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The role of CRISPR-Cas9 technology Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Reaching new horizons in Alzheimer's research 17/04/25, 10:24 Last updated: Published: 12/10/23, 10:50 The role of CRISPR-Cas9 technology The complexity of Alzheimer’s Alzheimer's disease (AD) is a formidable foe, marked by its relentless progression and the absence of a definitive cure. As the leading cause of dementia, its prevalence is expected to triple by 2050. Traditional therapies mainly focus on managing symptoms; however, advances in genetics research, specifically CRISPR-Cas9 gene-editing technology, offer newfound hope for understanding and treating this debilitating condition. The disease is characterized by progressive deterioration of cognitive function, with memory loss being its hallmark symptom. Primarily affecting individuals aged 65 and over, age is the most significant risk factor. Although this precise cause remains elusive, scientists believe that a combination of genetic, lifestyle and environmental factors contributes to its development. CRISPR’s role in Alzheimer’s research After the discovery of using CRISPR-Cas9 for gene editing, this technology is receiving interest for its potential ability to manipulate genes contributing to Alzheimer’s. Researchers from the University of Tokyo used a screening technique involving CRISPR-Cas9 to identify calcium, proteins, and integrin-binding protein 1, which is involved in the formation of AD. Furthermore, Canadian researchers have edited genes in brain cells to prevent Alzheimer’s using CRISPR. The team identified a genetic variant called A673T, found to decrease Alzheimer’s likelihood by a factor of four and reduce Alzheimer’s biomarker beta-amyloid (Aβ). Using CRISPR in petri dish studies, they managed to activate this A673T variant in lab-grown brain cells. However, the reliability and validity of this finding are yet to be confirmed by replication in animal studies. One final example of CRISPR application is targeting the amyloid precursor protein (APP) gene. The Swedish mutation in the APP gene is associated with dominantly inherited AD. Scientists were able to specifically target and disrupt the mutant allele of this gene using CRISPR, which decreased pathogenic Aβ peptide. Degenerating neurons are surrounded by Aβ fibrils, the production of Αβ in the brain initiates a series of events which cause the clinical syndrome of dementia. The results of this study were replicated both ex vivo and in vivo and demonstrated this could be a potential treatment strategy in the future. The road ahead While CRISPR technology’s potential in Alzheimer’s research is promising, its therapeutic application is still in its Infancy. Nevertheless, with the aid of cutting-edge tools like CRISPR, deepening our understanding of AD, we are on the cusp of breakthroughs that could transform the landscape of Alzheimer’s disease treatment. Written by Maya El Toukhy Related articles: Alzheimer's disease (an overview) / Hallmarks of Alzheimer's / Sleep and memory loss Project Gallery

Exploring the distinctive features that define and disrupt the brain Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A deep dive into the hallmarks defining Alzheimer’s disease 17/04/25, 10:20 Last updated: Published: 06/11/24, 12:02 Exploring the distinctive features that define and disrupt the brain The progressive decline in neurocognition, resulting in a detrimental effect on one’s activities of daily living, is referred to as dementia. It typically affects people over the age of 65. Multiple theories have been proposed to explain the pathogenesis of Alzheimer’s disease (AD), including the buildup of amyloid plaques in the brain and the formation of neurofibrillary tangles (NFT) in cells. Understanding the pathophysiology of AD is imperative to the development of therapeutic strategies. Therefore, this article will outline the major hallmarks and mechanisms of AD. Hallmark 1: amyloid plaques One of the most widely accepted hypotheses for AD is the accumulation of amyloid beta protein (Aβ) in the brain. Aβ is a 4.2 kDa peptide consisting of approximately 40–42 amino acids, originating from a precursor molecule called amyloid precursor protein. This process, defined as amyloidosis, is strongly linked to brain aging and neurocognitive decline. How do the amyloid plaques form? See Figure 1 . Reasons for the accumulation of amyloid plaques: Decreased autophagy: Amyloid