Discussing eutrophication and industrial activities Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link How human activity impacts the phosphorus cycle Last updated: 27/12/25, 17:55 Published: 15/01/26, 08:00 Discussing eutrophication and industrial activities Phosphorus is one of the most important chemical elements in biology because it is a component of nucleic acids, ATP, and the phospholipid bilayers that make up our cell membranes. Like carbon and nitrogen, there is a limited amount of phosphorus on Earth, which is continually cycled between inorganic, organic, terrestrial, and aquatic sources. However, human activity disrupts the phosphorus cycle, resulting in some places having too much phosphorus and others having too little. This article will describe what the phosphorus cycle is and how we are affecting it. What is the phosphorus cycle? The phosphorus cycle involves phosphate ions (PO 4 3- ) moving between rocks, living organisms, and water bodies. Phosphate enters ecosystems when wind and rain break off tiny pieces of phosphate rock, primarily apatite, in a process called weathering. Weathered phosphate rock enters soil, where micro-organisms transform it into a form that plants can absorb through their roots (see my previous article on this process, called phosphate solubilisation). Plants convert inorganic phosphate into organic phosphorus compounds, such as DNA, ATP, and phosphoproteins, which are then transferred along the food chain. At each step of the food chain, phosphorus is returned to the soil by excretion from living organisms or decomposition of dead organisms. I call this the ‘organic mini-cycle’ from soil, to plants, to animals, and back to soil. Occasionally, phosphorus leaves the organic mini-cycle and enters water bodies by leaching or soil erosion. Phosphorus settles on the seabed and turns back into phosphate rock over hundreds of millions of years, completing the cycle. An overview is shown in Figure 1 . Humans disrupt the phosphorus cycle by eutrophication Deforestation, farming, and sewage overload water bodies with nutrients like phosphorus in a process called eutrophication. Agriculture is a big source of eutrophication, specifically fertilisers, organophosphorus pesticides, and animal feed. When it rains, they are carried from farm soil to water bodies by surface runoff and soil erosion. Human-caused deforestation exaggerates eutrophication because without tree roots, soil erosion increases, so more agricultural phosphorus enters water bodies. The other big eutrophication source is domestic sewage, which is dumped directly into water bodies. Fertilisers, pesticides, animal feed, and sewage provide algae with excess nutrients, so they overgrow into an algal bloom ( Figure 2 ). Algal blooms block sunlight from reaching submerged aquatic plants, so they cannot photosynthesise, and may produce toxins that kill aquatic life. Once the algal bloom dies, it is decomposed by bacteria, which use up oxygen in the water. With oxygen used up and no photosynthesis to replace it, fish and other aquatic animals die. Therefore, human phosphorus inputs like fertilisers and domestic waste can destroy aquatic ecosystems. Industrial activity depletes non-renewable phosphate rock While human activities overload water bodies with phosphorus, they deplete land of phosphate rock. Phosphate rock is mined and chemically reacted with sulfuric acid to produce fertiliser. Since phosphate rock is non-renewable, mining it permanently removes a crucial phosphorus input from the local ecosystem. 85% of phosphate rock is found in only 5 countries (China, Morocco, South Africa, Algeria, and Syria), so these countries are being depleted of phosphorus, only to overload another ecosystem with fertiliser thousands of miles away ( Figure 3 ). Scientists have suggested using agricultural waste and domestic wastewater as an alternative phosphorus source for fertiliser production. This would rebalance the phosphorus cycle on both ends: reducing the demand for non-renewable phosphate rock, and preventing eutrophication. Phosphorus can be recovered from waste and reused in fertiliser production in a variety of ways – acid leaching, isolating iron phosphate using a magnet, metal precipitation, and polyphosphate-accumulating micro-organisms, which use and store phosphate in their cells. However, the pollution and diseases present in sewage and farm waste make them difficult to recycle. Conclusion Phosphorus is an essential element for plant growth, so humans have manufactured fertilisers to provide their crops with extra phosphorus. However, fertiliser production depletes some ecosystems of phosphate rock, while fertiliser application causes eutrophication in other ecosystems. Along with domestic sewage and deforestation, agriculture has disrupted the natural cycle, which transports phosphate between plants, animals, micro-organisms, the soil, water bodies, and rocks. Therefore, making fertiliser by recycling the phosphorus in our waste products could keep the human population fed without compromising natural ecosystems. Written by Simran Patel Related