Uncovering the role of IGF2BP1 in neuroblastoma and its potential as a therapeutic target Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Novel neuroblastoma driver: a potential target for therapeutics Last updated: 24/06/25, 15:16 Published: 03/07/25, 08:00 Uncovering the role of IGF2BP1 in neuroblastoma and its potential as a therapeutic target Introduction Neuroblastoma is a complicated cancer of the nervous system that primarily affects children, particularly those under the age of five. It is characterised by the development of tumours originating from neural crest cells involved in the formation of the adrenal glands and sympathetic nervous system. As the most common extracranial solid tumour in infancy and childhood, neuroblastoma represents a significant challenge in paediatric oncology due to its complex biology and variable prognosis. Recent advancements have brought hope by identifying a novel genetic driver, IGF2BP1 , implicated in the aggressive progression of the disease. The University Medicine Halle team's breakthrough in pinpointing IGF2BP1 's role is significant. It paves the way for understanding the molecular underpinnings of neuroblastoma. Additionally, it opens the door to potentially transformative targeted therapies. By elucidating the mechanisms through which IGF2BP1 drives tumour growth—specifically through its interaction with oncogenes such as MYCN —researchers are making significant progress. They are closer than ever to devising strategies that could arrest the disease's development. This progress could significantly improve patient outcomes. The importance of this discovery cannot be overblown, as it provides a crucial target for therapeutic intervention, potentially leading to the development of more effective, less toxic treatments. This is a significant step towards not only enhancing survival rates but also the quality of life for affected children worldwide. IGF2BP1: a key player in neuroblastoma and potentially other tumours The IGF2BP1 gene has emerged as a crucial element in neuroblastoma pathogenesis. It functions as an RNA-binding protein that enhances the stability and translation of mRNA transcripts. These transcripts encode oncogenic proteins, significantly impacting tumour behaviour. Oncogenes are genes that have the potential to cause cancer by promoting uncontrolled cell division and tumour growth. The activation of IGF2BP1 leads to the increased expression of several key oncogenes, including BIRC5 and MYCN. These are known to drive the growth and malignancy of neuroblastoma cells. This discovery marks a substantial leap in understanding the molecular dynamics at play within neuroblastoma cells, offering a novel avenue for targeted intervention. By stabilising and enhancing the translation of mRNA transcripts encoding these oncogenic proteins, IGF2BP1 plays a crucial role in promoting tumour growth and malignancy. Understanding this interaction provides a strategic point of intervention, potentially leading to targeted therapies that could inhibit the harmful effects of IGF2BP1 and significantly improve patient outcomes. Moreover, the IGF2BP1 role extends beyond neuroblastoma. Its expression has been detected in various other cancers, where it similarly promotes tumour growth and survival. For example, IGF2BP1 has been implicated in the progression of colorectal, breast, and lung cancers, suggesting a broader oncogenic role. This consistent pattern across different cancers underscores its potential as a universal therapeutic target. The broad impact of IGF2BP1 on multiple tumour types also highlights the potential for developing cross-cancer therapeutic strategies. By targeting IGF2BP1 , it may be possible to design treatments that are effective against multiple forms of cancer, thus maximising the impact of research and development efforts in oncology. This could lead to the creation of a new class of anticancer drugs that inhibit IGF2BP1 , offering hope to patients with various malignancies. However, targeting this gene presents challenges. IGF2BP1 is involved in beneficial processes such as normal cell growth and repair. For instance, it plays a role in stabilising mRNA during cell division, which is crucial for tissue regeneration. Inhibiting IGF2BP1 might impair these processes, leading to issues such as poor wound healing or reduced immune function. Additionally, its inhibition could potentially affect other normal cellular functions, posing a risk of unintended side effects. Thus, while targeting IGF2BP1 holds promise, understanding its role in healthy cells is essential to developing therapies that are both effective and safe. Research into IGF2BP1’s mechanisms has also revealed that it might be instrumental in initiating an “oncogene storm”. This is a rapid and intense expression of oncogenes that drives aggressive tumour growth. It also leads to resistance to conventional therapies. Conventional therapies typically refer to standard cancer treatments such as chemotherapy, radiation therapy, and surgery. For example, chemotherapy drugs like doxorubicin and cisplatin are designed to kill rapidly dividing cells, but the oncogene storm can enable tumour cells to become resistant to these drugs by enhancing their survival mechanisms. Similarly, radiation therapy aims to damage the DNA of cancer cells, but the increased expression of oncogenes can repair this damage more effectively, allowing the tumour to persist. This understanding provides a crucial insight into how cancer cells exploit molecular mechanisms to thrive and evade treatment, thereby pointing to strategic points of intervention. Current research is exploring how targeted therapies can be developed to specifically inhibit the effects of the oncogene storm, potentially overcoming resistance to these conventional treatments. This understanding provides a crucial insight into how cancer cells exploit molecular mechanisms to thrive and evade treatment, thereby pointing to strategic points of intervention. MYCN’s role in neuroblastoma: a pivotal transcriptional driver MYCN is a member of the MYC family of transcription factors, which play critical roles in cell cycle progression, apoptosis, and cellular transformation. In neuroblastoma, MYCN is particularly notorious for its strong association with high-risk disease and poor clinical outcomes, making it a main point of cancer research. High-risk disease in neuroblastoma is characterised by factors such as advanced stage at diagnosis, unfavourable histology, and the presence of MYCN amplification. For example, Stage 4 neuroblastoma, where the cancer has spread to distant lymph nodes, bone, bone marrow, liver, skin, or other organs, is considered high-risk. Poor clinical outcomes in these cases often include a lower survival rate and a higher likelihood of relapse after treatment. Studies have shown that children with MYCN -amplified neuroblastoma have a significantly lower 5-year survival rate compared to those without MYCN amplification. This is because MYCN amplification drives rapid tumour growth and metastasis, making the cancer more aggressive and difficult to treat. Additionally, these patients often exhibit resistance to conventional therapies such as chemotherapy and radiation, which further complicates treatment and negatively impacts prognosis. Specific examples of poor clinical outcomes include frequent relapses and the development of resistance to multiple lines of therapy. Despite intensive treatment regimens, including high-dose chemotherapy followed by stem cell transplant and radiation therapy, the overall survival rate for high-risk neuroblastoma remains below 50%. This bare reality underscores the critical need for novel therapeutic strategies that can effectively target MYCN and improve outcomes for patients with high-risk neuroblastoma. In general, MYCN amplifies in approximately 20% to 25% of neuroblastoma cases, leading to a dramatic increase in its protein expression. This overexpression is a known marker for aggressive disease and has been linked to rapid tumour progression and resistance to standard therapies. Standard therapies for neuroblastoma typically include a combination of surgery, chemotherapy, and radiation therapy. For instance, chemotherapy drugs such as cyclophosphamide and vincristine are commonly used to shrink tumours before surgical removal. However, the overexpression of MYCN can enhance the tumour’s ability to repair DNA damage caused by these treatments, making them less effective. Radiation therapy, which uses high-energy particles to destroy cancer