proteins are abnormally folded proteins. Autophagy in the brain is primarily carried out by neuronal and glial cells, involving key structures known as autophagosomes and lysosomes. When autophagy becomes downregulated, the metabolism of Aβ is impaired, eventually resulting in plaque buildup. Overproduction of acetylcholinesterase (AChE): Acetylcholine (Ach) is the primary neurotransmitter involved in memory, awareness, and learning. Overproduction of ACHE by astrocytes into the synaptic cleft can lead to excessive breakdown of Ach, with detrimental effects on cognition. Reduced brain perfusion: Blood flow delivers necessary nutrients and oxygen for cellular function. Reduced perfusion can lead to “intracerebral starvation”, depriving cells of the energy needed to clear Aβ. Reduced expression of low-density lipoprotein receptor-related protein 1: Low-density lipoprotein receptor-related protein 1 (LRP1) receptors are abundant in the central nervous system under normal conditions. They are involved in speeding up the metabolic pathway of Aβ by binding to its precursor and transporting them from the central nervous system into the blood, thereby reducing buildup. Reduced LRP1 expression can hinder this process, leading to amyloid buildup. Increased expression of the receptor for advanced glycation end products (RAGE): RAGE is expressed on the endothelial cells of the BBB, and its interaction with Aβ facilitates the entry of Aβ into the brain. Hallmark 2: neurofibrillary tangles See Figure 2 Neurofibrillary tangles are excessive accumulations of tau protein. Microtubules typically support neurons by guiding nutrients from the soma (cell body) to the axons. Furthermore, tau proteins stabilise these microtubules. In AD, signalling pathways involving phosphorylation and dephosphorylation cause tau proteins to detach from microtubules and stick to each other, eventually forming tangles. This results in a disruption in synaptic communication of action potentials. However, the exact mechanism remains unclear. Recent studies suggest an interaction between Aβ and tau, where Aβ can cause tau to misfold and aggregate, forming neurofibrillary tangles inside brain cells. Both Aβ and tau can self-propagate, spreading their toxic effects throughout the brain. This creates a vicious cycle, where Aβ promotes tau toxicity, and toxic tau can further exacerbate the harmful effects of Aβ, ultimately causing significant damage to synapses and neurons in AD. Hallmark 3: neuroinflammation Microglia are the primary phagocytes in the central nervous system. They can be activated by dead cells and protein plaques, where they initiate the innate immune response. This involves the release of chemokines to attract other white blood cells and the activation of the complement system which is a group of proteins involved in initiating inflammatory pathways to fight pathogens. In AD, microglia bind to Aβ via various receptors. Due to the substantial accumulation of Aβ, microglia are chronically activated, leading to sustained immune responses and neuroinflammation. Conclusion The contributions of amyloid beta plaques, neurofibrillary tangles and chronic neuroinflammation provide a framework for understanding the pathophysiology of AD. AD is a highly complex condition with unclear mechanisms. This calls for the need of continued research in the area as it is crucial for the development of effective treatments. Written by Blessing Amo-Konadu Related articles: Alzheimer's disease (an overview) / CRISPR-Cas9 to potentially treat AD / Sleep and memory loss REFERENCES 2024 Alzheimer’s Disease Facts and Figures. (2024). Alzheimer’s & dementia, 20(5). doi:https://doi.org/10.1002/alz.13809. A, C., Travers, P., Walport, M. and Shlomchik, M.J. (2001). The complement system and innate immunity. [online] Nih.gov. Available at: https://www.ncbi.nlm.nih.gov/books/NBK27100/ . Bloom, G.S. (2014). Amyloid-β and tau: the Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA neurology, [online] 71(4), pp.505–8. doi:https://doi.org/10.1001/jamaneurol.2013.5847. Braithwaite, S.P., Stock, J.B., Lombroso, P.J. and Nairn, A.C. (2012). Protein Phosphatases and Alzheimer’s Disease. Progress in molecular biology and translational science, [online] 106, pp.343–379. doi:https://doi.org/10.1016/B978-0-12-396456-4.00012-2. Heneka, M.T., Carson, M.J., El Khoury, J., Landreth, G.E., Brosseron, F., Feinstein, D.L., Jacobs, A.H., Wyss-Coray, T., Vitorica, J., Ransohoff, R.M., Herrup, K., Frautschy, S.A., Finsen, B., Brown, G.C., Verkhratsky, A., Yamanaka, K., Koistinaho, J., Latz, E., Halle, A. and