article: Meet the microbes that feed phosphorus to plants REFERENCES 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. R. Jupp A, Beijer S, C. Narain G, et al. Phosphorus Recovery and Recycling – Closing the Loop. Chemical Society Reviews 2021; 50: 87–101. Khan MN, Mohammad F. Eutrophication: Challenges and Solutions. In: Ansari AA, Gill SS (eds) Eutrophication: Causes, Consequences and Control: Volume 2 . Dordrecht: Springer Netherlands, pp. 1–15. Akinnawo SO. Eutrophication: Causes, consequences, physical, chemical and biological techniques for mitigation strategies. Environmental Challenges 2023; 12: 100733. Liu L, Zheng X, Wei X, et al. Excessive Application of Chemical Fertilizer and Organophosphorus Pesticides Induced Total Phosphorus Loss from Planting Causing Surface Water Eutrophication. Sci Rep 2021; 11: 23015. Project Gallery

Unveiling the paradigm shift in cognitive impairment through machine learning Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Brain metastasis hacks brain activity and jams neuronal communication Last updated: 29/05/25, 11:46 Published: 29/05/25, 08:00 Unveiling the paradigm shift in cognitive impairment through machine learning Understanding the impact of brain metastasis on neuronal communication Introduction Researchers from the Spanish National Research Council (CSIC) and the Spanish National Cancer Research Centre (CNIO) have made a ground-breaking discovery related to brain metastasis and its impact on brain activity and neuronal communication. This finding could potentially explain why half of all patients with brain metastasis experience cognitive impairment. Understanding the influence on neural circuits The research , published in Cancer Cell, aimed to comprehend how brain metastasis affects the functionality of neuronal circuits beyond the physical mass of the tumour. The researchers conducted multidimensional modelling of brain functional analyses in the context of brain metastasis and tested various preclinical models from different primary sources and oncogenic profiles. The study was able to separate the effect on local field potential oscillatory activity from cortical and hippocampal areas. This helped researchers learn more about the different ways that brain metastasis can affect people. The authors highlighted the importance of this comprehensive approach in unravelling the complex dynamics of brain metastasis. Detecting metastases through electrical activity Through the measurement of electrical activity in the brains of mice with and without metastases, the researchers discovered distinct electrophysiological differences between the two groups. The researchers used artificial intelligence to confirm that metastases were indeed to blame for these differences. Using an automatic algorithm trained with numerous electrophysiological recordings, the researchers developed a model that could accurately identify the presence of metastases. Furthermore, the algorithm demonstrated the ability to distinguish metastases originating from different primary tumours, such as skin, lung, and breast cancer. These findings provide clear evidence of the specific impact that metastasis has on the brain's electrical activity. Paradigm shift in understanding brain metastases The study represents a significant paradigm shift in the understanding of brain metastases. Traditionally, neurological dysfunction in patients with brain metastasis was attributed solely to the physical mass effect of the tumour. However, this research indicates that changes in brain activity resulting from tumour-induced biochemical and molecular alterations also contribute to these symptoms. The implications of this paradigm shift are far-reaching and have potential implications for the prevention, early diagnosis, and treatment of brain metastasis. By recognising that neurological symptoms are not solely due to the physical presence of the tumour, medical professionals can explore novel diagnostic and therapeutic strategies. Potential therapeutic targets Looking ahead, the researchers are eager to explore potential therapeutic targets that can protect the brain from cancer-induced disruptions in neuronal circuits. They aim to identify molecules involved in metastasis-induced changes in neuronal communication, intending to evaluate them as possible therapeutic targets. The researchers want to create strategies that might stop or lessen the neurological dysfunction that patients frequently experience by understanding the biochemical and molecular changes brought on by brain metastasis. This could lead to advancements in the prevention, early diagnosis, and treatment of brain metastasis, ultimately improving patient outcomes. Conclusion The groundbreaking studies carried out by the Spanish National Research Council and the Spanish National Cancer Research Centre have shed light on how brain metastasis affects brain activity and neuronal communication. By dissociating the effects of tumour mass from changes in brain activity, the study has revealed the complex dynamics of brain metastasis and its contribution to cognitive impairment