cells, also becomes less effective as MYCN overexpression promotes survival pathways within the cells. The interaction between MYCN and IGF2BP1 creates a formidable axis that drives the malignant characteristics of neuroblastoma cells. Functionally, MYCN amplifies the effects of IGF2BP1 by synergising its activity. This synergy is evident in their mutual enhancement of oncogenic signalling pathways. MYCN enhances the transcription of numerous genes involved in cellular proliferation and survival. While IGF2BP1 stabilises the mRNAs of these genes, ensuring their sustained expression and activity within the cell. This interaction not only accelerates tumour growth but also contributes to the genomic instability that is characteristic of high-risk neuroblastoma. Besides, the role of MYCN extends beyond merely amplifying gene expression. It fundamentally alters the cellular landscape by modulating the expression of genes involved in metabolism, differentiation, and angiogenesis, thus shaping the tumour microenvironment to favour cancer growth and metastasis. Recent studies have also uncovered MYCN ’s role in repressing the transcription of genes involved in cellular differentiation, thereby maintaining the cells in a more primitive, stem-like state that is conducive to cancer progression. The discovery of the “oncogene storm”, a phenomenon triggered by the cooperative action of MYCN and IGF2BP1 , highlights the critical need for targeted therapeutic strategies that can disrupt this deleterious synergy. By focusing on this interaction, researchers aim to develop novel treatments that can more effectively curb the aggressive nature of MYCN -amplified neuroblastoma. The potential for therapeutic intervention The discovery of the IGF2BP1 and MYCN interaction not only deepens our understanding of neuroblastoma pathogenesis but also marks a significant step towards developing targeted therapeutic interventions. The small molecule BTYNB , which disrupts this interaction, has shown promising results in preclinical studies. By inhibiting the oncogene-enhancing effect of IGF2BP1 on MYCN , BTYNB effectively reduces tumour growth and could potentially improve the efficacy of existing treatment protocols. Current research is exploring the application of BTYNB in combination with other therapeutic agents. Combining BTYNB with existing chemotherapy drugs or novel targeted therapies may enhance treatment efficacy and prevent the onset of resistance. This combinatorial approach could be particularly effective in high-risk neuroblastoma cases, where conventional treatments often fall short. Additionally, understanding the pharmacodynamics and optimising the dosing schedule of BTYNB are critical areas of ongoing research to maximise its therapeutic potential and minimise side effects. This includes studying how the drug is absorbed, distributed, metabolised, and excreted in the body to ensure optimal efficacy. For instance, researchers are investigating the timing and dosage that maximise tumour reduction while minimising toxicity. Examples include adjusting the frequency of administration to maintain therapeutic levels and combining BTYNB with other agents to enhance its effects. These efforts aim to maximise its therapeutic potential and minimise side effects. Furthermore, the ability of BTYNB to impair tumour growth without the severe side effects associated with conventional chemotherapy presents an opportunity to reduce the treatment burden on patients. This aspect is crucial, especially in paediatric oncology, where the long-term health of young patients is a significant concern. Future therapeutic strategies could see BTYNB becoming part of a first-line treatment for neuroblastoma, either as a standalone therapy or in combination with other treatments. Future directions The ground-breaking discovery of the IGF2BP1 - MYCN interaction in neuroblastoma provides solid initial results with BTYNB , and the identification of IGF2BP1 as a key driver in neuroblastoma opens several avenues for future research. One critical area involves further elucidation of the molecular mechanisms underlying IGF2BP1 ’s influence on neuroblastoma progression. Continued research is necessary to dissect the finer details of the molecular pathways modulated by IGF2BP1 and MYCN . This includes understanding the downstream effects of their interaction and identifying other molecular players involved in the signalling cascade. Insights from such studies could reveal novel personalised therapeutic targets and help in designing drugs that can more precisely disrupt these pathways. Additionally, given the role of IGF2BP1 in various cancers, research should also explore its potential as a universal cancer target. Comparative studies across different cancer types could identify shared patterns of IGF2BP1 activity, offering opportunities to develop broad-spectrum anticancer strategies. Developing targeted delivery mechanisms that can direct BTYNB or other similar drugs specifically to neuroblastoma cells could significantly enhance therapeutic outcomes and reduce side effects. Research into nanoparticle-based delivery systems or conjugated molecules that seek out cancer-specific markers could be particularly fruitful. Additionally, investigating other compounds that can target IGF2BP1 or MYCN could provide alternative therapeutic options or complementary strategies to overcome resistance. Strategic integration of new therapies into existing treatment protocols needs careful planning. This includes determining the optimal sequencing of therapies and identifying which combinations are most effective for various subtypes of neuroblastoma based on genetic characteristics. Clinical trials are essential to transitioning laboratory findings to clinical applications. Designing and implementing rigorous clinical trials to test the efficacy and safety of BTYNB , both as a monotherapy and in combination with other therapies, is crucial. These trials should incorporate robust biomarker studies to tailor therapies based on genetic profiles and monitor patient responses more effectively. Lastly, addressing the challenge of drug delivery remains paramount. Developing drug delivery systems that can effectively target tumour sites with minimal off-target effects could improve the therapeutic index of treatments like BTYNB . Research in this area will not only benefit neuroblastoma patients but also advance the field of targeted cancer therapy in general. Importantly, given the young age of neuroblastoma patients, it is imperative to consider long-term outcomes and quality of life in therapeutic development. Efforts must be made to ensure that new treatments are not only effective but also minimise the long-term health impacts often associated with aggressive cancer therapies. Conclusion The identification of IGF2BP1 as a pivotal driver in the pathogenesis of neuroblastoma, particularly in concert with MYCN , marks a significant milestone in paediatric oncology. This discovery not only enhances our molecular understanding of one of the most challenging childhood cancers but also sets the stage for the development of targeted therapeutic strategies that could revolutionise treatment paradigms. The potential of BTYNB , a small molecule inhibitor that disrupts the IGF2BP1 - MYCN interaction, underscores the power of targeted therapy. In preclinical models, BTYNB has demonstrated a promising ability to inhibit tumour growth effectively and with fewer side effects compared to traditional chemotherapy. Such advancements herald a new era in treatment where therapy is not only about fighting the disease but also preserving the quality of life for the youngest patients. However, the journey from laboratory to clinic is filled with challenges that require innovative solutions and collaborative efforts. These challenges include ensuring the safety and efficacy of new treatments, overcoming drug resistance, and achieving precise delivery to tumour sites. The future of neuroblastoma treatment lies in the ability to refine these emerging therapies through rigorous research, optimise their delivery, and integrate them seamlessly into existing treatment protocols. Additionally, the exploration of IGF2BP1 's role across various cancer types may provide insights that transcend paediatric oncology, offering new hope for comprehensive cancer treatment strategies. As the research advances, it will be crucial to maintain a multidisciplinary approach, combining the expertise of molecular biologists, clinical researchers, and pharmacologists to