Aim and Background: Lumbar disc degeneration (LDD) is thought to be multifactorial in origin. Very recently the focus has shifted to the involvement of a family of candidate genes in the pathogenesis of LDD. There is particular emphasis on the vitamin D receptor gene (VDR gene). The VDR polymorphisms FOK1, TAQ1, and APO1 have been variably associated with LDD. Objective: To evaluate the association between the FOK1/Taq1 genes and LDD. Materials and Methods: One hundred unrelated healthy (asymptomatic) individuals who presented for routine health checkup and 93 consecutive patients (43 males and 50 females) with no history of low back pain were enrolled in the study after informed consent was obtained. The MRI images of cases and controls were graded and peripheral blood samples were collected from all participants and sent for genetic analysis. Results: Individuals with the dominant genotype for Taq1 had a significantly higher association with LDD than those without it. There was no association between LDD and the Fok1 genotype. Conclusion: Genetic predisposition is an important risk factor for LDD.

Parkinson’s disease (PD) is a common multidimensional neurological disorder characterized by motor and non-motor features and is more prevalent in the elderly. Sleep disorders and cognitive disturbances are also significant characteristics of PD. Sleep is an important physiological process for normal human cognition and physical functioning. Sleep deprivation negatively impacts human physical, mental, and behavioral functions. Sleep disturbances include problems falling asleep, disturbances occurring during sleep, abnormal movements during sleep, insufficient sleep, and excessive sleep. The most recognizable and known sleep disorders, such as rapid-eye-movement behavior disorder (RBD), insomnia, excessive daytime sleepiness (EDS), restless legs syndrome (RLS), sleep-related breathing disorders (SRBDs), and circadian-rhythm-related sleep–wake disorders (CRSWDs), have been associated with PD. RBD and associated emotional disorders are common non-motor symptoms of PD. In individuals, sleep disorders and cognitive impairment are important prognostic factors for predicting progressing neurodegeneration and developing dementia conditions in PD. Studies have focused on RBD and its associated neurological changes and functional deficits in PD patients. Other risks, such as cognitive decline, anxiety, and depression, are related to RBD. Sleep-disorder diagnosis is challenging, especially in identifying the essential factors that disturb the sleep–wake cycle and the co-existence of other concomitant sleep issues, motor symptoms, and breathing disorders. Focusing on sleep patterns and their disturbances, including genetic and other neurochemical changes, helps us to better understand the central causes of sleep alterations and cognitive functions in PD patients. Relations between α-synuclein aggregation in the brain and gender differences in sleep disorders have been reported. The existing correlation between sleep disorders and levels of α-synuclein in the cerebrospinal fluid indicates the risk of progression of synucleinopathies. Multidirectional approaches are required to correlate sleep disorders and neuropsychiatric symptoms and diagnose sensitive biomarkers for neurodegeneration. The evaluation of sleep pattern disturbances and cognitive impairment may aid in the development of novel and effective treatments for PD.

The pilot study aimed to investigate the effects of GAMS on oral microbiota in healthy dog subjects. Thirty-eight dogs were recruited and randomly allocated to the placebo (n = 19) and treatment groups (n = 19). The dogs were treated with mouth spray once daily for 42 days. The changes in the gingival index (GI), plaque index (PI), and calculus index (CI) were measured at baseline (day 0) and end of the study (42nd day). The changes in the oral microbial composition of representative dogs (placebo, n = 7; and treatment, n = 7) were also evaluated at baseline and end of the study. Oral microbial composition was assessed by sequencing. The sequences were annotated using the QIIME 2.0TM. The GI, PI, and CI indexes were reduced after the GAMS usage. The abundance of the commensal bacterial phylum Actinobacteria and Chloroflexi, genera Frederiksenia, and Bergeyella was improved after six weeks of GAMS usage. GAMS reduced the pathogenic bacterial species, including Neisseria sp., Desulfobulbus sp., Capnocytophaga canis, and Corynebacterium mustelae. Moreover, some pathogenic bacterial abundances were increased at the end of the study. All the microbial variations were observed within the group. The inter-group analysis revealed that the changes were unrelated to GAMS usage. Further studies need to be carried out using more experimental subjects to confirm the effectiveness of GAMS. More metagenomic data are required to evidence the GMAS impact on the oral microbiome of healthy dogs.

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A multi-factorial illness that causes morbidity threatens life and affects the quality of life is the major depressive disorder (MDD). Serotonergic dysfunction is one of the most described theories of psychiatric symptoms. Several serotonergic genes have been reported in associated with MDD. Recent studies have suggested that serotonin transporter length polymorphic region (5HTTLPR), Tryptophan hydroxylase gene 1 (TPH1) and Tryptophan hydroxylase gene 2 (TPH2) are associated with MDD. In the present study, we have examined the possible correlation between serotonergic genes 5HTTLPR, TPH1 (A218C), and TPH2 (G703T) polymorphism in MDD patients in Coimbatore tertiary care hospital. Blood samples were collected from 245 major depressive disorder patients and 250 healthy volunteers belonging to the faculty of Karpagam College of Medical Science and Research. All the samples were analysed by PCR-RFLP method. The chi-square test has been used for comparing genotype and allele distribution of cases and controls. We observed the 5HTTLPR L/S genotype and allele frequencies (P=0.001and p= 0.001) and TPH2 (G703T) (P=0.0002 and P= 0.005) TPH1 (A218C) (P=0.48 and P=0.43) polymorphisms with MDD. We also observed higher homozygous genotype frequencies of the short allele of 5HTTLPR, the G allele of TPH2 G703T polymorphism in patients. In short, our preliminary study suggests that the 5HTTLPR L/S and TPH2 G703T gene polymorphism were associated with the MDD. Serotonergic genes polymorphism in MDD patients and control groups were compared. Further clinical trials are to be carried out to find the exact mechanisms of the serotonergic system in MDD.