in patients. The discovery of distinct electrophysiological differences and the development of an algorithm to detect metastases offer promising opportunities for early diagnosis and personalised treatment. This paradigm shift in understanding brain metastases opens the door for novel diagnostic and therapeutic strategies, as well as the exploration of potential therapeutic targets to protect the brain from cancer-induced disruptions. With further research, it is hopeful that advancements in the prevention, early diagnosis, and treatment of brain metastasis will improve patient outcomes and lead to a better understanding of neurological dysfunction in these patients. Written by Sara Maria Majernikova Related articles: Cancer on the move / Cancer magnets / Latent space transformations / Uploading brain to a computer REFERENCE Sanchez-Aguilera A, Masmudi-Martín M, Navas-Olive A, Baena P, Hernández-Oliver C, Priego N, Cordón-Barris L, Alvaro-Espinosa L, García S, Martínez S et al : Machine learning identifies experimental brain metastasis subtypes based on their influence on neural circuits . Cancer Cell 2023, 41 (9):1637-1649.e1611. 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

Seizures are not mainly uncontrolled jerking and losing consciousness Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Epilepsy 101: what are the different types of epilepsy seizures? Last updated: 29/04/25, 17:09 Published: 27/02/25, 08:00 Seizures are not mainly uncontrolled jerking and losing consciousness After previously covering a very generic overview into epilepsy – what it is, its different types, methods of diagnosis and treatment, it would be a good idea to really delve deeper into the different types of seizures. Are they just convulsions, shaking and losing consciousness? Or is there more to it? Read more to find out! But before we begin, it is important to cover some key terms and prefixes, to help us with understanding what the different types of seizures are: Myo-: muscle Clonic: repeated jerking Tonic: muscle stiffness Atonic: muscles become limp Motor: movement From our previous article , we know that the two main types of epilepsy are generalised and focal epilepsy. Each type of epilepsy has different types of seizures associated with it. Generalised epilepsy – it consists of 2 main types of seizures (motor and non-motor seizures): 1) Generalised Motor Seizures: Involves changes in muscle activity, where they either move abnormally, or don’t move at all. This includes: Myoclonic seizures: sudden body jerks (especially the hands or the legs) as if someone had been jolted with electricity. Tonic - Clonic (Grand mal) seizures: This seizure has 2 main phases – a tonic and clonic stage:- Initial tonic (stiffness) phase is followed by a clonic (repeated, uncontrolled jerking of the limbs) phase. During the 'tonic' phase, the person may become unconscious and fall to the floor. In the 'clonic' phase, the person might struggle to breathe or uncontrollably bite their tongue. This is probably the ‘typical’ seizure everyone thinks of when they hear about epilepsy! Atonic seizures: The muscles become limp, and the person might even collapse. 2) Generalised non-motor seizures: They are usually also referred to as 'absence seizures', and they don’t include any changes in muscle activity. Instead, the person might stare into space, and might have a pause in activity, or a repetition in movements, such as lip-smacking for around 15 seconds or less. The individual may not remember what happened during the seizure; however their normal state of alertness is regained immediately after. People might easily confuse this type of seizure with daydreaming! Focal epilepsy- This is split into 4 main types based on whether the person is aware of their seizure, and if there are any changes in muscle activity involved: 1) Focal awareness seizures: Patient is fully aware of what is happening during a seizure, even if they are unable to move or respond. Some people might experience an "aura" as a warning before this seizure. This could feel like a strange sensation, fear, euphoria, a sense of déjà vu, feeling that something bad is about to happen, visual changes or even tingling or stiffness in their body. 2) Focal impaired awareness seizures: The person isn’t aware of their seizure, nor can they remember having it, and can’t respond to anyone during the seizure. The seizure can include movements such as moving their hands and legs or making random noises. 3) Focal Motor Seizures: involves random muscle activity, such as twitching, stiffness, limpness, or other movements such as rubbing hands, lip-smacking and walking around. 