ensure that these new discoveries translate into safe and effective treatments. The engagement of global health communities in these efforts will be essential to address the diverse and complex nature of cancer treatment across different populations. All in all, the path forward is marked by significant potential and profound responsibility—to continue the search for knowledge and to translate that knowledge into therapies that not only extend life but also enhance the lived experiences of patients during and after treatment. With continued dedication and innovation, the future for children battling neuroblastoma looks increasingly hopeful. Written by Sara Maria Majernikova Related articles: Cancer on the move (metastasis) REFERENCES Hagemann, S., Misiak, D., Bell, J. L., Fuchs, T., Lederer, M. I., Bley, N., Hämmerle, M., Ghazy, E., Sippl, W., Schulte, J. H., & Hüttelmaier, S. (2023). IGF2BP1 induces neuroblastoma via a druggable feedforward loop with MYCN promoting 17q oncogene expression. Molecular cancer , 22 (1), 88. https://doi.org/10.1186/s12943-023-01792-0 Liu, Y., Guo, Q., Yang, H., Zhang, X. W., Feng, N., Wang, J. K., Liu, T. T., Zeng, K. W., & Tu, P. F. (2022). Allosteric Regulation of IGF2BP1 as a Novel Strategy for the Activation of Tumor Immune Microenvironment. ACS central science , 8 (8), 1102–1115. https://doi.org/10.1021/acscentsci.2c00107 Project Gallery

Research confirms anxiety disorders do have a genetic side Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Does anxiety run in families? Here's what genetics tells us Last updated: 10/07/25, 19:26 Published: 19/06/25, 08:00 Research confirms anxiety disorders do have a genetic side Have you ever noticed anxiety can pop up in several members of the same family? Maybe your sister worries constantly, or your brother gets nervous around people. It might feel like anxiety is passed down through generations. But is that really how it works, or is it just a coincidence? Here's what science has to say. Your DNA can affect anxiety Research confirms anxiety disorders do have a genetic side. That means you're more likely to have anxiety if someone in your family, like your mum, dad, sibling, or even a grandparent, has it too. But this doesn't mean anxiety is certain. Instead, genes increase your chances, accounting for about 30% to 40% of your risk. Scientists work this out by comparing identical and fraternal twins and by following anxiety diagnoses across generations; those studies repeatedly find that roughly one-third to two-fifths of a person’s risk is genetic. So, if genetics only make up part of the picture, what's the rest? That's where your environment steps in. Your life experiences matter a lot. Things like your relationships, stressful situations, and even your physical health can tip the scales one way or another. Genes set the stage, but they don't control the outcome. Think of your genes as nudging you towards anxiety rather than pushing you into it completely. The rest depends on what happens to you. How genes shape your brain Scientists have pinpointed several genes linked to anxiety. One of these genes affects serotonin, a brain chemical that helps regulate your mood and manage stress. When serotonin works well, you feel calm and can handle stressful events better. But if your genes make serotonin less effective, stress hits you harder. This can make anxiety more likely during tough times, even when others around you seem okay. There's another important point: your brain structure. Genes influence parts of your brain, especially the amygdala. Think of the amygdala as your internal alarm system. It warns you when something feels dangerous. In people with certain genes, the amygdala is extra sensitive. That means their "alarm" goes off more easily, causing anxiety even when there's no real danger present. However, not everyone with these genetic variations experiences anxiety. Your brain adapts throughout life, changing how genes affect you. This ongoing flexibility is called neuroplasticity: experience can strengthen or weaken neural circuits and can even add or remove chemical tags, such as DNA methylation, that switch genes on or off, reshaping how your stress system responds. Anxiety isn't just genetic; here's why It's tempting to blame your genes entirely if anxiety runs in your family. But life is more complicated. Even if you inherit genes that make anxiety more likely, the disorder usually develops when certain environmental conditions come into play. Stressful life events like losing a loved one, ongoing conflict at home, bullying, or trauma can trigger anxiety symptoms. Someone might have anxiety-related genes but never experience anxiety if their life stays relatively stress-free. On the other hand, someone without these genes can still develop anxiety if they experience severe stress or trauma. Lifestyle choices also make a big difference. Regular exercise, healthy eating, good sleep, and support from friends and family can protect against anxiety. Studies show these lifestyle habits are powerful, even if your genes are pushing in the opposite direction. Can you change your genetic destiny? Understanding that anxiety has a genetic basis can help. It means anxiety isn't just a character flaw or personal weakness. It's something partly built into your biology, something real and valid. Realising this can reduce shame and make people more willing to seek help. And here's another benefit: knowing your family history allows you to spot anxiety sooner. If you understand that anxiety might run in your family, you can pay attention to early signs, like trouble sleeping, excessive worry, or panic in social settings. Catching anxiety early means getting support earlier, making treatments like therapy or lifestyle changes more effective. Anxiety might run in your family, but you get to decide how far it goes. Written by Rand Alanazi Related articles: Depression / South Asian mental health / Physical and mental health / Does insomnia run in families? REFERENCES National Institute of Mental Health. Anxiety disorders [Internet]. Bethesda (MD): National Institute of Mental Health; 2024 [cited 2025 May 29]. Available from: https://www.nimh.nih.gov/health/topics/anxiety-disorders Mayo Clinic. Anxiety disorders [Internet]. Rochester (MN): Mayo Foundation for Medical Education and Research; 2018 [cited 2025 May 29]. Available from: https://www.mayoclinic.org/diseases-conditions/anxiety/symptoms-causes/syc-20350961 Leyfer O, Woodruff-Borden J, Mervis CB. Anxiety disorders in children with Williams syndrome, their mothers, and their siblings: implications for the aetiology of anxiety disorders. J Neurodev Disord . 2009 Feb 13;1(1):4-14. Martin EI, Ressler KJ, Binder EB, Nemeroff CB. The neurobiology of anxiety disorders: brain imaging, genetics, and psychoneuroendocrinology. Psychiatr Clin North Am [Internet]. 2009 Sep;32(3):549-75. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3684250/ McEwen BS, Eiland L, Hunter RG, Miller MM. Stress and anxiety: structural plasticity and epigenetic regulation as a consequence of stress. Neuropharmacology . 2012 Jan;62(1):3-12. Xie S, Zhang X, Cheng W, Yang Z. Adolescent anxiety disorders and the developing brain: comparing neuroimaging findings in adolescents and adults. Gen Psychiatry [Internet]. 2021 Aug 4;34(4):e100542. Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8340272/ Zhang K, Ibrahim GM, Venetucci Gouveia F. Molecular pathways, neural circuits and emerging therapies for self-injurious behaviour. Int J Mol Sci [Internet]. 2025 Feb 24;26(5):1938. Available from: https://www.mdpi.com/1422-0067/26/5/1938 Chaves T, Fazekas CL, Horváth K, Correia P, Szabó A, Török B, et al. Stress adaptation and the brainstem with focus on corticotropin-releasing hormone. Int J Mol Sci [Internet]. 2021 Jan 1;22(16):9090. Available from: https://www.mdpi.com/1422-0067/22/16/9090 Project Gallery

