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Bipolar disorder (BD) is a chronic, progressive illness characterized by fluctuations in mood. It is associated with psychosocial and cognitive impairment that can affect a person’s life at home, at work or school, and in interpersonal relationships. Children and adolescents diagnosed with BD experience similar functional impairments and risk for suicidal thoughts or actions compared to adults. Additionally, they are at an increased risk for poorer prognosis during adulthood given the negative outcomes associated with early illness onset, delayed treatment, misdiagnosis, and longer illness duration. The etiology and pathophysiology of bipolar disorder is incompletely understood. Peripheral blood biomarkers can provide insight into the mechanisms underlying the disease and can aid in identifying at-risk individuals, making an accurate diagnosis, monitoring illness activity and improving therapeutic intervention. A PubMed search was carried out and 12 studies were identified that assessed potential peripheral blood biomarkers in children and adolescents with bipolar disorder. These studies suggest that fatty acid biostatus, markers of lipid and protein oxidation, markers of inflammation and immune disturbance, neurotrophic factors and enzymes related to inflammation may serve as biomarkers of BD. These potential biomarkers of the disorder warrant further study in youth with BD. Current findings support a staging hypothesis of BD wherein cumulative episodes lead to disruptions of the pathways associated with the disorder and thus greater impairment in patients farther from their disease onset. However, these and other biomarkers will need to be evaluated in larger, longitudinal studies to validate their use and expand knowledge in the field.

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Alzheimer’s disease (AD), an age-related neurodegenerative disorder, progresses across a continuum of severity that leads to serious neurological dysfunction and eventually death. Initially manifesting as mild impairment in cognition and executive function, AD eventually leads to serious disturbances in memory, decision-making, language, mobility and sensing the environment. AD affects approximately 27 million people worldwide, over 5 million in the United States alone, and is one of the most debilitating diseases that costs society billions of dollars annually and is a primary cause of death in the elderly. Pharmacological treatments produce only moderate symptomatic benefits and do not attenuate or prevent the progression of AD with some medications associated with increased symptomatic behavior such as decreased motor function and increased likelihood of falls. Conversely, research utilizing animal models indicates exercise may play an important role to attenuate AD symptoms and delaying AD onset as regular aerobic activity increases the expression of brain-derived neurotrophic factor, a peptide that plays a major role in neural function, neural plasticity, and attenuation of neuritic plaque; a ß-amyloid derived plaque that is recognized as the primary cause of neural degradation associated with AD. To examine this exercise hypothesis, participants (N = 19; mean age 85.5 ±5.2 years) completed a single treatment, regular walking activity over time (30-min per day, 3 days per week for 12 weeks), with pre-test post-test evaluations undertaken utilizing valid research instruments designed to measure cognition, executive function, and motor capabilities in persons with AD. T-test with repeated measures ANOVA with various categorical variables as between-group factors were used to test the hypothesis. Analysis of change indicated significant change occurred in Cognitive function [t(18) = 5.74, p < .001], Balance [t(18) = 7.43, p < .001], and Mobility [t(18) = 3.82, p < .001], with no significant change in Activities of Daily Living (t[18] = 1.48, p < .156). A significant decrease in the number of falls was also found (z = 2.392, p < .017). No main effect was associated with AD stage, gender, or education level. The results of this study indicate regular aerobic activity enhances neural function in persons with AD, thus supporting the exercise hypothesis which posits regular aerobic exercise attenuates AD symptoms and delays AD onset. While the results provide important evidence regarding the impact of aerobic exercise on neural function in the AD populations, further research is necessary to identify the mechanisms by which brain-derived neurotrophic factor is induced with exercise and to examine the effectiveness of different exercise modalities (e.g., specificity, duration, and intensity) on neural function in the AD population. / Kinesiology

Schizophrenia is a debilitating neuropsychiatric disorder that affects approximately one percent of the global population. Aberrant N-methyl-D-aspartate receptors and endoplasmic reticulum stress have been implicated in the pathogenesis of schizophrenia. Despite a century of extensive research, outcomes from best-practice treatments remain dismal. Lurasidone hydrochloride is a novel atypical antipsychotic drug with a unique receptor binding profile that can potentially treat the heterogeneous symptomology of schizophrenia. However, discrepancies in experimental design (i.e. animal models used, symptoms assessed etc.) have yielded conflicting results surrounding the procognitive and antidepressant properties of lurasidone. Furthermore, the limited aqueous solubility of lurasidone poses a considerable challenge for improving antipsychotic drug delivery to the brain and limiting the prevalence of adverse side effects. These obstacles coupled with the elusive pathophysiology of schizophrenia and its incurable nature, highlight the importance of investigating novel therapeutic targets and their underlying mechanisms to improve treatment and enhance the quality of life of patients with schizophrenia. This thesis sought to accomplish three primary objectives: (1) validate the behavioural efficacy of lurasidone hydrochloride; (2) investigate the role of mesencephalic astrocyte-derived neurotrophic factor as a potential therapeutic target of lurasidone; and (3) evaluate the therapeutic potential of intranasal lurasidone administration as a novel method for antipsychotic drug delivery. The data presented within this thesis suggest that repeated lurasidone treatment may be effective at treating the positive, negative, and cognitive symptoms of schizophrenia, but not sensorimotor gating deficits. Furthermore, sub-chronic lurasidone treatment in rats significantly increased the relative expression of mesencephalic astrocyte-derived neurotrophic factor in the rat prefrontal cortex, a primary site of impairment observed in schizophrenia. Lastly, we conclude that lurasidone administered via the nasal route using a novel poly(oligo ethylene glycol methacrylate)-based nanogel formulation required four times less drug to achieve a therapeutic response comparable to traditional intraperitoneal routes. The findings presented within this thesis suggest that lurasidone might be a favourable atypical antipsychotic drug that exerts its therapeutic effects through the modulation of neurotrophic factor expression in the brain regions affected by schizophrenia. This thesis offers new insight that can help guide future studies toward improving the prognosis of patients suffering from schizophrenia. / Thesis / Master of Science (MSc)

Syfte Syftet med denna litteraturstudie var att redovisa vilken typ av träning (träningsform, intensitet, frekvens, träningspassduration och interventionsduration) som påverkar vilonivåer av BDNF hos friska vuxna. Metod För att besvara syftet gjordes en litteraturstudie. Litteratursökningar utfördes i databaserna PubMed, Web of Science och SPORTDisucs vilka gav 18 inkluderade artiklar. Träningsinterventionerna redovisades utifrån träningsform, intensitet, duration och frekvens. Resultatet redovisade de ingående gruppernas procentuella förändring gällande vilonivåer av BDNF samt tillhörande signifikansnivå. Resultat Av 18 inkluderade artiklar påvisade fem en signifikant skillnad i vilonivåer av BDNF, medan 13 artiklar inte visade någon signifikant skillnad. Slutsatser Utifrån resultatet kan inga generella slutsatser dras om träningsupplägg som påverkar vilonivåer av BDNF hos friska vuxna. Troligtvis skiljer sig den träningsinducerade responsen på vilonivåer av BDNF i olika kombinationer av träningsform, intensitet, frekvens, interventionsduration och träningspassduration. Responsen är således en komplex funktion beroende på ett flertal faktorer som såväl träningsupplägg och individuella faktorer. Regelbunden träning ger förmodligen en förändrad respons på BDNF-genuttryck, oavsett om vilonivåerna påverkas eller inte, vilket på sikt gynnar hjärnhälsan.