Browsing by Author "Siddik, Md Abu Bakkar"
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Item Examining the role of branched-chain amino acids in Alzheimer’s disease progression(2021-12) Siddik, Md Abu Bakkar; Hegde, Vijay; Shin, Andrew C.; Reddy, Arubala; Moghaddam, Masoud Zabet; Jung, KwangheeAlzheimer's disease (AD), an age-associated neurodegenerative disorder, is primarily characterized by accumulated amyloid-beta plaques, neurofibrillary phosphorylated Tau tangles, and diminished neurotransmitters in the brain. AD is strongly associated with type 2 diabetes (T2D). Emerging studies suggest that branched-chain amino acids (BCAAs), the essential amino acids we need to obtain from food, are involved in the pathogenesis of insulin resistance and T2D. Furthermore, high BCAAs can potentially reduce nerve growth factors, neuronal excitotoxicity, apoptosis, and an imbalance of crucial neurotransmitters in the brain. Interestingly, all these consequences caused by BCAA overload represent the key pathological features of AD, making BCAAs a potential contributor to this disease. Therefore, we examined if circulating BCAA levels are high in AD. We further tested if hepatic BCAA metabolism is impaired in AD since the liver is an organ with high BCAA degradation activity. Thus, plasma BCAA levels of eight-month-old wildtype or AD transgenic mice were measured by BCAA assay, and proteins and genes related to BCAA metabolism in the liver were determined by western blot and RT-qPCR, respectively. The plasma BCAA profile of healthy individuals, patients with AD, T2D, or AD+T2D after overnight fasting was analyzed using LC/MS. We observed that plasma BCAAs and/or their metabolites were higher in AD mice and humans than in healthy controls. This is further supported by the impairment in hepatic BCAA catabolism, evidenced by the key enzyme's inactivity in the BCAA degradation pathway. Even though high plasma BCAAs are present in AD, whether or not they can induce AD-like features in neurons is poorly understood. Therefore, we used mouse hippocampal HT-22 neurons to examine the direct effect of BCAAs on genes essential for neuronal functions. Mature HT-22 neurons were treated with 0, 1, 5, or 10 mM BCAAs for 24h, followed by protein and gene expression analysis. We found that BCAA supplementation to HT-22 neurons dose-dependently decreased expression of genes critical for neuronal functions, including mitochondrial biogenesis and fusion, autophagy, and synapse formation as it occurs in AD. So, our findings suggest that high plasma BCAAs resulting from inefficient degradation may potentially contribute to the development of AD. Considering the BCAA-induced AD-like features, our study further advocates the possibility of targeting BCAA intake and/or metabolism as a novel strategy to treat AD. Therefore, we extended our research to test if restriction of dietary BCAAs can ameliorate AD pathogenesis in transgenic AD mice. 10-12 months old WT or APP/PS1 mice were placed on either a chow diet (CD) or a CD with 50% BCAA restriction for two months. The BCAA-restricted diet was adjusted for all other amino acids to make it iso-caloric and iso-nitrogenous compared to the CD. For assessing cognitive function, Y-maze was used at baseline and after BCAA restriction. Animals were sacrificed after 5 hours of fasting, blood and tissues were collected for biochemical analysis. Baseline and post-restriction blood glucose, insulin, and BCAAs were also measured. To evaluate changes in neuropathological hallmarks of AD following dietary BCAA restriction, cortical or hippocampal protein, mRNA, or neurotransmitters were measured. Our findings suggest that BCAA restriction improved cognition and lowered fasting blood glucose, inflammation, pTau, and Aβ-42 levels in AD mice compared to control diet-fed mice. BCAA restriction also increased the production of cortical and hippocampal neurotransmitters crucial for neurotransmission. Combining all these findings, our study presents the potentials of a BCAA lowering approach to mitigate AD.Item Psychological disorders among college going students: A post Covid-19 insight from Bangladesh(2024) Siddik, Md Abu Bakkar; Ali, Akher; Miah, Sumon; Hasan, Mahedi (TTU); Ahmed, Minhaz; Sunna, Tachlima ChowdhuryThe COVID-19 pandemic has been found to result in adverse effects on both the physical and mental well-being of individuals. The adolescent population emerged as one of the most susceptible cohorts affected by the ongoing pandemic. They experienced significant adversity due to various mental health conditions. The objective of this study was to evaluate the present prevalence rates of depression, anxiety, and internet addiction among college-going students in Bangladesh following the post-COVID period. The study involved a cohort of 7667 students. A cross-sectional study was conducted to evaluate the levels of depression, anxiety, and internet addiction among college-going adolescents. The assessment utilized the Patient Health Questionnaire (PHQ-9), Generalised Anxiety Disorder (GAD-7), and Young's Internet Addiction Test (IAT) scales. The data was analyzed using the Pearson chi-square test and binary logistic regression. Participants averaged 15.3 years old and 64.3 % female. 63 % of students fulfilled the criterion for internet addiction, 37 % did not, 75 % met depression criteria, 25 % did not, and 60 % met anxiety requirements. Girls were more depressed and anxious than boys. Boys were more internet-addicted than girls. Social media usage from COVID-19, daily exercise, online courses, and financial concerns throughout the pandemic affected participants' mental health. Still, the students were suffering from internet addiction, depression, and anxiety after COVID-19. Early identification and intervention may lessen these difficulties' influence on adolescents' academic and personal lives. Colleges may provide mental health services, encourage healthy lives, and educate on mental health.