Biology subjects

Khayrullina, G.

Publications and source records attributed to Khayrullina, G..

3 recordsLinked to original sources

bioRxiv2024

The heart rate dynamics and antioxidant capacity under cognitive load in Obsessive-Compulsive disorder

The research of the oxidants-antioxidants homeostasis and its connection to autonomic nervous system (ANS) dysfunction in patients with obsessive-compulsive disorder (OCD) is a relatively uncharted field of study. We recruited 31 patients diagnosed with OCD and 29 healthy volunteers to analyze their saliva antioxidant capacity before and after a three-block behavioral task with cognitive and emotional load, during which we assessed heart rate (HR) and heart rate variability (HRV) patterns. We found that the OCD group had a significantly lower antioxidant capacity (AOC) and showed no increase in AOC after the cognitive task as compared with healthy volunteers. The notable negative correlation between HR and AOC changes led us to select two subgroups inside the OCD and control group: one with high HR and another with low HR. The AOC changes for OCD and healthy participants with high HR were similar, while OCD sub-group with low HR exhibited significantly different changes in AOC compared with the control group. Although HRV did not show a correlation with AOC, the OCD group demonstrated substantially higher increase of very low frequencies (VLF) of HRV during the cognitive task performance and significantly elevated low frequency powers of HRV expressed in normal units (LFnu). OCD sub-group with lower HR exhibited higher LFnu compared to both the patient and the control group with high HR. Our findings imply that OCD patients with elevated sympathetic tone of ANS reflected by initially increased HR show more adaptive AOC to cognitive load

neuroscience↗

bioRxiv2023

Increased error rate and delayed response to negative emotional stimuli in antisaccade task in obsessive-compulsive disorder

Ample evidence links impaired inhibitory control, attentional distortions, emotional dysregulation, and obsessive-compulsive disorder (OCD). However, it remains unclear what underlies the deficit that triggers the OCD cycle. The present study used an antisaccade paradigm with emotional stimuli to compare eye movement patterns reflecting inhibitory control and attention switching in OCD and healthy control groups. Thirty-two patients with OCD and thirty healthy controls performed the antisaccade task with neutral, positive, and negative visual images. The groups differed significantly in the number of errors to negative stimuli. The latency of correct antisaccades varied between valences in OCD group when negative and neutral stimuli served as target ones. The OCD group showed more errors to negative stimuli than the control group and they also performed antisaccades more slowly to negative and neutral stimuli than positive ones. Other patterns, including mean velocity of correct antisaccades and anticipatory saccades, did not differ between groups. The mean velocity of correct antisaccades was higher for negative and positive stimuli than for neutral stimuli; however, there were more anticipatory saccades for neutral stimuli than for negative and positive stimuli in both groups. The peak velocity parameter did not show any differences either between groups or between valences. The findings support a hypothesis that an attentional bias towards threatening stimuli interferes with inhibitory control in OCD.

neuroscience↗

bioRxiv2021

Viral mediated knockdown of GATA6 in SMA iPSC-derived astrocytes prevents motor neuron loss and microglial activation

Spinal muscular atrophy (SMA), a pediatric genetic disorder, is characterized by the profound loss of spinal cord motor neurons and subsequent muscle atrophy and death. Although the mechanisms underlying motor neuron loss are not entirely clear, data from our work and others support the idea that glial cells contribute to disease pathology. GATA6, a transcription factor that we have previously shown to be upregulated in SMA astrocytes, is negatively regulated by SMN and can increase the expression of inflammatory regulator NF{kappa}B. In this study, we identified upregulated GATA6 as a contributor to increased activation, pro-inflammatory ligand production, and neurotoxicity in spinal-cord patterned astrocytes differentiated from SMA patient induced pluripotent stem cells. Reducing GATA6 expression in SMA astrocytes via lentiviral infection ameliorated these effects to healthy control levels. Additionally, we found that SMA astrocytes contribute to SMA microglial phagocytosis, which was again decreased by lentiviral-mediated knockdown of GATA6. Together these data identify a role of GATA6 in SMA astrocyte pathology and further highlight glia as important targets of therapeutic intervention in SMA.

neuroscience↗