It's extremely pronounced in a technical environment Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link You're not a fraud: battling imposter syndrome in STEM Last updated: 22/05/25, 11:01 Published: 17/04/25, 08:00 It's extremely pronounced in a technical environment Background If you work in STEM or take even a keen interest in the field, it’s highly likely you’d have heard of and possibly experienced the term 'imposter syndrome'. Despite the glamorised success stories and carefully curated achievements we see in professional circles and on social media, let’s take a realistic step back - people struggle no matter how qualified they are. It’s okay to admit that, and it’s time we remove the stigma of this common experience. Coming into the Scientist Training Programme, I felt a sense of excitement and pride in my achievement of having even managed to get a place on the programme. As I settled in, this quickly turned into something else – fear, anxiety, worry. Feelings that I may not be good enough or I’m not where I belong. I seemed like the only one in my department without a postgraduate qualification. I began feeling out of place. It was only until I was able to put a label on this feeling – imposter syndrome, that I could take active steps to fix it. So, what is imposter syndrome? Put simply, it's the persistent feeling of self-doubt and inadequacy despite evident success. It makes you question whether you truly deserve your accomplishments, fearing that at any moment, someone will expose you as a fraud. This is extremely pronounced in a technical environment where your success is largely measured by your ability to tackle complex problems. Understanding its purpose While frustrating, imposter syndrome stems from a mechanism designed to keep us grounded and striving for growth. As social beings, we evolved to be highly attuned to hierarchies and belonging, and self-doubt may have once served as a protective mechanism, preventing reckless decisions. However, in today’s world, particularly in STEM fields, this innate caution can turn into chronic self-evaluation. The role of social media Imposter syndrome can be exacerbated through the often-unrealistic lens of social media. As I scroll through various social media platforms, I encounter countless posts showcasing often unrealistically flawless careers. Despite what you see in those 'day in the life' posts, not every STEM professional wakes up at 4am and has a cold shower. Rarely do we see the setbacks, rejections, or moments of self-doubt behind those polished posts, yet they exist for everyone. The distortion of what we see online is undoubtably a catalyst for imposter syndrome, but we can take a sensible step back and look at things through a realistic lens. Comparison truly can be the thief of joy if you let it. Coping strategies The good news is, it’s not all doom and gloom and there are strategies we can employ to handle our mischievous minds. As STEM professionals, sometimes we become isolated in our work, deeply ingrained in fixing a problem and not realising there are countless others to share your thoughts and feelings with. This is something I pushed myself to do and as I reached out to the wider community of trainee scientists, I quickly realised that I wasn’t alone. Almost everyone I had spoken to had shared a similar sentiment of having experienced imposter syndrome to some extent. It is important to remember that imposter syndrome is something that has been a universal experience for a very long time. It is certainly not a feeling that is exclusive to those in the early stages of their career as I surprisingly found out having networked with senior figures in the STEM community. My supervisor – a consultant clinical scientist with over 40 years of experience still experiences imposter syndrome as he tackles new challenges in the ever-evolving world of science. I have found that keeping a journal has been incredibly beneficial in logging my achievements -whether personal or career-related. Having a record of successes, no matter how small, serves as a tangible reminder that progress is being made, even when self-doubt tries to convince me otherwise. But the most effective tool I’ve discovered is something I’m still learning myself - self-compassion instead of self-criticism. It’s easy to be too hard on yourself, especially in STEM, where learning new things daily is the norm. The pressure to always have the right answers can make mistakes feel like failures rather than part of the learning process. But the reality is that growth comes from pushing through discomfort, not from perfection. Learning to extend yourself the same kindness you would offer a friend can make a world of difference in battling imposter syndrome. Reframing its meaning If you have experienced imposter syndrome I do have some good news for you – you’re pushing yourself out of your comfort zone in some way and challenging yourself. That is something to be proud of and its important to realise that experiencing imposter syndrome can sometimes simply be a mandatory byproduct of self-growth. You are exactly where you need to be. Even the greatest of minds can experience imposter syndrome. Albert Einstein himself once remarked: The exaggerated esteem in which my lifework is held makes me very ill at ease. I feel compelled to think of myself as an involuntary swindler. So, remember, you’re not alone in this struggle. When to seek help While imposter syndrome is something that a large majority of people experience, you should know when to seek help. If it manifests into something much more than occasional self-doubt, there is no shame in reaching out for help. Speaking to trusted friends or family about how you’re feeling is crucial to keep your mind in the right place. A qualified therapist will be well equipped to help you deal with imposter syndrome and keep you grounded. There are a wealth of online resources that can be used to help you; such as articles, self-help guides, and professional development communities – including the team here at Scientia News who offer strategies to build confidence and reframe negative thinking. Acknowledging imposter syndrome is the first step, but learning to challenge it is what truly allows you to move forward. And the next time you begin to doubt yourself, take a step back and think about your achievements and how they themselves were born from the ashes of self-doubt. Written by Jaspreet Mann Related articles: My role as a clinical computer scientist / Mental health strategies / Mental health in South Asian communities REFERENCES “Imposter Syndrome: A Curse You Share with EinsteinThesislink « Thesislink.” Thesislink, 10 July 2018, https://thesislink.aut.ac.nz/?p=6630 . NHS Inform (2023) ‘Imposter syndrome’, NHS Inform. Available at: https://www.nhsinform.scot/healthy-living/mental-wellbeing/stress/imposter-syndrome . Mind (2022) ‘Understanding imposter syndrome’, Mind. Available at: https://www.mind.org.uk/information-support/types-of-mental-health-problems/imposter-syndrome/ . Healthline (2021) ‘What is imposter syndrome and how can you combat it?’, Healthline. Available at: https://www.healthline.com/health/mental-health/imposter-syndrome . Psychology Today (2020) ‘Overcoming imposter syndrome’, Psychology Today. Available at: https://www.psychologytoday.com/gb/blog/think-well/202002/overcoming-imposter-syndrome . beanstalk. Feel Like a Fraud? How to Overcome Imposter Syndrome - Employee and Family Resources . 1 Jan. 2023, https://efr.org/blog/feel-like-a-fraud . Ling, Ashley. “3 Ways to Get Past Imposter Syndrome.” Thir.St , 13 Aug. 2024, https://thirst.sg/3-ways-to-get-past-imposter-syndrome/ . Project Gallery

This requires a strategy accounting for different factors, as well as other wider determinants of health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Addressing Health Inequalities Last updated: 03/05/26, 18:09 Published: 02/04/26, 08:00 This requires a strategy accounting for different factors, as well as other wider determinants of health This is the fourth and final article in a series on health inequalities. Previous article: Ethnic health equalities. Welcome to the final article in a series of articles about health inequalities. This article will look more in detail at how to address health inequalities. Introduction Health inequalities are systematic and avoidable differences in health outcomes. They carry heavy human and economic costs, including over £31bn in lost productivity annually. Previous articles in this series explored how factors like geography, income, and ethnicity drive these disparities. However, addressing healthcare inequalities requires a strategy accounting for these factors, as well as other wider determinants of health. The impact of the environment Scientists have published research which found that environmental factors, including smoking, physical activity, and socioeconomic status, have a greater impact on a person’s health and premature death compared to their genes. They analysed data from the UK Biobank, a dataset of biological, health and lifestyle information. Their analysis showed that environmental exposure explains 17% of the variation in risk of death, while genetic predisposition