4) Focal Non-motor Seizures: no muscle movements or stiffness (as this is a non-motor seizure), but there is a change in a patient’s feelings and thoughts, causing strange feelings, a racing heart, and waves of heat or cold. Now that we’ve covered the key seizures, what triggers epilepsy seizures, causing those lights in the city (which in this case, is our brain) to start flickering or shut completely? There are many different causes, and they vary from one person to another. They could include: Stress Lack of sleep Drinking alcohol Consuming illegal drugs Not taking your anti-seizure medication (ASMs) Some types of medication Menstrual Cycle and hormonal changes Flashing lights (for individuals with photosensitive epilepsy) Photosensitive epilepsy is epilepsy that is triggered by flashing of lights, causing seizures such as myoclonic seizures. It is interesting to see how many people hold the misconception that seizures are mainly uncontrolled jerking and losing consciousness, when in fact there’s a huge variety of seizure! It is important that we know what different seizures look like, so we could help these individuals appropriately. Don’t be afraid to read further about epilepsy and seizures, and how to help people out there! Written by Hanin Salem Related articles: Epilepsy 101 (overview) / Traumatic brain injuries REFERENCES Dhanyamraju, S. (2019). What is a Seizure? - Lone Star Neurology . [online] Lone Star Neurology. Available at: https://lonestarneurology.net/seizures/seizures/ . [Accessed 19 Dec. 2024]. Ditki medical & biological sciences. (n.d.). Neurological System Glossary: Tonic-Clonic Seizure . [online] Available at: https://ditki.com/course/neurological-system/glossary/eeg-findings/tonic-clonic-seizure . [Accessed 19 Dec. 2024]. Epilepsy action (2022). Focal seizures | Epilepsy Action . [online] www.epilepsy.org.uk . Available at: https://www.epilepsy.org.uk/info/seizures/focal-seizures [Accessed 18 Dec. 2024]. John Hopkins Medicine (n.d.). Generalized Seizures . [online] Available at: https://www.hopkinsmedicine.org/health/conditions-and-diseases/epilepsy/generalized-seizures#:~:text=Generalized%20seizures%20include%20absence%2C%20atonic [Accessed 17 Dec.2024]. NHS (2020). Symptoms - Epilepsy . [online] NHS. Available at: https://www.nhs.uk/conditions/epilepsy/symptoms/ [Accessed 17 Dec. 2024]. Project Gallery

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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

Behaviours in birds, mammals, and invertebrates Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Same-sex attraction in non-human animals Last updated: 17/06/25, 12:20 Published: 11/09/25, 08:00 Behaviours in birds, mammals, and invertebrates Biased science communication can have detrimental consequences. For example, facts about animal reproduction have been twisted to justify discrimination against the LGBTQIA+ community. Some people call homosexuality a “Darwinian paradox”, because it does not fit their preconceived belief that an animal’s job is to stay alive and make babies. This belief ignores how some animals, like humans, have complex social structures and do things just for fun. Same-sex sexual behaviours (SSSB) have been observed in 1500 animal species, none of whom do it to make babies. This article describes some of these behaviours in birds, mammals, and invertebrates. Same-sex sexual behaviour (SSSB) in birds The first recorded example of SSSB in non-human animals comes from Aristotle about 2300 years ago. He wrote about male pigeons, partridges, and quails mating with other male conspecifics. Since then, same-sex relationships have been recorded in other bird species. Greylag geese form “gander pairs” of two males, whose behaviours resemble pairs of opposite-sex mates. In Oahu, Hawaii, female-female Laysan albatross pairs looked after 31% of nests between 2004 and 2007. These pairs, one of which is pictured in Figure 1 , were equally good at raising chicks as male-female pairs. SSSB was also observed in unbonded king penguins, meaning penguins which had not committed to a mate for that breeding season. Using DNA to assess individual sex, 26.4% of courtship displays between unbonded king penguin couples were same-sex. There was also one male-male and one female-female pair of bonded king penguins, but both couples broke up and re-bonded with opposite-sex mates in the same season. The most famous same-sex bird couple is Roy and Silo from Central Park Zoo. They were a pair of chinstrap penguins who raised a chick named Tango when given a fertile egg. This family was the subject of a children’s book ( Figure 2 ) and an American culture war. Thus, many bird species pair with individuals of the same sex in captivity and more importantly, in the wild. SSSB in mammals Humans are not the only mammals to mate with individuals of the same sex. Male bats from the Myotis genus have been observed getting intimate with each other, and Mytois lucifugus releases sperm during this activity. In another bat species called the Bonin flying fox, males groomed each other in a way scientists perceived as sexual. Japanese macaques have monogamous female-female pairs called consortships, in which females carry out the same mating behaviours seen with male-female pairs. SSSB in insects In addition to birds and mammals, some insects conduct sexual activities to others of the same sex. In a 2012 study, 16% of male field crickets did courtship displays to and/or tried to mate with another male. The authors conducted experiments to rule out some leading Darwinian causes of