Biology subjects

Karunanayaka, P.

Publications and source records attributed to Karunanayaka, P..

6 recordsLinked to original sources

bioRxiv2026

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↗

bioRxiv2024

Neurocognitive Mechanism of Radiologists Perceptual Errors: Results of Preliminary Studies

BackgroundThe most prevalent type of radiologist error is failing to detect abnormalities on images, the so-called "perceptual error." The prevalence of this type of false-negative (FN) error remains essentially unchanged since it was first described in 1949. PurposeThe purpose of this research is to identify a potential neurocognitive mechanism contributing to radiologists susceptibility to perceptual error, in order to inform intervention strategies to reduce such errors in practice. These experiments evaluated the relationship between brain network activation states and radiologists perceptual errors on two distinct visual tasks utilizing functional MRI (fMRI) and functional Near Infrared Spectroscopy (fNIRs). Materials and MethodsA prospective study consisting of three experiments was carried out on a small number of radiologist subjects. The first two experiments used fMRI, with participants performing two distinct types of visual tasks, respectively: the first was a task requiring subjects continuous attention and the second task required visual search. For the first of these experiments, simultaneous functional Near-Infrared Spectroscopic Imaging (fNIRs) was utilized along with fMRI. The second experiment was combined fMRI and eye-tracking. A third experiment using fNIRs alone was an observational study of subjects neurocognitive states during their usual practice. ResultsAn approximately threefold increased risk of FN perceptual errors (misses) was observed in the presence of a particular error-prone neurocognitive state (EPS) involving simultaneous co-activation of elements of the Default Mode Network (DMN) and Frontoparietal Network (FPN), which was detectable by both functional imaging modalities, with high concordance. EPS episodes appeared to be stochastic in occurrence, and occurred without operator awareness. We also found a high prevalence of the EPS in radiologists performing their normal interpretive tasks in their actual practice setting. ConclusionOur results suggest that dynamic interactions between brain networks leading to a particular error-prone state (EPS) may underlie a substantial fraction of radiologists perceptual errors. We demonstrate that this EPS can be detected unobtrusively in the clinical setting. These results suggest potential intervention strategies for perceptual error, the largest class of radiologist errors in practice. Key Results/HighlightsO_LIPeriodic episodes of a discrete neurocognitive state were observed in radiologists during specific visual tasks and in actual clinical settings. C_LIO_LIThere was an approximately threefold increased risk of perceptual error during this state. Most FN errors for the two visual tasks occurred during these brief episodes (p < 0.01). C_LIO_LIThere was also a highly significant anti-correlation of the prevalence of the error-prone neurocognitive state (EPS) with subject age (p < 0.001). C_LI ConflictsThe authors report no conflicts of interest or potential competing interests. Summary StatementWe report experimental results corelating perceptual errors by radiologists to episodic fluctuations in brain network activation, which appear to occur on a stochastic basis. These produce an error-prone neurocognitive state outside of operator awareness or control that is associated with an approximately threefold increase in the risk of perceptual error.

neuroscience↗

bioRxiv2023

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↗

bioRxiv2021

IMPAIRED OLFACTORY NETWORK FUNCTIONAL CONNECTIVITY IN PARKINSON'S DISEASE: A NOVEL MARKER FOR DISEASE PROGRESSION

ObjectiveDetermine the neural basis of olfactory impairment in akinetic-rigid (PDAR) and tremor predominant (PDT) Parkinsons disease subtypes. MethodsWe combined resting-state fMRI (rs-fMRI) with seed based functional connectivity (FC) in order to delineate the olfactory networks functional connectivity (ON FC) between PDAR and PDT patients. We then contrasted their ON FC patterns with cognitively normal (CN) subjects. All three groups were closely matched in age, demographic variables, and adjusted for relative cognitive performance. Olfactory function was measured using the University of Pennsylvania Smell Identification Test (UPSIT). ResultsUPSIT scores were lower in akinetic-rigid vs tremor subtypes; ON FC values were lower in PDAR compared to PDT and CN, and followed the trend observed in UPSIT scores. UPSIT scores and ON FC values were significantly correlated, reflecting the effects of PD pathologies. ConclusionsThe results show that olfactory function differs between PDAR and PDT suggesting a correlation between PD-related motor symptoms and olfactory deficits. ON FC differences accounts for the impaired olfactory functions observed between PDAR and PDT. PDAR is known to have worse clinical outcomes and faster cognitive decline compared to PDT; therefore, PD-related olfactory dysfunction may serve as a novel metric for enhancing PD prognosis.