explains less than 2%. Of the 25 factors that were analysed, smoking was linked to 21 diseases, followed by 19 diseases for socioeconomic factors like household income, home ownership, and employment status. While genetics still dominates for specific conditions like dementia and breast cancer, these findings emphasise that the vast majority of health outcomes are determined by our environment rather than our biology. Therefore, to address health inequalities, targeted strategies and collaborative methods like co-design need to be used to ensure interventions meet the genuine needs of the most vulnerable communities. Core20PLUS5 The NHS’s Core20PLUS5 is one of these targeted strategies, defining a target population (the “Core20PLUS”) and identifying 5 areas of healthcare that require improvement. For both groups (adults, children and young people), the target population is the same: CORE20 refers to the most deprived 20% of the population identified by the national Index of Multiple Deprivation, while the PLUS population includes those who experience health inequalities the most, such as ethnic minority groups, individuals with a learning disability, autistic individuals, and individuals with multiple long-term health conditions. The differences between the strategy for adults and that for children and young people are in the 5 areas of healthcare requiring improvement. As seen in Figure 1 , for adults, the 5 areas are continuity and improvement of maternity care (specifically for women from Black, Asian and ethnic minority groups and from the most deprived groups), improved services for individuals with severe mental illness, improved services for those with chronic respiratory disease, early cancer diagnosis, and improved management of hypertension. Smoking cessation is another area of focus that covers all the 5 priorities. For children and young people, the 5 areas of healthcare improvement are specific to this population: asthma care, diabetes care, epilepsy care, oral health, and mental health, as seen in Figure 2 . Co-design for addressing health inequalities Another method to address health inequalities is through co-design, which is a participatory methodology where stakeholders, including service users (e.g., patients, their carers, etc) and providers (healthcare professionals and other staff), collaborate to jointly create and refine services, products, or solutions. A diagram of three key factors needed in co-design can be seen in Figure 3 . This joint approach helps to ensure that interventions align with the genuine needs and preferences of the people who will be using that service, and the findings that providers see coming up frequently from comments by service users. Co-design can be used to address health inequalities by co-producing strategies with people from those communities and backgrounds. For example, individuals from ethnic minority groups can participate, so researchers can genuinely understand and try to address racism's impact on health. This is supported by research published in the BMJ , where co-design with service users and providers from ethnic minority groups found that more culturally appropriate mental healthcare was needed, and that there needed to be more open discussions about the impacts of ethnicity, culture and racism in mental health. In the context of Figure 3 , this study involved “committed” ethnic minority groups with the “capability” of sharing their lived experience with researchers. This shows how co-design can be used as a tool that allows others to share their experiences for the benefit of themselves and others. Conclusion There needs to be a cross-government strategy that aligns current policy, funding, and practice around health equity. Because these inequalities are systematic and avoidable failures, they require a holistic approach that moves beyond clinical care to address the PLUS populations who experience the greatest disadvantage. Trust in the healthcare system has been eroded among ethnic minority groups due to repeated negative experiences, cultural insensitivity, and discriminatory treatment. To rebuild it, lived experiences need to be accounted for, and solutions need to be co-designed. Furthermore, determinants of good health, like stable housing, fair pay, and high-quality education, must be provided to the people most affected by health inequalities. These inequalities must be addressed to ensure everyone has the ability and opportunity to have a long and healthy life. Written by Naoshin Haque Related article: Reflection on global health injustices Project Gallery

Causes, symptoms, diagnosis and management Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hypertension: a silent threat to global health Last updated: 08/10/26, 18:58 Published: 13/03/25, 08:00 Causes, symptoms, diagnosis and management Introduction Did you know that hypertension, also known as high blood pressure, is a leading cause of premature death, affecting 1.28 billion adults aged 30-79 worldwide? According to the World Health Organisation (WHO), two-thirds of these individuals live in low and middle-income countries. Despite its widespread prevalence, many people remain undiagnosed as most cases are asymptomatic, and individuals are unaware they have the condition. Hypertension can lead to serious clinical manifestations such as heart disease. It can also cause eye retinopathy, causing vision problems and kidney damage, including proteinuria. It also contributes to vascular contributions like atherosclerosis, leading to stenosis and aneurysms. It also significantly raises the risk of stroke and heart failure (Figure 1 ). Addressing hypertension through early diagnosis, improved access to treatment and lifestyle changes is essential to reducing its global burden. This article aims to explore the causes, diagnosis and treatments. What drives hypertension? Hypertension is characterised by persistently elevated BP in the systemic arteries. Blood pressure is typically presented as a ratio: systolic BP, which measures the pressure on arterial walls during heart contraction, and diastolic BP, which reflects the pressure when the heart is at rest. Hypertension is diagnosed when the systolic blood pressure is 130 mmHg or higher and/or diastolic blood pressure exceeds 80 mmHg based on multiple readings taken over time ( Figure 2 ). In contrast, secondary hypertension occurs only in 5% of cases and is caused by an underlying condition, such as kidney disease, hormonal imbalances, or vascular problems. This form of hypertension is often reversible if the underlying cause is treated. Common causes of secondary hypertension include chronic kidney disease, polycystic kidney disease, hormone excess (such as aldosterone and cortisol), vascular issues like renovascular stenosis and certain medications. Drugs that can cause secondary hypertension include chronic use of non-steroidal inflammatory drugs (NSAIDs), antidepressants and oral contraceptives. Hypertension, regardless of its cause, can be exacerbated by certain health behaviours, including excessive dietary salt, a sedentary lifestyle, heavy alcohol consumption, and diets low in essential nutrients, such as potassium. These factors contribute to the development and worsening of high blood pressure. However, blood pressure can be improved by reversing these behaviours, as well as following a diet rich in fruits and vegetables, which helps to mitigate the negative impact on blood pressure. Spotting hypertension: how it is diagnosed Hypertension is usually detected when blood pressure (BP) is measured during regular checkups. Since it often doesn’t show symptoms, all adults must check their BP regularly. The most common way to diagnose hypertension is by measuring BP several times in a doctor’s office. To get an accurate reading, BP must be measured carefully. Since BP can vary throughout the day, multiple measurements are needed. Doctors have recently started using home BP monitoring (HBPM) and ambulatory BP monitoring (ABPM) to check BP outside of the office. ABPM records BP every 20-30 minutes over 24 hours, while HBPM lets patients measure BP at home. These methods help identify conditions like 'white coat hypertension' (high BP in the doctor’s office but normal at home) or 'masked hypertension' (normal BP at the doctor’s office but high at home). When diagnosing hypertension, doctors also look for other health issues related to high BP, such as heart disease or kidney problems. If high BP is sudden or difficult to control, doctors may suspect secondary hypertension, which