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"No civil discourse, no cooperation; misinformation, mistruth." These were the words of former Facebook Vice President Chamath Palihapitiya who publicly expressed his regret in a 2017 interview over his role in co-creating Facebook. Palihapitiya shared that social media is ripping apart the social fabric of society and he also sounded the alarm regarding social media’s unavoidable global impact. He is only one of social media’s countless critics. The more disturbing issue resides in the empirical evidence supporting such notions. At least 95% of adolescents own a smartphone and spend an average time of two to four hours a day on social media. Moreover, 91% of 16-24-year-olds use social media, yet youth rate Instagram, Facebook, and Twitter as the worst social media platforms. However, the social, clinical, and neurodevelopment ramifications of using social media regularly are only beginning to emerge in research. Early research findings show that social media platforms trigger anxiety, depression, low self-esteem, and other negative mental health effects. These negative mental health symptoms are commonly reported by individuals from of 18-25-years old, a unique period of human development known as emerging adulthood. Although emerging adulthood is characterized by identity exploration, unbounded optimism, and freedom from most responsibilities, it also serves as a high-risk period for the onset of most psychological disorders. Despite social media’s adverse impacts, it retains its utility as it facilitates identity exploration and virtual socialization for emerging adults. Investigating the “user-centered” design and neuroscience underlying social media platforms can help reveal, and potentially mitigate, the onset of negative mental health consequences among emerging adults. Effectively deconstructing the Facebook, Twitter, and Instagram (i.e., hereafter referred to as “The Big Three”) will require an extensive analysis into common features across platforms. A few examples of these design features include: like and reaction counters, perpetual news feeds, and omnipresent banners and notifications surrounding the user’s viewport. Such social media features are inherently designed to stimulate specific neurotransmitters and hormones such as dopamine, serotonin, and cortisol. Identifying such predacious social media features that unknowingly manipulate and highjack emerging adults’ brain chemistry will serve as a first step in mitigating the negative mental health effects of today’s social media platforms. A second concrete step will involve altering or eliminating said features by creating a social media platform that supports and even enhances mental well-being.
Environmental and genetic factors influence schizophrenia risk. Individuals who have direct family members with schizophrenia have a much higher incidence. Also, acute stress or life crisis may precede the onset of the disease. This study aims to understand the effects of environment on genes related to schizophrenia risk. It investigates the impact of sleep deprivation as an acute environmental stressor on the expression of Htr2a in mice, a gene that codes for the serotonin 2A receptor (5-HT2AR). HTR2A is associated with schizophrenia risk through genetic association studies and expression is decreased in post-mortem studies of patients with the disease. Furthermore, sleep deprivation as a stressor in human trials has been shown to increase the binding capacity of 5-HT2AR. We hypothesize that sleep deprivation will increase the number of cells expressing Htr2a in the mouse anterior prefrontal cortex when compared to controls. Sleep deprived that mice express EGFP under control of the Htr2a promoter displayed anteroposterior gradients of expression across sagittal sections, with concentrations seen most densely within the prefrontal cortex as well as the anterior pretectal nucleus, thalamic nucleus, as well as the cingulate gyrus. Htr2a-EGFP expression was most densely visualized in cortical layer V and VI pyramidal neurons within the lateral prefrontal cortex of coronal sections. Furthermore, the medial prefrontal cortex contained significantly cells expressing Htr2a¬-EGFP than the lateral prefrontal cortex. Ultimately, the hypothesis was not supported and sleep deprivation did not result in more ¬Htr2a-EGFP expressing cells compared to basal levels. However, expressing cells appeared visibly brighter in sleep-deprived animals when compared to controls, indicating that the amount of intracellular Htr2a-GFP expression may be higher. This study provides strong visual representations of expression gradients following sleep deprivation as an acute stressor and paves the way for future studies regarding 5H-T2AR’s role in schizophrenia.
Neurological manifestations may be more prominent and have a larger role in ankylosing spondylitis than previously thought. Ankylosing Spondylitis is a rheumatic disease primarily identified by its autoinflammatory characteristics and is highly associated with the HLA-B27 gene. While it’s cause is not yet fully understood and it’s symptoms widely vary, neurological impairment is not uncommon. The neurological manifestations of Ankylosing Spondylitis include but are not limited to pain sensitization, altered brain phenotype, and disrupted cardiac conduction. Central and peripheral nervous system involvement may be more significant than previously thought and have the potential to cause demyelinating diseases, spinal cord, and nerve root injuries. Altered connectivity throughout various regions within the brain further exemplify the need for a better understanding of the disease and better treatment development. Higher instances of depression and dementia were also reported and coincide with not only a less active lifestyle, but altered brain activity. Studies on cardiac conduction and arrhythmias in AS patients revealed parasympathetic and sympathetic nervous system dysregulation. These studies have explored the possibility of new targets for treatment involving cardiac mechanisms. Treatments for diseases of a similar suspected pathology, new prospective targets for therapy, and a more thorough understanding of current treatments for the disease may be the key in providing more substantial relief. By further investigation in the role of the nervous system in Ankylosing Spondylitis, the disease may become more manageable for patients and greatly increase quality of life in the future.