Human brain imaging methods such as postiron emission tomography and functional magnetic resonance imaging have recently achieved widespread use in the study of both normal cognitive processes and neurological disorders. While many of these studies have begun to yield important insights into human brain function, the relationship between these measurements and the underlying neuronal activity is still not well understood. One open question is how neuronal inhibition is reflected in these imaging results. In this paper, we describe how large-scale modeling can be used to address this question. Specifically, we identify three factors that may play a role in how inhibition affects imaging results: (1) local connectivity; (2) context; and (3) type of inhibitory connection. Simulation results are presented that show how the interaction among these three factors can explain seemingly contradictory experimental results. The modeling suggests that neuronal inhibition can raise brain imaging measures if there is either low local excitatory recurrence or if the region is not otherwise being driven by excitation. Conversely, with high recurrence or actively driven excitation, inhibition can lower observed values.
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http://dx.doi.org/10.1016/s0361-9230(00)00435-4 | DOI Listing |
Neurocrit Care
January 2025
Division of Neurocritical Care, Departments of Neurology and Neurosurgery, New York University Langone Medical Center, 530 First Avenue, MSB-2-206, New York, NY, 10016, USA.
Background: The Uniform Determination of Death Act requires brain death/death by neurologic criteria (BD/DNC) determination to be in accordance with "accepted medical standards." The medical organizations responsible for delineating these guidelines are only specified statutorily in two states. State health organizations (SHOs) are composed of policy experts and medical professionals who are responsible for addressing medical, ethical, and legislative problems related to health.
View Article and Find Full Text PDFJ Neural Transm (Vienna)
January 2025
Section of Adult Neurology, Department of Internal Medicine, Chong Hua Hospital, Fuente, Cebu, Philippines.
Joubert Syndrome (JS) is a congenital cerebellar ataxia typically inherited in an autosomal recessive pattern, although rare X-linked inheritance can occur. It is characterized by hypotonia evolving into ataxia, global developmental delay, oculomotor apraxia, breathing dysregulation, and multiorgan involvement. To date, there are 40 causative genes implicated in JS, all of which encode proteins of the primary cilium.
View Article and Find Full Text PDFJ Neurol
January 2025
Vienna Cognitive Science Hub, University of Vienna, Vienna, Austria.
Background: Conventional medical management, while essential, cannot address all multifaceted consequences of Parkinson's disease (PD). This pilot study explores the potential of a co-designed creative arts therapy on health-related quality of life, well-being, and pertinent non-motor symptoms.
Methods: We conducted an exploratory pilot study with a pre-post design using validated questionnaires.
Eur J Nucl Med Mol Imaging
January 2025
Laboratory of Neuroimaging and Innovative Molecular Tracers (NIMTlab), Geneva University Neurocenter and Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Purpose: As dual-phase amyloid-PET can evaluate amyloid (A) and neurodegeneration (N) with a single tracer injection, dual-phase tau-PET might be able to provide both tau (T) and N. Our study aims to assess the association of early-phase tau-PET scans and F-fluorodeoxyglucose (FDG) PET and their comparability in discriminating Alzheimer's disease (AD) patients and differentiating neurodegenerative patterns.
Methods: 58 subjects evaluated at the Geneva Memory Center underwent dual-phase F-Flortaucipir-PET with early-phase acquisition (eTAU) and F-FDG-PET within 1 year.
Nat Methods
January 2025
Department of Computer Science, Princeton University, Princeton, NJ, USA.
Spatially resolved transcriptomics technologies provide high-throughput measurements of gene expression in a tissue slice, but the sparsity of these data complicates analysis of spatial gene expression patterns. We address this issue by deriving a topographic map of a tissue slice-analogous to a map of elevation in a landscape-using a quantity called the isodepth. Contours of constant isodepths enclose domains with distinct cell type composition, while gradients of the isodepth indicate spatial directions of maximum change in expression.
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