Executive Functions, Fatigue And Eye-blink Rate: A Comparison Between Healthy Aging And Multiple Sclerosis Patients Across Ages - Info and Reading Options

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Dopamine modulates different Central Nervous System (CNS) functions and regulates neuroimmune interaction in MS (Melnikov, Pashenkov and Boyko, 2021). Many studies (Carandini et al., 2021; Dobryakova et al., 2015; Grech et al., 2019; Manjaly et al., 2019) have shown the involvement of dopamine in fatigue, cognitive impairment, and depression in MS. Changes in brain structure (e.g. structures critical for dopaminergic projections being damaged) cause dopamine imbalance (Dobryakova et al., 2015). For example, a study indicated that high Fatigue Severity Scale (FSS) scores showed reduced regional synaptic activity in dopamine-related areas, in MS patients (Roelcke et al., 1997). Another study supporting the dopamine imbalance hypothesis reported that MS patients with high fatigue showed reduced mesocorticolimbic connectivity compared to healthy adults when performing a working memory task (Engstrom et al., 2013). Most research on the dopamine imbalance hypothesis and its relation to fatigue in MS comes from pharmacological studies (Krupp et al.,1995; Pucci et al., 2007; Stankoff et al., 2005; Ledinek et al., 2013) reporting that dopamine agonist reduces fatigue. Further, animal and human research have reported the influence of dopamine on cognition as well, showing an inverted-U shape pattern (Cools and D’Esposito, 2011; Seamans and Yang, 2004), with too little or too much dopamine leading to cognitive impairment. Fatigue seems to follow a similar mechanism (Dobryakova et al., 2015). In a study by Gibbs and D’Esposito (2005) healthy participants that received dopamine agonist showed increased working memory performance. Later, Haret et al., (2009) reported similar results in MS patients. As a result, the dopamine imbalance hypothesis supports a unifying framework of fatigue in research. Lastly, as fatigue and cognitive functions rely on similar neural networks, there is a possibility that dopamine has a modulating effect on fatigue (Dobryakova et al., 2015). Eye-blink rate has long been linked as an indirect measure of dopamine activity. When it comes to neurological and psychiatric disorders, EBR showed significance to dopamine dysregulation. For example, Parkinson’s disease patients show reduced EBR (Agostino et al., 2008, 1987; Aksoy et al., 2014; Biousse et al., 2004; Bologna et al., 2014, 2012; Deuschl and Goddemeier, 1998; Fitzpatrick et al., 2012; Karson et al., 1984b, 1982b; Kimber and Thompson, 2000; Korosec et al., 2006; Reddy et al., 2013; Tamer et al., 2005) as there is progressive loss of dopaminergic neurons in the striatum (Dauer and Przedborski, 2003). Schizophrenic patients on the other hand, show increased EBR (Adamson, 1995; Chen et al., 1996; Helms and Godwin, 1985; Karson et al., 1984a, 1983, 1981a; Kleinman et al., 1984; Mackert et al., 1988; Ostow and Ostow, 1945; Stevens, 1978b, 1978a; Swarztrauber and Fujikawa, 1998), as their disorder is associated with excessive dopamine activity (Howes et al., 2015). In the same vein, individuals with mild cognitive impairment show increased EBR, which correlates negatively with cognitive performance (Ladas et al., 2014). Further, examining EBR in MS has only been done through startle eyeblink modulation (SEM) (Fox et al., 2016). SEM involves the examination of the size and the speed of the startle eyeblink reflex elicited in the presence and absence of a non-startling “prepulse” stimulus that is paired with the startle stimulus. In a study by Dezmalj-Grbelja et al., 2021), they examined the neurophysiological characteristics of BR in MS and in individuals with clinically isolated syndrome (CIS), however they examined blink reflex through visual evoked potentials. They concluded that BR is a useful diagnostic tool in brainstem assessment. Even though there is a well-established link between the role of both dopamine and EBR in MS, there is a surprising lack of research examining EBR in relation to fatigue and executive functions in MS. Such a relationship is notable given the evidence of the imbalance dopamine hypothesis in MS-related symptoms of fatigue and cognitive dysfunction. As a result, we aim to investigate EBR, as an indirect measure of dopamine activity, and its relation to fatigue and executive functions in MS. Our study will represent a critical gap in research and might provide insights into the neurochemical mechanisms of MS. We aim to explore the relationship between MS and EBR in adults. The first section of our study will focus on comparing and matching a sample of MS patients with a control group of healthy older adults. We will examine the differences in EBR between these two groups to better understand the neurochemical implication of MS in relation to Efs, fatigue and aging. We expect that correlation between EBR and EF in MS patients will differ from our first study. In the second section of our study, we will shift our focus on MS patients across different age groups. Our objective will be centered on the progression of MS and its relation to fatigue, EF deficits and potential dopamine imbalance, as measured by EBR. Specifically, we will examine how fatigue changes throughout the lifespan in MS patients comparing the different age groups, and if such effect also affects EBR. By analyzing age-related differences we can better understand if EBR can serve as a reliable marker for fatigue levels in MS in different stages of life. We hypothesize that there will be a distinction between older and younger groups of MS patients in terms of fatigue and EBR patterns. Further we will explore EF deficits across different age groups in MS to gain a better insight into how MS can impact EF over time. Finally, we will further examine whether any EF deficit in MS will correlate to EBR.

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