SSSB, such as establishing dominance relationships (similar to an ‘alpha male’) or defusing hostile encounters. SSSB is well studied in flour beetles, where the males mount other males and release capsules of sperm like they would to females. In these beetles, the sexes are sexually dimorphic - distinguishable by appearance, smell, and/or sound - so a male beetle is intentionally choosing to mate with another male. When 59 male damselflies were offered a male and female in the same cage, 10 approached and began mating with the male. More damselflies chose the male over the female after spending a few days in a male-only population, perhaps because they were used to only having males to choose from. Therefore, analogies to both homoromantic and homosexual partnerships in humans exist in insects. Conclusion Since mammals, birds, insects, and molluscs all have evidence of SSSB in the wild, it is normal and certainly not unnatural for humans to do the same. These behaviours range from preferentially approaching the same sex to intentional, intimate actions. All the papers I used in this article are over a decade old, with the earliest evidence of non-human same-sex behaviour being 2300 years old. This means using biology to justify homophobia is very outdated, and factually incorrect. Written by Simran Patel REFERENCES Young LC, Zaun BJ, VanderWerf EA. Successful same-sex pairing in Laysan albatross. Biol Lett [Internet]. 2008 Aug 23 [cited 2025 Feb 1];4(4):323–5. Available from: https://royalsocietypublishing.org/doi/10.1098/rsbl.2008.0191 Richardson J, Parnell P, Cole H. And Tango makes three. First Little Simon board book edition. New York: Little Simon; 2015. 1 p. Sugita N. Homosexual Fellatio: Erect Penis Licking between Male Bonin Flying Foxes Pteropus pselaphon . Pellis S, editor. PLoS ONE [Internet]. 2016 Nov 8 [cited 2025 Feb 1];11(11):e0166024. Available from: https://dx.plos.org/10.1371/journal.pone.0166024 Bailey NW, French N. Same-sex sexual behaviour and mistaken identity in male field crickets, Teleogryllus oceanicus . Animal Behaviour [Internet]. 2012 Oct [cited 2025 Feb 1];84(4):1031–8. Available from: https://linkinghub.elsevier.com/retrieve/pii/S0003347212003508 Huber R, Martys M. Male-male pairs in Greylag Geese ( Anser anser ). J Ornithol [Internet]. 1993 Apr [cited 2025 Feb 1];134(2):155–64. Available from: https://link.springer.com/10.1007/BF01640084 Levan KE, Fedina TY, Lewis SM. Testing multiple hypotheses for the maintenance of male homosexual copulatory behaviour in flour beetles. J of Evolutionary Biology [Internet]. 2009 Jan [cited 2025 Feb 1];22(1):60–70. Available from: https://academic.oup.com/jeb/article/22/1/60-70/7324140 Pincemy G, Dobson FS, Jouventin P. Homosexual Mating Displays in Penguins. Ethology [Internet]. 2010 Dec [cited 2025 Feb 1];116(12):1210–6. Available from: https://onlinelibrary.wiley.com/doi/10.1111/j.1439-0310.2010.01835.x Riccucci M. Same-sex sexual behaviour in bats. Hystrix, the Italian Journal of Mammalogy [Internet]. 2010 Sep 24 [cited 2025 Feb 1];22(1). Available from: https://doi.org/10.4404/hystrix-22.1-4478 Van Gossum H, De Bruyn L, Stoks R. Reversible switches between male–male and male–female mating behaviour by male damselflies. Biol Lett [Internet]. 2005 Sep 22 [cited 2025 Feb 1];1(3):268–70. Available from: https://royalsocietypublishing.org/doi/10.1098/rsbl.2005.0315 Vasey PL, Jiskoot H. The Biogeography and Evolution of Female Homosexual Behavior in Japanese Macaques. Arch Sex Behav [Internet]. 2010 Dec [cited 2025 Feb 1];39(6):1439–41. Available from: http://link.springer.com/10.1007/s10508-009-9518-2 Project Gallery

The newest pillar of chemical research Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Not all chemists wear white coats: computational organic chemistry Last updated: 01/02/26, 20:04 Published: 05/02/26, 08:00 The newest pillar of chemical research Introduction 'Not all chemists wear white coats,' aptly describes the newest pillar of chemical research. Coined by the Royal Society of Chemistry, computational modelling has become an essential tool across all areas of traditional chemistry. As artifical intelligence (AI) and machine learning become increasingly prevalent in research, the future of chemistry may unfold computationally before ever touching a test tube. Given the breadth of the field, this article will focus specifically on computational advancements in organic chemistry. Analytical Chemistry Density Functional Theory (DFT) is a quantum computational method that models molecules based upon the distribution of their electron density. It can be utilised by organic chemists to determine the stereochemistry of a product by modelling Vibrational Circular Dichroism spectra (VCD). VCD is a spectroscopic technique which measures the difference in absorption of left versus right-handed circularly polarised light by chiral molecules. By using DFT to compute the VCD spectra of each enantiomer, chemists can compare them to experimental spectra. A match between the compound and the experimental spectrum indicates an accurate assignment of the molecule’s stereochemistry. See