Petzold, G.C. (2015). Neuroinflammation in Alzheimer’s disease. The Lancet. Neurology, 14(4), pp.388–405. doi:https://doi.org/10.1016/S1474-4422(15)70016-5. Kempf, S. and Metaxas, A. (2016). Neurofibrillary Tangles in Alzheimer′s disease: Elucidation of the Molecular Mechanism by Immunohistochemistry and Tau Protein phospho- proteomics. Neural Regeneration Research, 11(10), p.1579. doi:https://doi.org/10.4103/1673-5374.193234. Kumar, A., Tsao, J.W., Sidhu, J. and Goyal, A. (2022). Alzheimer disease. [online] National Library of Medicine. Available at: https://www.ncbi.nlm.nih.gov/books/NBK499922/. Ma, C., Hong, F. and Yang, S. (2022). Amyloidosis in Alzheimer’s Disease: Pathogeny, Etiology, and Related Therapeutic Directions. Molecules, 27(4), p.1210. doi:https://doi.org/10.3390/molecules27041210. National Institute on Aging (2024). What Happens to the Brain in Alzheimer’s Disease? [online] National Institute on Aging. Available at: https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/what-happens-brain- alzheimers-disease. Stavoe, A.K.H. and Holzbaur, E.L.F. (2019). Autophagy in Neurons. Annual Review of Cell and Developmental Biology, 35(1), pp.477–500. doi: https://doi.org/10.1146/annurev-cellbio-100818-125242 . Project Gallery

Recent prospects for carbon monoxide indicate so Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can carbon monoxide unlock new pathways in inflammation therapy? 20/03/25, 12:03 Last updated: Published: 01/09/24, 10:31 Recent prospects for carbon monoxide indicate so Carbon monoxide (CO) is a colourless, odourless and tasteless gas which is a major product of the incomplete combustion of carbon-containing compounds. The toxic identity CO stems from its strong affinity for the haemoglobin in our blood which is around 300 times as strong as the affinity of oxygen. As a result, once the gas is inhaled, CO binds to the haemoglobin instead and reduces the amount of oxygen our blood can transport, which can cause hypoxia (low levels of oxygen in tissue) and dizziness, eventually leading to death. However, an intriguing fact is that CO is also endogenously produced in our body, due to the degradation of haem in the blood. Moreover, recent prospects for CO indicate that it may even be developed as an anti-inflammatory drug. How CO is produced in the body See Figure 1 Haem is a prosthetic (non-peptide) group in haemoglobin, where the oxygen binds to the iron in the molecule. When red blood cells reach the end of their lifespan of around 120 days, they are broken down in a reaction called haemolysis. This occurs in the bone marrow by macrophages that engulf the cells, which contain the necessary haem-oxygenase enzyme. Haem-oxygenase converts haem into CO, along with Fe2+ and biliverdin, the latter being converted to bilirubin for excretion. The breakdown of haem is crucial because the molecule is pro-oxidant. Therefore, free haem in the blood can lead to oxidative stress in cells, potentially resulting in cancers. Haem degradation also contributes to the recycling of iron for the synthesis of new haem molecules or proteins like myoglobin. This is crucial for maintaining iron homeostasis in the body. The flow map illustrates haemolysis and the products produced, which either protect cells from further stress or result in cell injury. CO can go on to induce anti-inflammatory effects- see Figure 2 . Protein kinases and CO Understanding protein kinases is crucial before exploring carbon monoxide (CO) reactions. Protein kinases phosphorylate (add a phosphate group to) proteins using ATP. Protein kinases are necessary to signal the release of a hormone or regulating cell growth. Each kinase has two regulatory (R) subunits and two catalytic (C) subunits. ATP as a reactant is usually sufficient for protein kinases. However, some kinases require additional mitogens – specific activating molecules like cytokines (proteins regulating immune cell growth), that are involved in regulating cell division and growth. Without the activating molecules, the R subunits bind tightly to the C subunits, preventing phosphorylation. Research on obese mice showed that CO binding to a Mitogen-Activated Protein Kinase (MAPK) called p38 inhibits inflammatory responses. This kinase pathway enhances insulin sensitivity, reducing obesity effects. The studies used gene therapy, modifying haem-oxygenase levels in mice. Mice with