neuroscience↗

bioRxiv2020

Neural Basis of Olfactory and Trigeminal Integration

Humans naturally integrate signals from the olfactory and intranasal trigeminal systems. A tight interplay has been demonstrated between these two systems, and yet the underlying neural circuitry that mediates olfactory-trigeminal integration remains poorly understood. Using functional magnetic resonance imaging (fMRI), combined with psychophysics, this study investigated the neural mechanisms underlying olfactory-trigeminal integration. Fifteen participants with normal olfactory function performed a localization task with air-puff stimuli, phenylethyl alcohol (PEA; rose odor), or a combination thereof while being scanned. The ability to localize PEA to either nostril was at chance. Yet, its presence significantly improved the localization accuracy of weak, but not strong, air-puffs, relative to air-puff localization without concomitant PEA when both stimuli were delivered concurrently to the same nostril, but not when different nostrils received the two stimuli. This enhancement in localization accuracy, exemplifying the principles of spatial coincidence and inverse effectiveness in multisensory integration, was associated with multisensory integrative activity in the primary olfactory (POC), orbitofrontal (OFC), superior temporal (STC), inferior parietal (IPC) and cingulate cortices, and in the cerebellum. Multisensory enhancement in most of these regions, except the OFC, correlated with behavioral multisensory enhancement, as did increases in connectivity between some of these regions. We interpret these findings as indicating that the POC is part of a distributed brain network mediating integration between the olfactory and trigeminal systems. HIGHLIGHTSO_LIPsychophysical and neuroimaging study of olfactory-mechanosensory (OM) integration C_LIO_LIBehavior, cortical activity and network connectivity show OM integration C_LIO_LIOM integration obeys principles of inverse effectiveness and spatial coincidence C_LIO_LIBehavioral and neural measures of OM integration are correlated C_LI

neuroscience↗

bioRxiv2020

18F-FDG-PET Hyperactivity in Alzheimers Disease Cerebellum and Primary Olfactory Cortex

Cerebellar involvement in Alzheimers disease (AD) has not been studied to the extent that cortical neuropathological changes have. Historical and recent histopathological literature demonstrate cerebellar AD pathology while functional investigation has demonstrated disrupted intrinsic cortical - cerebellar connectivity in AD. Additionally, olfactory deficits occur early in AD, prior to the onset of clinical symptoms. The neurological basis for the involvement of the cerebellum and olfactory system in the disease course remain unclear. 18F-fludeoxyglucose (FDG) positron emission tomography (PET) data from the Alzheimers Disease Neuroimaging Initiative (ADNI) were analyzed to characterize metabolism in the cerebellum and olfactory region of AD, mild-cognitive impaired (MCI), and age-matched cognitively normal (CN) controls. In contrast to known parietal and temporal lobe FDG hypo-metabolism within the default mode network in AD, a significant FDG hyper-metabolism was found in the cerebellum and olfactory cortical regions (including the piriform cortex, olfactory tubercle, anterior olfactory nucleus, and nucleus accumbens shell). The increase in cerebellum glucose utilization was shown also in late- verses early-MCI patients. The cerebellar and olfactory regions both contain inhibitory distal and inter-neuronal connections that are vulnerable to disruption in AD. The hyper-metabolism in the cerebellum and olfactory structures may reflect disruption of local and system-wide inhibitory networks due to AD neurodegeneration, suggesting a hypothetical mechanism for susceptibility of the olfactory system to early AD pathology.

neuroscience↗