is caused by another condition, like kidney disease or hormonal imbalances. A thorough medical history is essential. This includes asking about past BP readings, medications, and lifestyle factors such as smoking and diet. Doctors also check for other risk factors like diabetes or high cholesterol, increasing heart disease risk. A physical exam helps confirm the diagnosis of hypertension and checks for any damage to organs like the heart and kidneys. BP should be measured on both arms and if there's a significant difference in readings, further tests may be needed. If necessary, doctors may also check for conditions like atrial fibrillation or perform ultrasounds to look for heart or kidney problems. Blood tests can also help identify risk factors, confirm or rule out secondary hypertension, and assess overall heart health. Managing hypertension, from lifestyle changes to medications Studies show that weight loss can reduce systolic blood pressure by 5 to 20 mmHg, making it an effective strategy for managing hypertension. However, the exact "ideal" body weight or Body Mass Index (BMI) for controlling blood pressure is not clearly defined, but small weight reductions can make a difference. Reducing salt intake, staying active, and managing sleep apnoea also help. While smoking does not directly raise blood pressure, quitting reduces long-term heart risks. Overall, lifestyle changes alone can cut cardiovascular events by up to 15%. Most national and international guidelines recommend the use of angiotensin-converting enzyme inhibitors (ACE inhibitors), angiotensin II receptor blockers (ARBs), calcium channel blockers (CCBs), and thiazide or thiazide-like diuretics as first-line pharmacological treatments for hypertension. Conclusion Hypertension is a prevalent and often silent condition with serious health consequences, including heart disease, stroke, and kidney failure. Its widespread impact on global health, particularly in low- and middle-income countries, underscores the importance of early diagnosis and proactive management. While lifestyle modifications are crucial in managing blood pressure, medications remain essential for many individuals. By raising awareness, promoting regular blood pressure checks, and ensuring access to both preventative and therapeutic measures, we can reduce the burden of hypertension and improve long-term health outcomes globally. Written by Michelle Amoah Related articles: Related mechanisms of hypertension / Cardiac regeneration REFERENCES Iqbal, A. M., and Jamal, S. F. (2023). Essential hypertension. In StatPearls [Internet]. StatPearls Publishing. Retrieved from [ https://www.ncbi.nlm.nih.gov/books/NBK539859/ ] Schmieder, R. E. (2010). End Organ Damage In Hypertension. Deutsches Ärzteblatt International. https://doi.org/10.3238/arztebl.2010.0866 Touyz, R. M., Camargo, L. L., Rios, F. J., Alves-Lopes, R., Neves, K. B., Eluwole, O., Maseko, M. J., Lucas-Herald, A., Blaikie, Z., Montezano, A. C., and Feldman, R. D. (2022). Arterial Hypertension. In Comprehensive Pharmacology (pp. 469–487). Elsevier. World Health Organization. (2023). Hypertension. Retrieved [24th January 2025], from https://www.who.int/news-room/fact-sheets/detail/hypertension Project Gallery

Psilocybin's active metabolite, psilocin, acts as a serotonin receptor agonist Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The promising effects of magic mushrooms for depression Last updated: 05/04/26, 15:37 Published: 19/02/26, 08:00 Psilocybin's active metabolite, psilocin, acts as a serotonin receptor agonist This is Article 3 in a series on psychiatric disorders and the brain. Previous article: Inside out: the chemistry of depression . Next article coming soon. What is psilocybin? Psilocybin is a naturally occurring psychedelic tryptamine alkaloid found in over 200 species of mushrooms (Psilocybin mushrooms), commonly known as magic mushrooms or shrooms. Upon ingestion, the body converts psilocybin into its active metabolite, psilocin, which acts as a serotonin receptor agonist, primarily impacting 5-HT2A receptors. What is psilocybin useful for? In recent years, clinical research has shown that psilocybin-assisted therapy, can quickly and meaningfully reduce symptoms of depression, often within days rather than weeks, when given in a safe, controlled medical setting with psychological support. Importantly, these studies don’t just look at mood while someone is under the influence. They measure long-term changes weeks or months after treatment. Studies, such as Gukasyan et al. , 2022 and Goodwin et al. , 2022, have shown that 1-2 doses of psilocybin plus therapy have led to sustained reductions in depressive symptoms that last at least 8-12 weeks, and in some cases 12 months later. Research has also demonstrated potential benefits for individuals whose depression has not responded to conventional antidepressant treatments. A large phase II double-blinded trial, by Griffiths et al. , 2016, involving people with treatment-resistant depression found that those given a therapeutic dose (25 mg) of psilocybin had noticeably greater improvement in their depression scores compared with a very low dose (10 mg). Scientists, for example Daws et al. , 2022, believe psilocybin works differently from standard antidepressants. It appears to temporarily increase connections between different parts of the brain and may help break rigid patterns of negative thinking that are typical in depression. If psilocybin is effective, why is it not currently used in treatment for depression? Psilocybin remains classified as a Schedule I controlled substance under the United Nations 1971 Convention on Psychotropic Substances, meaning it is considered to have a high potential for abuse and no accepted medical use. For psilocybin to become an approved clinical treatment for depression, it must be rescheduled through formal regulatory review, a process that involves extensive clinical testing and bureaucratic steps. In many countries, including the United States, rescheduling controlled substances can be slow and complex. For example, in 2022-2023, the U.S. government reviewed the scheduling of marijuana (cannabis) after presidential direction to federal agencies, but a final rescheduling decision was still pending as of late 2025. According to the U.S. Drug Enforcement Administration, Schedule III drugs are defined as substances with moderate to low potential for physical and psychological dependence, whereas Schedule I substances are defined as having no currently accepted medical use and a high potential for abuse. Because psilocybin is still Schedule I in most jurisdictions, it cannot yet be prescribed as a mainstream treatment for depression, despite promising clinical trial results. Written by Chloe Kam Related article: What does depression do to your brain? Project Gallery

The finches are a classic example of adaptive radiation, which is the rapid diversification of an organism into many different species with different ecological roles. Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Beak diversity in Darwin's finches Last updated: 24/09/26, 20:33 Published: 10/09/26, 08:00 The finches are a classic example of adaptive radiation, which is the rapid diversification of an organism into many different species with different ecological roles. Darwin’s finches are a family of birds from the Geospiza , Platyspiza , and Certhidea species on the Galápagos Islands, located in the Pacific Ocean. They are named after their contribution to Charles Darwin’s theories on evolution by natural selection. The finches are a classic example of adaptive radiation, which is the rapid diversification of an organism into many different species with different ecological roles. In this example, an ancestral bird on the Galápagos Islands evolved into about 18 species over 1-2 million years. Restricted gene flow with South America, climatic oscillations from the El Niño phenomenon, glacial cycles, and volcanic activity created the conditions for this rapid evolution. Different Galápagos islands vary in size, elevation, and food availability, so Darwin’s finches diversified by adapting to these different islands. This created a wide range of beak shapes and sizes, both within and between finch species. This article will describe Darwin’s finch beak diversity and the molecular basis behind it. How beak morphology varies in Darwin’s finches Darwin’s finches have diverse beak sizes and shapes, which match their diverse diets. Their beaks vary in length, depth, and curvature. Warbler finches have pointy