reduced haem-oxygenase levels had more adipocytes (fat-storing cells) and increased insulin resistance, suggesting CO treatment potential for chronic obstructive pulmonary disease (COPD), which causes persistent lung inflammation and results in 3 million deaths annually. Carbon-monoxide-releasing molecules As a result of these advancements, specific CO-releasing molecules (CORMs) have been developed to release carbon monoxide at specific doses. Researchers are particularly interested in the ability of CORMs to regulate oxidative stress and improve outcomes in conditions during organ transplantation, and cardiovascular diseases. Advances in the design of CORMs have focused on improving their stability, and targeted release to specific tissues or cellular environments. For instance, CORMs based on transition metals like ruthenium, manganese, and iron have been developed to enhance their efficacy and minimize side effects. This is achieved through carbon monoxide forming a stable ‘ligand’ structure with metals to travel in the bloodstream. Under an exposure to light or a chemical, or even by natural breakdown, these structures can slowly distribute CO molecules. Although the current research did not find any notable side effects within mouse cells, this does not reflect the mechanisms in human organ systems, therefore there is still a major risk of incompatibility due to water insolubility and toxicity issues. These problems could lead to potentially lead to disruption in the cell cycle, which may promote neurodegenerative diseases. Conclusion: the future of carbon monoxide Carbon monoxide has transitioned from being a notorious toxin to a valuable therapeutic agent. Advances in CO-releasing molecules have enabled its safe and controlled use, elevating its anti-inflammatory and protective properties to treat various inflammatory conditions effectively. This shift underpins the potential of CO to revolutionise inflammation therapy. It is important to remember that while carbon monoxide-releasing molecules (CORMs) have potential in controlled therapeutic settings, carbon monoxide gas itself remains highly toxic and should be handled with extreme caution to avoid serious health risks. Written by Baraytuk Aydin Related articles: Schizophrenia, inflammation and ageing / Kawasaki disease REFERENCES Different Faces of the Heme-Heme Oxygenase System in Inflammation - Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/The-colorimetric-actions-of-the-heme-HO-system-heme-oxygenase-mediated-heme-degradation_fig3_6531826 (accessed 11 Jul, 2024). Nath, K.A. (2006) Heme oxygenase-1: A provenance for cytoprotective pathways in the kidney and other tissues, Kidney International. Available at: https://www.sciencedirect.com/science/article/pii/S0085253815519595 (Accessed: 12 July 2024). Gáll, T. et al. (2020) ‘Therapeutic potential of carbon monoxide (CO) and hydrogen sulfide (H2S) in hemolytic and hemorrhagic vascular disorders—interaction between the heme oxygenase and H2S-producing systems’, International Journal of Molecular Sciences, 22(1), p. 47. doi:10.3390/ijms22010047. Venkat, A. (2024) Protein kinase, Wikipedia. Available at: https://en.wikipedia.org/wiki/Protein_kinase (Accessed: 12 July 2024). Goebel, U. and Wollborn, J. (2020) Carbon monoxide in intensive care medicine-time to start the therapeutic application?! - intensive care medicine experimental, SpringerOpen. Available at: https://icm-experimental.springeropen.com/articles/10.1186/s40635-020-0292-8 (Accessed: 07 July 2024). Bansal, S. et al. (2024) ‘Carbon monoxide as a potential therapeutic agent: A molecular analysis of its safety profiles’, Journal of Medicinal Chemistry, 67(12), pp. 9789–9815. doi:10.1021/acs.jmedchem.4c00823. DeSimone, C.A., Naqvi, S.L. and Tasker, S.Z. (2022) ‘Thiocormates: Tunable and cost‐effective carbon monoxide‐releasing molecules’, Chemistry – A European Journal, 28(41). doi:10.1002/chem.202201326. Project Gallery