Figure 1 . Predicting molecular conformation While the Cahn-Ingold-Prelog naming system allows chemists to describe the 3D arrangement of a molecule, computational analysis can help predict which molecular shape is preferred in practice. Molecular Mechanics (MM) is a computational method that treats molecules using classical physics, modelling atoms and bonds as ‘balls’ connected by ‘strings’. A force field is used to calculate the potential energy of a molecule, accounting for bond stretching, angle bending, bond rotation, van der Waals interactions and electrostatic forces. A simple example of how this method supports organic chemistry is the determination of the most stable conformation of butane. By rotating the central C-C bond through 360°, the energy of each conformation can be plotted against the dihedral angle. This analysis shows that the anti-conformation is the most stable, as the two methyl groups are positioned 180° apart to minimise steric strain. See Figure 2 . Drug discovery Computational chemistry has also transformed drug discovery by enabling chemists to simulating how potential drug compounds will bind to their target active site. In the past, drug development has often relied on synthesising a large number of candidates and testing each experimentally to see which worked. Today, advances in computational chemistry, combined with X-ray crystallographic data, allows both a drug candidate and its protein binding site to be modelled before any lab work begins. This helps researchers save both time and resources. Known as structural based drug design, this approach commonly relies on hybrid computational methods, particularly Quantum Mechanics/ Molecular Mechanics (QM/MM). In this case, the chemically active regions, such as the drug molecule and protein active site are treated using QM while the rest of the proteins is treated using MM. By combining these techniques, a balance is struck between computational accuracy and calculation time, especially important for larger molecules. See Figure 3. Conclusion In conclusion, computational chemistry is an essential tool for interpreting experimental results and generating new scientific insight. While this article has focused on its role in supporting organic chemistry research, the reach of computational chemistry extends far beyond this field. From modelling batteries and solid state materials to organometallic catalysis, computational chemistry is now firmly embedded in modern chemical research. Written by Antony Lee Related articles: Quantum- chemistry , computing REFERENCES The Royal Society of Chemistry - https://edu.rsc.org/resources/not-all-chemists-wear- white-coats/1654.article (Accessed January 2026) Y.L. Zeng, X.Q. Huang, C.R. Huang, H. Zhang, F. Wang, Z.X. Wang, Angew. Chem. Int. Ed., 2021, 60, 10730-10735 Chemistry LibreTexts https://chem.libretexts.org/Bookshelves/Organic_Chemistry/Organic_Chemistry_%28Mor sch_et_al.%29/03%3A_Organic_Compounds_Alkanes_and_Their_Stereochemistry/3.07% 3A_Conformations_of_Other_Alkanes (Accessed January 2026) Ecole des Bio-Industries - https://www.ebi-edu.com/en/coup-de-coeur-research-9/ (Accessed January 2026) Project Gallery

How your gut is your second brain (an opinion piece) Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Microbes in charge Last updated: 16/06/25, 17:09 Published: 26/06/25, 08:00 How your gut is your second brain (an opinion piece) Imagine this: you have just won ten million dollars in the lottery, or you have just eaten the most delicious, warm, chocolate brownie. In these situations, our brains produce chemicals called neurotransmitters, which give us these great feelings of pleasure and happiness. Now, imagine this: you're about to sit an exam. In this situation, our brains, instead, produce different chemicals, making us feel stressed and anxious. Our emotions control the highs and lows of life. I have always heard that the brain inside all of us controls everything that we feel, think and do. However, I've always found it strange that every feeling, thought, and behaviour is controlled by a three-pound, soggy lump of cells inside our heads, until I learned about gut microbiota. We each have a second brain, which controls as much of our physical and mental functions as the brain in our heads, and plays a role in preventing diseases. This second brain is our gut microbiota. However, we have completely underestimated their role as the second brain. I learned this first through the intriguing story of the rat. If the rat becomes colonised with the microbe Toxoplasma gondii, a fascinating thing happens: they lose their fear of cats. The cat's smell was chosen as a measure. The infected rat preferred the areas that had the smell of cats. So, the microbes take control of the brain and change the way you think. In another study, a research group at University College Cork in Ireland fed Lactobacillus rhamnosus , a good bacteria—or 'probiotic' you can usually find in yoghurt—to one of two groups of mice. The probiotic mice were much more likely to succeed in the face of adversity tests than those not treated