beaks to spear insects, while tee finches have triangular beaks suitable for eating fruits and insects in tree canopies. Ground finches have blunt beaks suitable for crushing seeds, and birds with bigger beaks eat bigger seeds ( Figure 1 ). This partitioning of food between finches with different beaks is most prominent during the dry season, when there is more competition for food; in the wet season, there is more diet overlap between finches with different beaks. Beaks play the dual role of hands and mouth – foraging, feeding, communicating, nest building and more – so even small changes in beak morphology can have big impacts on finch lifestyles. Therefore, beak morphology is a hallmark of adaptive radiation in Darwin’s finches. Evolution of beak size within a species While Figure 1 highlights different beak sizes between species, the Galápagos' changing environment makes beak size evolve within a species too. A well-known example is the medium ground finch ( Geospiza fortis ) , which eats seeds and whose beak size varies depending on the size of available seeds. When there was a drought on the Galápagos Island of Daphne Major in 1977, small seeds did not survive, so G. fortis could only eat large seeds with hard shells. Finches survived if they had larger beaks that could crack open these larger, harder seeds. Since natural selection favoured larger beaks, the average beak size of the species increased in the late 1970s. However, the large ground finch ( Geospiza magnirostris ) colonised Daphne Major island in late 1982 and outcompeted the native G. fortis for large seeds. This meant G. fortis was left with smaller seeds, creating a selection pressure which reduced G. fortis beak size for the next 15 years. Figure 2 shows how opposing selection pressures have made the beak size of G. fortis vary over time. Molecular basis of beak morphology Evolution of beak size within and between species of Darwin’s finches has a complex molecular basis. Beak morphology has to be heritable (i.e. have a genetic basis) for natural selection to act on it: birds with beaks more suitable to their environment pass down genes for those beaks to their offspring. Beaks are made of bone and cartilage, so genes involved in the formation and development of bone and cartilage are suspected to control beak morphology. The ALX1, CALM1, GSC, RDH14, FGF10, and FOXC1 genes have different variants in Darwin’s finch species with blunt and sharp beaks, meaning nucleotide sequence differences in these genes are responsible for changes in beak shape. These variations are not necessarily in the coding sequence of those genes: often, the variations are in transcription factor genes, promoters, and other DNA sequences which regulate the expression of genes like ALX1 and CALM1 ( Figure 3 ). Therefore, beak morphology is heritable, but it involves a complex combination of developmental genes. Conclusion The size and shape of beaks in Darwin’s finches are diverse because of an adaptive radiation over 1-2 million years. Changes in interspecific competition and geography of the Galápagos Islands affected food availability over space and time. Finches with different beaks adapted to eating different types of food, as natural selection acted on various genes involved in beak development both directly and indirectly. Molecular and phenotypic studies of Darwin’s finches have revealed the complex interaction between developmental genes and the environment in controlling beak morphology. Nearly 200 years after Charles Darwin’s expedition to the Galápagos, his finches remain a classic example of natural selection and adaptive radiation. Written by Simran Patel Related articles: Galapagos tortoises / The diversity of bat faces REFERENCES De León LF, Podos J, Gardezi T, et al. Darwin’s finches and their diet niches: the sympatric coexistence of imperfect generalists. J Evol Biol 2014; 27: 1093–1104. Grant PR, Grant BR. Evolution of character displacement in Darwin’s finches. Science 2006; 313: 224–226. Foster DJ, Podos J, Hendry AP. A geometric morphometric appraisal of beak shape in Darwin’s finches. J Evol Biol 2008; 21: 263–275. Boag PT, Grant PR. Intense natural selection in a population of Darwin’s finches (Geospizinae) in the Galápagos. Science 1981; 214: 82–85. Grant PR, Grant BR. From microcosm to macrocosm: adaptive radiation of Darwin’s finches. Evol J Linn Soc 2024; 3: kzae006. Lamichhaney S, Berglund J, Almén MS, et al. Evolution of Darwin’s finches and their beaks revealed by genome sequencing. Nature 2015; 518: 371–375. Cheng Y, Miller MJ, Lei F. Molecular Innovations Shaping Beak Morphology in Birds. Annu Rev Anim Biosci 2025; 13: 99–111 Project Gallery

Exploring neuroplasticity after brain injury Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can we really ‘rewire’ our brain? Last updated: 06/05/26, 21:11 Published: 07/05/26, 08:00 Exploring neuroplasticity after brain injury Can the brain really rebuild what has been lost after a brain injury? This idea derives from neuroplasticity – the nervous system’s capacity to change and adapt, reorganising its connections and overall structure as a result of an experience. In other words, the brain strengthens, weakens, and forms new neural connections over time. In psychology, neuroplasticity is crucial for understanding learning, as repeated behaviours and thoughts can strengthen neural pathways, resulting in increased automatic responses. Neuroplasticity plays a large role in recovery following a brain injury. Joy & Carmichael (2020) found that after a stroke, the brain becomes temporarily plastic, during which new axons and synapses may form, functions can be reassigned to undamaged brain regions, and the brain becomes flexible to training, allowing for recovery. A key takeaway is that after a stroke, the brain not only repairs itself but also enters a temporary state of reorganisation and recovery. Repeated practice during rehabilitation supports the formation of new pathways, helping lost skills to be regained. This is a core psychological principle: learning requires repetition, and without it, new neural pathways will not be produced or maintained. This reorganisation is driven by cellular processes that modify neural connections. Specialised immune cells, known as microglia, reshape connections between neurons and assist in incorporating new cells into preexisting networks, as demonstrated by Sandvig et al. (2018). This emphasises that recovery is not solely biological but also behavioural, as the way one interacts with their environment influences the way the brain reorganises itself. For example, when an individual performs a behaviour, such as moving their leg in rehab, neural pathways for that certain behaviour are activated frequently. Here, microglia respond to this activity by strengthening frequently used connections and removing unused ones, a process known as “use it or lose it”, in relation to neural pathways. So, can we really ‘rewire’ our brains? Yes, but to an extent! Neuroplasticity illustrates that the brain is capable of change, through reinforced behaviour and experience, though it should be noted that this process rarely results in complete normalcy. From a psychological perspective, neuroplasticity highlights that recovery is about how behaviour, experience, and learning intertwine to allow the brain’s ability to adapt. Written by Shreya Dhaliwal Related articles: Brain injury / Synaptic plasticity REFERENCES Cleveland Clinic. (2023, December 13). Brainwork: The Power of Neuroplasticity . https://health.clevelandclinic.org/neuroplasticity . Joy , M. T., & Carmichael, S. T. (2020). Encouraging an excitable brain state: mechanisms of brain repair in stroke. Nature Reviews Neuroscience, 22 (1), 38–53. https://doi.org/10.1038/s41583-020-00396-7 . Kreber, L. (2025). Neuroplasticity . Centre for Neuro Skills. https://www.neuroskills.com/neuroplasticity/ . Mateos-Aparicio, P., & Rodríguez-Moreno, A. (2019). The impact of studying brain plasticity. Frontiers in Cellular Neuroscience, 13 . https://doi.org/10.3389/fncel.2019.00066 . Sandvig, I., Augestad, I. L., Håberg, A. K., & Sandvig, A. (2018). Neuroplasticity in stroke recovery. The role of microglia in engaging and modifying synapses and networks. European Journal of Neuroscience, 47 (12), 1414–1428. https://doi.org/10.1111/ejn.13959 Project Gallery

