Catalpol, classified as an iridoid glucoside, is recognized for its significant role in medicine, particularly in the treatment of various conditions such as diabetes mellitus, neuronal disorders, and inflammatory diseases. This review aims to evaluate the biological implications of catalpol and the mechanisms underlying its diverse pharmacological effects. A thorough exploration of existing literature was conducted utilizing the keyword "Catalpol" across prominent public domains like Google Scholar, PubMed, and EKB. Catalpol has demonstrated a diverse array of pharmacological effects in experimental models, showcasing its anti-diabetic, cardiovascular-protective, neuroprotective, anticancer, hepatoprotective, anti-inflammatory, and antioxidant properties. In summary, catalpol manifests a spectrum of biological effects through a myriad of mechanisms, prominently featuring its anti-inflammatory and antioxidant capabilities. Its diverse pharmacological profile underscores its potential for therapeutic applications across a range of conditions. Further research is warranted to fully elucidate the clinical implications of catalpol and optimize its use in medical practice.

Sleep is regarded as one of the most crucial factors in keeping a healthy lifestyle. To function normally, a person needs at least 6–8 h of sleep per day. Sleep influences not only our mood but also the efficiency with which we complete tasks. Sleep disorders exhibit diverse etiologies across different conditions and populations, with genetic and environmental factors playing a significant role in their development. Many issues emerge as a result of inadequate sleep. Unhealthy food and lifestyle choices have increased our susceptibility to sleep disorders. A well-balanced diet rich in essential vitamins and minerals can have a profound impact on sleep patterns, enhancing both the duration and quality of rest. The primary categories of sleep disorders include insomnia, sleep apnea (SA), narcolepsy, parasomnias, circadian rhythm disorders, and restless legs syndrome (RLS). The drugs used to treat sleep disorders are primarily habit-forming and have a history of withdrawal effects. This insufficiency in medication has prompted the hunt for newer, better options. Nutraceuticals are well-suited to the treatment of such illnesses. Its non-toxic, non-habit-forming properties, and practical efficiency have made it an outstanding choice. This review provides nutraceuticals used in sleep disorders. A comprehensive literature search was conducted utilizing several databases, including Google Scholar, Elsevier, Springer Nature, Wiley, PubMed, and EKB. Nutraceuticals are products that employ food or dietary components to treat or prevent disease. In the therapy of sleep disorders, nutraceuticals such as Artemisia annua, valerian, rosemary, jujube, Passionflower, lemon balm, ashwagandha, kava-kava, lavender, and chamomile have been shown to have remarkable benefits. These remedies exert their effects through multiple mechanisms, both directly by modulating neurotransmitter and hormonal pathways within sleep circuits, and indirectly by enhancing sleep quality through the alleviation of stress, inflammation, and oxidative stress. Clinical studies were piloted to validate the efficacy of natural sleep aids. Future research should focus on elucidating the precise mechanisms through which natural products influence sleep.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterised by the death of motor neurons leading to paralysis and death generally 3–5 years post-symptom onset. ALS is a cell- and non-cell-autonomous disease, with glia such as astrocytes influencing disease pathology and progression. Our laboratory has previously identified purine metabolism dysfunction in induced neural progenitor cell-derived astrocytes (iAstrocytes) from sporadic ALS (SALS) cases, driven by loss of the enzyme adenosine deaminase (ADA). Here, we have demonstrated that loss of ADA, along with changes to ecto-5′-nucleotidase and hypoxanthine-guanine phosphoribosyl transferase led to disruption in purine metabolite levels, linked to the level of the ADA enzyme. These alterations were recapitulated in SALS CSF and post-mortem tissue, with ageing and sex affecting purine metabolite levels downstream of ADA and positively correlating with disease progression. Loss of ADA led to reduced 53BP1-mediated DNA repair and increased P16 levels, which was recapitulated in control iAstrocytes via ADA inhibition. Our findings indicate that TDP43 dysfunction drives impairment of ADA-mediated purine metabolism in vitro, leading to downstream effects that include DNA damage, likely through inhibition of DNA repair mechanisms, and the induction of cellular senescence. Furthermore, these results suggest that therapeutic targeting of the ADA pathway may help slow ALS disease progression.