👤 Manjula Subbanna

Hypertension is recognized as a modifiable risk factor for cardiovascular diseases, alongside dyslipidemia. Studies have revealed that between 15 and 31% of individuals have both hypertension and dyslipidemia. However, emerging evidence suggests that natural therapies and yoga can help manage mild increases in blood pressure. This study aimed to evaluate the impact of yogic and naturopathy treatments on lipid profiles in hypertensive patients, thereby contributing to the existing literature. A randomized controlled experiment was conducted, involving 262 hypertensive patients randomly assigned to either the study group (SG) or control group (CG). The SG, consisting of 131 individuals, received yoga and naturopathic treatments for 10 days, while the CG (n = 131) did not. The lipid profile was measured at the beginning and end of the 10 days, and they were followed up and reassessed after 9 months. The study involved a total of 262 individuals, with 111 in the SG and 125 in the CG. After the 10-day intervention period, the SG showed significant reductions in total cholesterol, triglycerides, high-density lipoprotein, low-density lipoprotein, very low-density lipoprotein, apolipoprotein-A (Apo-A), apolipoprotein-B (Apo-B), and lipoprotein-A (Lp-A) (p < 0.001) compared to the CG. Also, the change was observed after 9 months in Apo-A, Apo-B, and Lp-A significantly (p < 0.001). These findings underscore the potential of naturopathic and yogic interventions in improving lipid profiles in hypertensive patients, thereby contributing to the current literature. In conjunction with conventional management, these specific interventions could be considered as a safer form of complementary therapy in the treatment of dyslipidemia among hypertensive patients. Thus, these findings hold promise for the integration of naturopathic and yogic therapies in the standard care of hypertensive patients. Show less

Endosomal system dysfunction within neurons is a prominent early feature of Alzheimer's disease (AD) pathology. Multiple AD risk factors are regulators of endocytosis and known to cause hyperactivity of the early endosome small GTPase rab5, resulting in neuronal endosomal pathway disruption and cholinergic neurodegeneration. Adaptor protein containing Pleckstrin homology domain, Phosphotyrosine binding domain, Leucine zipper motif (APPL1), an important rab5 effector protein and signaling molecule has been shown in vitro to interface between endosomal and neuronal dysfunction through a rab5-activating interaction with the BACE1-generated C-terminal fragment of amyloid precursor protein (APP-βCTF), a pathogenic APP fragment generated within endosomal compartments. To understand the contribution of APPL1 to AD-related endosomal dysfunction in vivo, we generated a transgenic mouse model overexpressing human APPL1 within neurons (Thy1-APPL1). Strongly supporting the important endosomal regulatory roles of APPL1 and their relevance to AD etiology, Thy1-APPL1 mice (both sexes) develop enlarged neuronal early endosomes and increased synaptic endocytosis due to increased rab5 activation. We demonstrated pathophysiological consequences of APPL1 overexpression, including functional changes in hippocampal long-term potentiation (LTP) and long-term depression (LTD), degeneration of large projection cholinergic neurons of the basal forebrain, and impaired hippocampal-dependent memory. Our evidence shows that neuronal APPL1 elevation modeling its functional increase in the AD brain induces a cascade of AD-related pathological effects within neurons, including early endosome anomalies, synaptic dysfunction, and selective neurodegeneration. Our in vivo model highlights the contributions of APPL1 to the pathobiology and neuronal consequences of early endosomal pathway disruption and its potential value as a therapeutic target. Show less

T helper 17 (Th17) pathway has been reported to be abnormal in schizophrenia; however, it is not known whether variation within genes of this pathway has any impact on schizophrenia. Herein, the impact of genetic variations and gene-gene interactions of Th17 pathway-related genes on the risk, psychopathology, and brain volume was examined in schizophrenia patients. Functional polymorphisms within interleukin 6 ( IL6 )(rs1800795 and rs1800797), IL10 (rs1800872 and rs1800896), IL17A (rs2275913 and rs8193036), IL22 (rs2227484 and rs2227485), IL23R (rs1884444), and IL27 (rs153109 and rs181206) genes were studied in 224 schizophrenia patients and 226 healthy controls. These variants were correlated with the brain morphometry, analyzed using MRI in a subset of patients ( n = 117) and controls ( n = 137). Patients carrying CC genotype of rs2227484 of IL22 gene had significantly higher apathy total score [ F (1,183) = 5.60; P = 0.019; partial ɳ 2 = 0.030]. Significant epistatic interactions between IL6 (rs1800797) and IL17A (rs2275913) genes were observed in schizophrenia patients. GG genotype of rs2275913 of IL17A gene was associated with reduced right middle occipital gyrus volume in schizophrenia patients ( T = 4.56; P < 0.001). Interactions between genes of Th17 pathway impact the risk for schizophrenia. The variants of Th17 pathway-related genes seem to have a determining effect on psychopathology and brain morphometric changes in schizophrenia. Show less