Looking at p53 mutations and cancer predisposition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Decoding p53: the guardian against cancer 05/02/25, 16:21 Last updated: Published: 23/11/23, 11:38 Looking at p53 mutations and cancer predisposition Being a tumour suppressor protein, p53 encoded by the TP53 gene plays a critical role in regulating cell division and preventing the formation of tumours. Its function in maintaining genome stability is vital in inhibiting cancer development. Understanding p53 Located on chromosome locus 17p13.1, TP53 encodes the p53 transcription factor 1. Consisting of three domains, p53 can directly initiate or suppress the expression of 3661 different genes involved in cell cycle control and DNA repair 2. With this control, p53 can influence cell division on a massive scale. Cancer is characterised by uncontrolled cell division, which can occur due to accumulated mutations in either proto-oncogenes or tumour suppressor genes. Wild-type p53 can repair mutations in oncogenes such that they will not affect cell division. However, if p53 itself is mutated, then its ability to repair DNA and control the cell cycle is inhibited, leading to the emergence of cancer. Mutations in TP53 are actually the most prevalent genetic alterations found in patients with cancer. The mechanisms by which mutated p53 leads to cancer are manifold. One such mechanism is p53’s interaction with p21. Encoded by CDKN1A , p21 is activated by p53 and prevents cell cycle progression by inhibiting the activity of cyclin-dependent kinases (CDKs). Therefore, we can see that a non-functional p53 would lead directly to uncontrolled cell division and cancer. Clinical significance The importance of p53 in preventing cancer is highlighted by the fact that individuals with inherited TP53 mutations (a condition known as Li-Fraumeni syndrome or LFS) have a significantly greater risk of developing any cancer. These individuals inherit one defective TP53 allele from one parent, making them highly susceptible to losing the remaining functional TP53 allele, ultimately leading to cancer. Loss of p53 also endows cells with the ability to ignore pro-apoptotic signals such that if a cell becomes cancerous, it is far less likely to undergo programmed cell death 3. Its interactions with the apoptosis-inducing proteins Bax and Bak, are lost when mutated, thus leading to cellular apoptosis resistance. The R337H mutation in TP53 is an example of the founder effect at work. The founder effect refers to the loss of genetic variation when a large population descends from a smaller population of fewer individuals. The descendants of the initial population are much more likely to harbour genetic variations that are less common in the species as a whole. In southern Brazil, the R337H mutation in p53 is present at an unusually high frequency 4 and is thought to have been introduced by European settlers several hundred years ago. It is responsible for a widespread incidence of early-onset breast cancers, LFS, and paediatric adrenocortical tumours. Interestingly, individuals with this mutation can trace their lineage back to the group of European settlers that set foot in Brazil hundreds of years ago. Studying p53 has enabled us to unveil its intricate web of interactions with other proteins and molecules within the cell and unlock the secrets of cancer development and potential therapeutic strategies. By restoring or mimicking the functions of p53, we may be able to provide cancer patients with some relief from this life-changing condition. Written by Malintha Hewa Batage Related articles: Zinc finger proteins / Anti-freeze proteins Project Gallery

Psychology delves into the human mind and behaviour. Read on for compelling articles ranging from reward sensitivity to evolutionary, and empathy-altruism theories. Discover the psychology of emotions: embarrassment, and aggression. Psychology Articles Psychology delves into the human mind and behaviour. Read on for compelling articles ranging from reward sensitivity to evolutionary, and empathy-altruism theories. Discover the psychology of emotions: embarrassment, and aggression. You may also like: Biology, Medicine Motivating the mind Effect of socioeconomic status on reward sensitivity The evolutionary theory by Darwin vs empathy-altruism Explaining altruism through different theories A perspective on well-being Hedonic vs eudaimonic: based on the principles of Aristotle and Aristippus Nature vs. nurture in childhood intelligence What matters most? The psychology of embarrassment Why do we feel this emotion? Models and theories A primer on the Mutualism theory of intelligence A detailed review on different studies Unmasking aggression Is this fierce emotion the result of personal, or social triggers? Mental health strategies Raising awareness to look after mental health Imposter syndrome in STEM Have you ever had this feeling in your STEM education or job? Mental health in the South Asian community Why is it not yet such an open discussion?

Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and the other sciences. Log In Welcome to Scientia News DELIVERING INFORMATIVE CONTENT Scientia News is full of STEM blogs, articles and resources freely available across the globe for students. Browse all of our fascinating content written by students and professionals showing their passion in STEM and other sciences. We hope this platform helps you discover something that inspires your curiosity, and encourages you to learn more about important topics in STEM. Meet the Official Team NAVIGATE AND CLICK THE PHOTOS BELOW TO LEARN MORE ABOUT US! To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. To play, press and hold the enter key. To stop, release the enter key. Latest Articles psychology Addressing mental health within the South Asian community View More biology The interaction between circadian rhythms and nutrition View More biology Yemen- a neglected humanitarian crisis View More biology The effects of nanoparticles on health View More CONTACT CONTACT US Scientia News welcomes anyone who wants to share their ideas and write for our platform. If you are interested in realising your writing potential with us AND live in the UK; and/ or would like to give feedback: Email us at scientianewsorg@gmail.com or fill in our GET IN TOUCH form below and we'll be in contact... Follow us on our socials for the latest updates. Comment, like and share! Join our mailing list below for latest site content. You can also sign up to become a site member . SUBSCRIPTION Join our mailing list to receive alerts for new articles and other site content. Be sure to check your spam/ junk folders in case emails are sent there. Email Subscribe GET IN TOUCH First Name Last Name Email Message Send Thanks for submitting!

It’s been found that the species Dicrurus adsimilis (fork-tailed drongos) uses deception by flexible alarm mimicry to target and carry out food-theft attempts. The deceptive tactics of the fork-tailed drongo were studied which includes the use of false alarm calls and mimicked calls. Research was done on 64 wild drongos in the Kalahari Desert and it was found that the drongos spent more than a quarter of their time watching their target species which included southern pied babblers and meerkats Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Deception by flexible alarm mimicry in an African bird Last updated: 05/11/24 Published: 28/12/22 It’s been found that the species Dicrurus adsimilis (fork-tailed drongos) uses deception by flexible alarm mimicry to target and carry out food-theft attempts. The deceptive tactics of the fork-tailed drongo were studied which includes the use of false alarm calls and mimicked calls. Research was done on 64 wild drongos in the Kalahari Desert and it was found that the drongos spent more than a quarter of their time watching their target species which included southern pied babblers and meerkats. The other species’ would listen to the alarm calls made by drongos and would rush to take cover as they would if it was an alarm call from their species. These alarm calls were beneficial to them as it increased the number of returns from foraging and reduced their vigilance. However, the drongos used this to their advantage and if the target species was to find a large item of food the drongos could produce a false alarm call to make the target species run to cover out of fear which allowed the observing drongo to steal the deserted food. In 42% of cases of false alarms the drongos used a mimicked cry and in another 27% it was a mixture of mimicked and drongo-specific. This could be because target species are more likely to respond to a mimicked alarm call. In the case of babblers, if they heard a mimicked alarm call they would take longer to carry on foraging than with a drongo-specific call. The results show that false alarm calls by drongos work to distract their target but the call should also be frequently changed and not overused for best results. Written by Areebah Khan Related article: Conserving the Californian condor SUMMARISED FROM Flower, T.P., Gribble, M. and Ridley, A.R. (2014) “Deception by flexible alarm mimicry in an African bird,” Science, 344(6183), pp. 513–516.