with the probiotic. They repeated a similar study in humans, with the probiotic-fed humans displaying improved resilience to negative emotions compared to those without the probiotic. As I mentioned earlier, neurotransmitters are these chemicals that can change how we think, behave, and feel. As it turns out, neurotransmitters are also produced in our gut, 50% of the dopamine and 90% of serotonin (nature's antidepressant): two neurotransmitters that drastically affect your mood, happiness and pleasure. According to some studies, dopamine also plays a role in memory and learning, so gut microbiota controls how you think and behave and is also involved in cognitive functions like memory and learning. Let’s now turn to mental health! One study by Venket Rao studied 39 individuals with chronic fatigue syndrome (a syndrome characterised by severe anxiety, depression, and long-term exhaustion), split the individuals into two groups. The first group received a bacterial strain for two months while the other group received only a placebo. The group that received the bacterial strain showed a significant decrease in anxiety with respect to the other group. Noticeably, there is a vital link between the gut microbiota and the immune system. 70-80% of immune cells are present in the gut. Additionally, studies have shown that Germ-free mice have fewer immune system structures in their intestines than wild-type mice. These immune structures in the gut are referred to as the gut-associated lymphoid tissues (GALT) and Peyer's patches. Another study explored the gut microbiota of 42 patients affected by Rheumatoid Arthritis and 10 healthy controls. They observed that rheumatoid arthritis patients have a higher population of Lactobacillaceae family and the Lactobacillus genus, and fewer Faecalibacterium , a butyrate producer. Butyrate is the fuel source for our intestinal cells to produce mucin, which then repairs the intestinal lining and mucosal membrane and reduces inflammation. Our gut and brain are physically and biochemically connected in several ways. First, our intestines are physically linked to our brain through the vagus nerve, which sends signals in both directions. Interestingly, even if this is cut off (severed), our intestines can continue to function fully without a connection to the brain, suggesting they have a mind of their own. Secondly, our brains are made up of a hundred billion neurons, which continuously send messages to tell our bodies how to work and behave. Well, interestingly, our guts have a hundred million neurons. Our gut microbiota, the unsung hero behind our feelings, thoughts, immune system and behaviour - proving that sometimes, it's not just all in our heads, but in our "guts" too! Written by Prabha Rana Related articles: The gut microbiome / The dopamine connection REFERENCES Webster J. P. (2007). The effect of Toxoplasma gondii on animal behavior: playing cat and mouse. Schizophrenia bulletin , 33 (3), 752–756. https://doi.org/10.1093/schbul/sbl073 Bravo, J. A., Forsythe, P., Chew, M. V., Escaravage, E., Savignac, H. M., Dinan, T. G., Bienenstock, J., & Cryan, J. F. (2011). Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proceedings of the National Academy of Sciences of the United States of America , 108 (38), 16050–16055. https://doi.org/10.1073/pnas.1102999108 Strandwitz P. (2018). Neurotransmitter modulation by the gut microbiota. Brain research , 1693 (Pt B), 128–133. https://doi.org/10.1016/j.brainres.2018.03.015 Rao, A. V., Bested, A. C., Beaulne, T. M., Katzman, M. A., Iorio, C., Berardi, J. M., & Logan, A. C. (2009). A randomized, double-blind, placebo-controlled pilot study of a probiotic in emotional symptoms of chronic fatigue syndrome. Gut pathogens , 1 (1), 6. https://doi.org/10.1186/1757-4749-1-6 Wiertsema, S. P., van Bergenhenegouwen, J., Garssen, J., & Knippels, L. M. J. (2021). The Interplay between the Gut Microbiome and the Immune System in the Context of Infectious Diseases throughout Life and the Role of Nutrition in Optimizing Treatment Strategies. Nutrients , 13 (3), 886. https://doi.org/10.3390/nu13030886 Round, J. L., & Mazmanian, S. K. (2009). The gut microbiota shapes intestinal immune responses during health and disease. Nature reviews. Immunology , 9 (5), 313–323. https://doi.org/10.1038/nri2515 Picchianti Diamanti, A., Panebianco, C., Salerno, G., Di Rosa, R., Salemi, S., Sorgi, M. L., Meneguzzi, G., Mariani, M. B., Rai, A., Iacono, D., Sesti, G., Pazienza, V., & Laganà, B. (2020). Impact of Mediterranean Diet on Disease Activity and Gut Microbiota Composition of Rheumatoid Arthritis Patients. Microorganisms , 8 (12), 1989. https://doi.org/10.3390/microorganisms8121989 Han, Y., Wang, B., Gao, H., He, C., Hua, R., Liang, C., … Xu, J. (2022). Vagus Nerve and Underlying Impact on the Gut Microbiota-Brain Axis in Behavior and Neurodegenerative Diseases. Journal of Inflammation Research , 15 , 6213–6230. https://doi.org/10.2147/JIR.S384949 Project Gallery

