Publications by authors named "Alzahra J Al Omran"

Stress has been implicated in the etiology of neurological and psychological illnesses. Chronic social isolation (SI) is a psychological stressor that provokes neurobehavioral changes associated with psychiatric disorders, including anxiety disorders. Mitochondria dysfunction and oxidative stress are hallmarks of anxiety pathogenesis.

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We have previously reported social isolation induces anxiety-like behavior, cognitive decline, and reduction in brain ATP levels in mice. These changes were ameliorated by treatment with dihydromyricetin (DHM), a compound that positively modulates γ-aminobutyric A (GABA) receptor. To gain further insight into the subcellular mechanisms underlying these changes, we utilized a social isolation-induced anxiety mouse model and investigated changes in mitochondrial oxidative capacity via the electron transport chain.

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Article Synopsis
  • - Anxiety disorders are common and costly in the U.S., with their prevalence rising due to factors like the pandemic, leading to increased treatment resistance and side effects in patients.
  • - In a study, male mice subjected to social isolation exhibited heightened anxiety, changes in neuroimmune responses, and alterations in brain cell activity, especially affecting microglia and stress hormone levels.
  • - Treatment with dihydromyricetin (DHM) showed potential to alleviate these negative effects of social isolation by improving neuroinflammation and reducing anxiety-like behaviors.
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Article Synopsis
  • Anxiety disorders are the most common mental illnesses in the U.S., significantly impacting treatment costs and heightening during the COVID-19 pandemic due to social isolation.
  • Research shows that dihydromyricetin (DHM), a flavonoid, may help reduce anxiety by counteracting negative impacts on the brain and immune system caused by prolonged social isolation in mice.
  • The study demonstrated that social isolation leads to increased anxiety and neuroinflammation, but DHM treatment helped restore normal brain functions and reduce inflammation associated with anxiety.
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Research focusing on the gut-brain axis is growing, but the interplay of ethanol (alcohol molecule), the gut microbiome, the brain and behavior is poorly understood. In the current study, we remodeled the gut microbiota by providing adult male C57BL/6J mice with a non-absorbable antibiotic cocktail (ABX) in the drinking water and tested ethanol consumption behavior in a binge-like "Drinking in the Dark" model. Notably, 2 weeks of ABX pre-treatment significantly increased ethanol consumption during the 6 weeks of ethanol exposure in the DID paradigm.

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Ependymal cilia protrude into the central canal of the brain ventricles and spinal cord to circulate the cerebral spinal fluid (CSF). Ependymal cilia dysfunction can hinder the movement of CSF leading to an abnormal accumulation of CSF within the brain known as hydrocephalus. Although the etiology of hydrocephalus was studied before, the effects of ethanol ingestion on ependymal cilia function have not been investigated in vivo.

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Primary cilia are sensory organelles that extend from the cell surface and sense extracellular signals. Endothelial primary cilia protruding from the inner surface of blood vessel walls sense changes in blood flow and convert this mechanosensation into an intracellular biochemical/molecular signal, which triggers a cellular response. Primary endothelial cilia dysfunction may contribute to the impairment of this response and thus be directly implicated in the development of vascular abnormalities such as hypertension and aneurysms.

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Multiciliated ependymal cells line the ventricles in the adult brain. Abnormal function or structure of ependymal cilia is associated with various neurological deficits. The current ex vivo live imaging of motile ependymal cilia technique allows for a detailed study of ciliary dynamics following several steps.

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