In today's fast-paced and often overwhelming world, taking care of our mental well-being is more crucial than ever. In this article, we will explore practical strategies that can easily be incorporated into our day-to-day lives, allowing us to establish a solid foundation for our mental well-being and sustain it in the long run. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Empowering your mental health journey with practical strategies Last updated: 22/05/25 Published: 18/05/23 In today's fast-paced and often overwhelming world, taking care of our mental well-being is more crucial than ever. In this article, we will explore practical strategies that can easily be incorporated into our day-to-day lives, allowing us to establish a solid foundation for our mental well-being and sustain it in the long run. 1. Embracing mindfulness Mindfulness is a powerful practice that helps us stay present, cultivate awareness, and manage stress. Imagine starting your day by dedicating a few minutes to mindful breathing or meditation, allowing yourself to set a calm and focused tone for the day. Engage in activities with a mindful mindset, whether it's taking a peaceful walk in nature, relishing a cup of tea, or fully immersing yourself in the present moment. 2. Exercise Physical activity is another essential self-care strategy that not only benefits our physical health but also plays a profound role in nurturing our mental well-being. Find an exercise routine that that brings you joy and that easily fits into your life. Whether it's walking, jogging, yoga, or any other form of movement that resonates with you, the key is to find something you enjoy and can stick to. Even small bursts of exercise throughout the day, like a short walk during your lunch break or opting for the stairs instead of the elevator, can make a significant difference in your overall well-being. 3. Sleep Hygiene Adequate sleep is vital for mental and emotional wellbeing. Establishing good sleep hygiene is crucial. Maintain a consistent sleep schedule by going to bed and waking up at the same time each day. Create a relaxing bedtime routine that signals to your body that it's time to unwind. Consider reading a book, taking a warm bath, or practicing gentle stretches to prepare your mind and body for restful sleep. Ensure your bedroom provides an optimal sleep environment by keeping it dark, quiet, and cool, and minimize exposure to screens before bed. 4. Online mental health platforms In our digital age, online mental health platforms have become invaluable resources for supporting our mental well-being. Platforms like Headspace , Better Help , and Calm offer a range of services, including meditation exercises, therapy sessions with licensed professionals, and stress reduction tools. Exploring these platforms can provide the support and guidance needed on your mental health journey. Self-care apps that can be installed on phones Prioritising self-care is essential for maintaining good mental health. By incorporating these practices into your daily routine, you can nurture your mind, body, and soul. By investing time and energy into yourself, you are fostering a stronger foundation for a happier and healthier life. Written by Viviana Greco Related articles: Physical and mental health / Imposter syndrome in STEM / Mental health in the South Asian community

Our planet's ecosystems are teeming with life! Navigate the intricate web of interactions in these intriguing articles. How do organisms relate to one another and their surroundings? Ecology Articles Our planet's ecosystems are teeming with life! Navigate the intricate web of interactions in these intriguing articles. How do organisms relate to one another and their surroundings? You may also like: Biology, Zoology Galápagos Tortoises An end at the beginning: their conservation Beavers are back in Britain The role of beavers in the ecosystem and their reintroduction in the UK. Article #3 in a series on animal conservation around the world. Pangolins in China From poached to protected. Article #4 in a series on animal conservation around the world. Gorongosa National Park, Mozambique From conflict to community. Article #5 in a series on animal conservation around the world.

This page features articles which tackle imminent health problems such as smoking, childhood obesity and depression, and pre-diabetes. Skin disease, Crohn's disease, anaemias, and endometriosis are also explored.  Medicine Articles This page features articles which tackle imminent health problems such as smoking, childhood obesity and depression, and pre-diabetes. Skin disease, Crohn's disease, anaemias, and endometriosis are also explored. You may also like: Dentistry , Biology Interventions for smoking cessation Public smoking health interventions The problem with childhood obesity What is childhood obesity? How many does it affect, and what can we do to tackle this? Pre-diabetes Pre-diabetes is the period before the onset of diabetes Anaemias Anaemia is a blood disease. Article #1 in a series about anaemia. Endometriosis breakthrough The latest breakthrough in endometriosis: the bacterium theory AI in medicinal chemistry How can it help the field? Depression in children And how we can help them Iron-deficiency anaemia Anaemia is a blood disease. Article #2 in a series about anaemia. The power of probiotics And how they are effective Blood: a vital fluid The role and importance of blood Smart bandages What are they and how can they be better than traditional bandages? Why whales don't get cancer Discussing from Peter's Paradox perspective Anaemia of chronic disease The second most-common anaemia. Article #3 in a series about anaemia. Erasing memory Is it possible to wipe your memories clean? Herpes vs. skin disease From foe to ally: a Herpes-based gene therapy treats dystrophic epidermolysis bullosa. Article #3 in a series on Rare diseases. The foremothers of gynaecology An International Women's Month collab with Publett Healthcare serial killers A disturbing reality The gut microbiome Also known as: the microbiota, gut microflora Crohn's disease A summary of the condition Sideroblastic anaemia A problem synthesising haem. Article #4 in a series about anaemia. Next