgia.
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View Article and Find Full Text PDFAlzheimers Dement
December 2024
Cornell University, Ithaca, NY, USA.
Background: Alzheimer's disease (AD) is characterized by progressive, irreversible neurodegeneration, leading to memory loss and cognitive decline. In mouse models of AD, global decreases in cerebral blood flow (CBF) are brought on by the plugging of capillaries by arrested neutrophils, and the administration of the neutrophil-specific antibody against Ly6G (anti-Ly6G) reduces these capillary stalls in minutes and improves cognitive function within hours. This suggests that at least some aspects of neural activity impairment are reversible, but the mechanism of this recovery - and what specific neural activity is normalized - is not yet known.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Milano - Bicocca, Monza, Monza, Italy, iCAB International Network, University of Milano - Bicocca, Monza, Italy.
ARIA-E/H (amyloid-related imaging abnormalities-Edema/Hemorrhage) is an umbrella term that defines the radiographic appearance of MRI images abnormality during treatments with Aβ-lowering monoclonal antibodies (mAbs) for Alzheimer's disease immunotherapy. Today, it is well-recognized that ARIA-E events can also occur spontaneously in patients with cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare autoimmune encephalopathy associated with raised cerebrospinal fluid (CSF) concentrations of spontaneous auto-antibodies against Aβ (aAbs). In this framework, the last years of research and experience of the iCAB international Network generated an increased consensus that therapy-induced ARIA is the iatrogenic manifestation of CAA-ri.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of California San Francisco, San Francisco, CA, USA.
Background: Neural circuit hyperexcitability and impaired excitation-to-inhibition (E/I) activity is believed to be a key contributor to synaptic and network degeneration in Alzheimer's disease (AD). Extensive preclinical research on transgenic animal models of AD have demonstrated neuronal and circuit level E/I imbalance mediated by amyloid-beta (Aβ) and tau proteins. Synaptic and network deficits are also integral changes of aging.
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