Examining disconnection strategies and Functional Group Interconversion (FGI) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Molecular blueprints: the art of synthetic planning Last updated: 05/03/26, 14:47 Published: 19/02/26, 08:00 Examining disconnection strategies and Functional Group Interconversion (FGI) This is article no. 1 in a two-part series on retrosynthesis. Next article: Synthesis of ibuprofen . Introduction Science is often seen as rigid, driven solely by facts and logic. Yet, in the world of chemical synthesis, molecular design and retrosynthetic analysis can be considered an art form. Synthetic creativity can be measured by the number of steps, environmental considerations, or the clever assembly of chemical building blocks. Widely used in the pharmaceutical industry and responsible for many Nobel Prize‑winning discoveries, retrosynthetic planning is central to modern synthetic chemistry. 1. Disconnection Strategy Retrosynthesis begins with deconstructing a target molecule into simpler starting materials known as synthons. A synthon is hypothetical but represents a fragment that could react to form a target molecule. Chemists then match synthons to real‑life equivalents (R.L.E.) which can be used in the lab. For example, if a target molecule contains an ester group, cleaving the oxygen–carbonyl bond produces four possible synthons ( Figure 1 ). Of these synthons, the positively charged oxygen has no R.L.E., so pairing the negatively charged oxygen with a carbonyl‑containing R.L.E., such as a carboxylic acid or acid chloride, and an alcohol will effectively synthesise the desired ester. 2. Functional Group Interconversion (FGI) FGIs are exploited by chemists when a functional group is difficult to manipulate directly. In these cases, the target functional group is converted to another functional group which is easier to work with. For instance, this strategy is commonly used to synthesise alkene and carboxylic acid fragments. As alkenes mainly participate in addition reactions, forming C–C bonds can prove difficult; therefore, converting the alkene to an alkyne can make this simpler. As an alkyne‑to‑alkene transformation is relatively simple, using either Lindlar’s catalyst (Z‑alkene) or Na/NH₃ (E‑alkene), alkynes can be used to build up the carbon chain before a final reduction. This is done by simple nucleophilic substitutions promoted by base deprotonation (NaNH₂) of the alkyne. The same idea is used for installing carboxylic acids, as a common FGI is to use a nitrile group (CN). These can be easily transformed back to the target carboxylic acid using acid in aqueous conditions. 3. Synthesis of Aspirin Retrosynthetic analysis can be used to design synthetic routes to common pharmaceuticals. For aspirin, a good disconnection strategy would be to break the ester bond and derive R.L.E. as shown above. To install the carboxylic acid, an FGI can be used. In Figure 3, two possible syntheses are highlighted utilising these strategies. While the synthetic methods presented previously will produce aspirin in high yields, they often create large amounts of waste and use harsh acidic conditions. Bhuyan et al. have proposed a more sustainable synthesis using blue LED light to catalyse the reaction under an O₂ atmosphere ( Figure 4) . Conclusion In conclusion, retrosynthesis and synthetic planning are essential tools for designing complex molecules. While the disconnection strategy and FGIs are relatively simple concepts, their application is used routinely in both industry and academia, regardless of the complexity of the target molecule. While one strategy may be used routinely, there are often many more ways to synthesise a particular compound more efficiently or with more flair. Stay tuned for Part 2, where the techniques discussed here are applied to the synthesis of ibuprofen. Written by Antony Lee Project Gallery

About phosphate-solubilising micro-organisms and their role in the phosphorus cycle Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Meet the microbes that feed phosphorus to plants Last updated: 15/01/26, 19:00 Published: 27/11/25, 08:00 About phosphate-solubilising micro-organisms and their role in the phosphorus cycle Plants need phosphorus to make biological molecules like DNA, ATP, and the phospholipid bilayers that form cell membranes. Most phosphorus on Earth is found in its most oxidised form, phosphate (PO 4 3- ). Plant roots can only absorb soluble phosphate ions, but 80% of the phosphate in soil is insoluble and therefore unavailable for plant growth. Enter phosphate-solubilising micro-organisms. What are phosphate-solubilising micro-organisms? Phosphate solubilisation is the process by which micro-organisms convert insoluble phosphorus sources, like rocks or the biomass of dead organisms, into bioavailable phosphate ions (Figure 1). Examples of phosphate-solubilising bacteria come from the genera Bacillus , Pseudomonas , Rhizobium, Escherichia , Streptomyces , and Micromonospora , as well as some cyanobacteria. Phosphate-solubilising fungi include Aspergillus , Penicillium , Mucor , Rhizopus , Rhizophagus, and Glomus . The latter two fungal genera are arbuscular mycorrhizal (AM) fungi - more on them later. The chemistry underpinning phosphate solubilisation is complex but can broadly be split into inorganic and organic processes ( Figure 1 ). Some of these inorganic and organic processes are described in the rest of this article. Solubilising inorganic phosphate Inorganic insoluble phosphate is solubilised by microbial acids. When phosphate-containing rocks like apatite are broken down by weathering, the resulting smaller rock particles enter the soil. Micro-organisms secrete organic acids – usually gluconic acid but occasionally lactic, citric, oxalic, or other acids – to solubilise these rock particles. Acids work on inorganic phosphate in two ways. Firstly, they dissolve weathered rock pieces due to their low pH. Secondly, negatively charged acid anions (lactate, citrate, etc) displace the phosphate captured by aluminium, iron, magnesium, and calcium minerals in the rock. Organic acids are just some of the chemicals secreted by microbes to solubilise inorganic phosphate. Solubilising organic phosphorus On the other hand, microbial enzymes solubilise organic phosphorus during the decomposition of organic matter. The two types of phosphate-solubilising enzymes are phosphatases, which solubilise 90% of organic phosphorus, and phytases, which solubilise the remaining 10%. Both types of enzyme break the ester bonds linking a PO 4 3- group to the rest of a biological molecule. By expressing genes encoding phytases and phosphatases, soil micro-organisms make phosphorus available for plants. Arbuscular mycorrhizae (AM) AM fungi provide plants with phosphorus in a symbiotic relationship. These fungi consist of hyphae, which are long, thin strands of cells that extend a plant’s root network and access phosphorus where roots cannot (Figure 2). AM fungi have a three-pronged approach to improving a plant’s phosphorus uptake: firstly, they absorb phosphate from the soil and give it to the plant in exchange for carbon. Secondly, they solubilise phosphate by secreting acids and phosphatases. Finally, AM fungi recruit phosphate-solubilising bacteria to the root system by feeding them sugars and amino acids. Conclusion Phosphate-solubilising bacteria and fungi provide plants with phosphorus, an essential element for making nucleic acids and ATP. Most phosphate is inaccessible to plants, locked up in rocks and biomass. By secreting organic acids and enzymes, soil micro-organisms convert this inaccessible phosphate into a form that plant roots can absorb and incorporate into their own biomass. When that plant dies, the organic phosphorus is solubilised again for another plant to use, so phosphorus never runs out. Therefore, phosphate-solubilising microbes are a small part of the invisible world that keeps our planet green. Written by Simran Patel Related article: Human activity and the phosphorus cycle REFERENCES Silva LI da, Pereira MC, Carvalho AMX de, et al. Phosphorus-Solubilizing Microorganisms: A Key to Sustainable Agriculture. Agriculture 2023; 13: 462. Pang F, Li Q, Solanki MK, et al. Soil Phosphorus Transformation and Plant Uptake Driven by Phosphate-solubilizing Microorganisms. Front Microbiol ; 15. Epub ahead of print 27 March 2024. DOI: 10.3389/fmicb.2024.1383813 . Schipanski ME, Bennett EM. Chapter 9 - The Phosphorus Cycle. In: Weathers KC, Strayer DL, Likens GE (eds) Fundamentals of Ecosystem Science (Second Edition) . Academic Press, pp. 189–213. Tian J, Ge F, Zhang D, et al. Roles of Phosphate Solubilizing Microorganisms from Managing Soil Phosphorus Deficiency to Mediating Biogeochemical P Cycle. Biology 2021; 10: 158. Project Gallery