Role of neurotransmitters in depression Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Inside out: the chemistry of depression Last updated: 19/02/26, 19:35 Published: 05/06/25, 08:00 Role of neurotransmitters in depression This is Article 2 in a series on psychiatric disorders and the brain. Next article: The promising effects of magic mushrooms for depression . Previous article: What does depression do to your brain? Ever wondered what’s going on inside your brain when you’re feeling down? Imagine the scene from Inside Out , where Sadness takes over the control room, overshadowing the other emotions. That’s actually not too far from what happens during depression, but the changes in your brain are much more than just a battle of emotions. Depression is the most common mental illness globally. It is typically marked by a persistently low mood and energy, and a loss of interest or pleasure in everyday activities. Risk factors include chronic stress, traumatic life events, genetic vulnerability, ageing, and female sex. While these influences are widely recognised, have you ever thought about what is actually happening inside your brain when you're depressed? You've probably heard phrases like “I need a serotonin boost,” but what does that really mean? What is serotonin, and how does it influence our emotions and mental health? What are neurotransmitters? Think of neurotransmitters as messenger pigeons between neurons. They are involved in communication between different neurons. Communication between neurons is called synaptic transmission. In synaptic transmission, neurotransmitters are released from vesicles in one neuron into the synaptic cleft (the gap between two neurons) and then bind to receptors on the receiving neuron. This is how information travels through the brain, allowing us to think, feel, and act. Serotonin is an example of a neurotransmitter. Others include dopamine, noradrenaline, acetylcholine. The monoamine theory of depression One of the most widely supported explanations for the neurobiology of depression is the monoamine theory. This theory suggests that depression results from an imbalance or deficiency of monoamines in the brain. Monoamines are a group of neurotransmitters, including serotonin, dopamine, and noradrenaline, that are synthesised from the amino acids L-tryptophan and L-tyrosine. Fun fact: Did you know around 95% of the body's serotonin is produced in the gut? This is why there is growing interest in the gut-brain axis in mental health! Different neurotransmitter systems are involved in depression and even everyday emotion processing and regulation. The dopamine (DA) system plays a key role in experiencing reward and pleasure, often linked to feelings of joy. In contrast, the serotonin (5-HT) system is more associated with responses to punishment and aversive experiences, such as sadness or disgust. Noradrenaline (NE), on the other hand, is closely tied to fear, anger, and the activation of the "fight or flight" response during stressful situations. These neurotransmitters are thought to underlie three fundamental emotional states, which can combine in different ways to form a wide range of complex emotions. In the brain, these monoamines regulate mood, motivation, pleasure, and emotional stability. When levels are low, people may experience sadness, fatigue, apathy, and changes in appetite or sleep. This is why many antidepressant medications, such as selective serotonin reuptake inhibitors (SSRIs), aim to increase the availability of these monoamines in the synapse, improving communication between neurons and, over time, alleviating symptoms. SSRI treatment, in particular, is based on the serotonin hypothesis, a subset of the broader monoamine theory of depression, which suggests that reduced serotonin levels contribute to depressive symptoms. Conclusion: why depression is more than a mood Depression isn’t just “feeling sad”; it is a real condition that involves real chemical changes in the brain. The monoamine theory helps explain this by focusing on key neurotransmitters like serotonin, dopamine, and noradrenaline, which help control mood, motivation, and emotional balance. When these chemicals are out of sync, too low or not working properly, it can lead to the emotional numbness, low energy, and hopelessness that many people with depression experience. These neurotransmitters do not work in isolation; they influence how we respond to rewards, stress, and even daily activities. By understanding the biological changes behind depression, we take an important step toward not only understanding the condition but also reducing the stigma around it. Written by Chloe Kam Related articles: Emotional chemistry / Embarrassment / Postpartum depression in adolescent mothers REFERENCES Barchas, J.D. and Altemus, M. (1999) ‘Monoamine Hypotheses of Mood Disorders’, in Basic Neurochemistry: Molecular, Cellular and Medical Aspects. 6th edition . Lippincott-Raven. Available at: https://www.ncbi.nlm.nih.gov/books/NBK28257/ (Accessed: 3 May 2025). Jiang, Y. et al. (2022) ‘Monoamine Neurotransmitters Control Basic Emotions and Affect Major Depressive Disorders’, Pharmaceuticals , 15(10), p. 1203. Available at: https://doi.org/10.3390/ph15101203 . Project Gallery