From the last few decades, there are increasing incidences of disorders like premature aging, cardiovascular disease, multiple sclerosis, fibromyalgia, and Alzheimer’s disease In addition to medication, researchers have found that yoga, a mind-body therapy, can be used as an alternative medicine. Yoga combines specific physical postures, breathing techniques, relaxation and meditation that improve mental and physical health of the body. The purpose of this review is to collate the research evidences claiming health benefits of performing traditional yogic practices. What are the biological and other reliable indicators to suggest that doing asanas, pranayama, and meditation could reduce or treat wide range of life style disorders are discussed. Importantly, these indicators are otherwise used to assess the severity of disorders. In many of the study it has been shown that yoga improves the redox health of body whose imbalance has been well proven to cause many health complications. The impact of yoga on neurodegenerative diseases have revealed that it reverses memory loss, reduce anxiety, depression and stress, the biological indicators of disease. However, most studies have several limitations and therefore further research into yoga is needed to validate these findings.

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There is mounting evidence of circadian rhythm disruption in Alzheimer's disease (AD); however, the cause-and-effect relationship between them is not understood. Chronic constant light exposure effectively disrupts circadian rhythm in rats. On the basis of previous publications, we hypothesized that chronic constant light exposure might contribute significantly to development of AD-like-phenotype in rats and that fluoxetine (Flx) treatment might protect the brain against it. Adult male rats were exposed to normal light-dark cycles, constant light (LL), constant dark, and LL+Flx (5 mg/kg/day, ZT5) for four months. The expression of molecular markers of circadian rhythm: Per2 transcripts; and protein expression of peroxiredoxin-1 (PRX1) and hyperoxidized peroxiredoxins (PRX-SO 2/3 ) were significantly dysregulated in the suprachiasmatic nuclei (SCN) of LL rats, which was prevented with concomitant fluoxetine administration. The levels of glutamate and γ-aminobutyric acid were dysregulated, and oxidative damage was observed in the SCN and hippocampi of LL rats. Fluoxetine treatment conferred protection against oxidative damage in LL rats. Constant light exposure also impaired rats' performance on Y-maze, Morris maze, and novel object recognition test, which was prevented with fluoxetine administration. A significant elevation in soluble Aβ 1−42 levels, which strongly correlated with upregulation of Bace1 and Mgat3 transcripts was observed in the hippocampus of LL rats. Further, the expression of antiaging gene Sirt1 was downregulated, and neuronal damage indicator Prokr2 was upregulated in hippocampus. Fluoxetine rescued Aβ 1−42 upregulation and AD-related genes' dysregulation. Our findings show that circadian disruption by exposure to chronic constant light may contribute to progression of AD, which can be prevented with fluoxetine treatment.

Peroxiredoxins (Prxs) are antioxidant proteins that are involved in cellular defence against reactive oxygen species and reactive nitrogen species. Humans have six peroxiredoxins, hPrxI-VI, out of which hPrxI and hPrxII belongs to the typical 2-Cys class sharing 90% conservation in their amino acid sequence including catalytic residues required to carry out their peroxidase and chaperone activities. Despite the high conservation between hPrxI and hPrxII, hPrxI behaves differently from hPrxII in its peroxidase and chaperone activity. We recently showed in yeast that in the absence of Tsa1 and Tsa2 (orthologs of hPrx) hPrxI protects the cells against different stressors whereas hPrxII does not. To understand this difference, we expressed catalytic mutants of hPrxI in yeast cells lacking the orthologs of hPrxI/II. We found that the catalytic mutants lacking peroxidase function including hPrxI C52S , hPrxI C173S , hPrxI T49A , hPrxI P45A and hPrxI R128A were not able to grow on media with nitrosative stressor (sodium nitroprusside) and unable to withstand heat stress, but surprisingly they were able to grow on an oxidative stressor (H 2 O 2 ). Interestingly, we found that hPrxI increases the expression of antioxidant genes, GPX1 and SOD1, and this is also seen in the case of a catalytic mutant, indicating hPrxI can indirectly reduce oxidative stress independently of its own peroxidase function and thus suggesting a novel role of hPrxI in altering the expression of other antioxidant genes. Furthermore, hPrxI C83T was resistant to hyperoxidation and formation of stable high molecular weight oligomers, which is suggestive of impaired chaperone activity. Our results suggest that the catalytic residues of hPrxI are essential to counter the nitrosative stress whereas Cys83 in hPrxI plays a critical role in hyperoxidation of hPrxI.