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Ekanayake, A.

Publications and source records attributed to Ekanayake, A..

3 recordsLinked to original sources

A DERIVED RELAXATION CONTRAST FROM SYNTHETIC MRI FOR DETECTING NETWORK MICROSTRUCTURAL VULNERABILITY

BackgroundOdor identification impairment is an early marker of Alzheimers disease (AD) that predicts memory decline, yet its underlying microstructural basis remains unclear. We hypothesized that mild cognitive impairment (MCI) involves early myelin and lipid disruption within olfactory-limbic circuits, detectable using a synthetic MRI-derived contrast that provides complementary sensitivity to myelin volume fraction (MVF). MethodsThirty-three older adults (healthy controls [HC], n = 16; mild cognitive impairment [MCI], n = 17) completed olfactory and cognitive testing and underwent 3T brain MRI using a QALAS sequence. An MVF map and synthetic FLAIR and DIR images were generated, and a FLAIR-DIR-derived metric (FD) was computed as FD = (FLAIR - DIR) / FLAIR. We investigated ROI-based group differences in olfactory-limbic gray-matter regions and associated white-matter tracts, voxel-wise regressions investigating FD-odor identification associations, and ROI-based MCI vs HC classification using cross-validated logistic regression models. ResultsCompared with HC, MCI showed significantly lower FD across olfactory-limbic gray-matter regions and white-matter pathways--including hippocampus, amygdala, orbitofrontal cortex, thalamus, and corpus callosum--whereas MVF differences were more limited. FD achieved moderate discrimination, with baseline performance comparable to MVF. Voxel-wise analyses revealed that better odor identification was associated with higher FD in the hippocampus/parahippocampal and insula; the association persisted after adjusting for voxel-wise MVF. MVF also showed significant positive voxel-wise associations with odor identification in the insula and genu of the corpus callosum. ConclusionFD is a practical, myelin- and lipid-sensitive contrast derived from routinely acquired synthetic FLAIR & DIR images that complement quantitative MVF. It captures behaviorally relevant variance beyond local myelin content and may improve detection of early olfactory-limbic microstructural changes in MCI. These findings support FD as a scalable candidate marker linking early network disruption to olfactory symptoms across the AD continuum.

neuroscience↗

Monorhinal and Birhinal Odor Processing in Humans: an fMRI investigation

The olfactory nerve, also known as cranial nerve I, is known to have exclusive ipsilateral projections to primary olfactory cortical structures. It is still unclear whether these projections also correspond to functional pathways of odor processing. In an olfactory functional magnetic resonance imaging (fMRI) study of twenty young healthy subjects with a normal sense of smell, we tested whether nostril specific stimulation with phenyl ethyl alcohol (PEA), a pure olfactory stimulant, asymmetrically activates primary or secondary olfactory-related brain structures such as primary olfactory cortex, entorhinal cortex, and orbitofrontal cortex. The results indicated that without a challenging olfactory task, passive (no sniffing) and active (with sniffing) nostril-specific PEA stimulation did not produce asymmetrical fMRI activation in olfactory cortical structures.

neuroscience↗

Targeting CTP Synthetase 1 to Restore Interferon Induction and Impede Nucleotide Synthesis in SARS-CoV-2 Infection

The newly emerged SARS-CoV-2 caused a global pandemic with astonishing mortality and morbidity. The mechanisms underpinning its highly infectious nature remain poorly understood. We report here that SARS-CoV-2 exploits cellular CTP synthetase 1 (CTPS1) to promote CTP synthesis and suppress interferon (IFN) induction. Screening a SARS-CoV-2 expression library identified ORF7b and ORF8 that suppressed IFN induction via inducing the deamidation of interferon regulatory factor 3 (IRF3). Deamidated IRF3 fails to bind the promoters of classic IRF3-responsible genes, thus muting IFN induction. Conversely, a shRNA-mediated screen focused on cellular glutamine amidotransferases corroborated that CTPS1 deamidates IRF3 to inhibit IFN induction. Functionally, ORF7b and ORF8 activate CTPS1 to promote de novo CTP synthesis while shutting down IFN induction. De novo synthesis of small-molecule inhibitors of CTPS1 enabled CTP depletion and IFN induction in SARS-CoV-2 infection, thus impeding SARS-CoV-2 replication. Our work uncovers a strategy that a viral pathogen couples immune evasion to metabolic activation to fuel viral replication. Inhibition of the cellular CTPS1 offers an attractive means for developing antiviral therapy that would be resistant to SARS-CoV-2 mutation.

microbiology↗