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Famine-induced epigenetic changes and public health strategies in affected populations Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why South Asian genes remember famine Last updated: 18/09/25, 08:44 Published: 23/01/25, 08:00 Famine-induced epigenetic changes and public health strategies in affected populations Our genes are often thought of as a fixed blueprint, but what if our environment could change how they work? This is the intriguing idea behind epigenetics—a field that shows how our environment, combined with the body’s adaptive responses for survival, can influence gene expression without altering our DNA. In South Asia, famines such as the infamous Bengal Famine of 1943 caused immense suffering, and these hardships may have triggered genetic changes that continue to affect generations. Today, South Asians face an increased risk of developing Type 2 diabetes by age 25, whereas White Europeans generally encounter this risk around age 40. What is driving this difference in risk? This article will explore the science behind these epigenetic changes, their impact on the descendants of famine survivors and how these insights can shape public health, policy, and research. The legacy of historical famines In 1943, the Bengal Famine claimed around three million lives. Nobel laureate Amartya Sen argues that the severity of the famine was not merely a result of prior natural disasters and disease outbreaks in crops. Instead, it was primarily driven by wartime inflation, speculative buying, and panic hoarding, which disrupted food distribution across the Bengal region. Consequently, for the average Bengali citizen, death from starvation, disease, and malnutrition became widespread and inevitable. The impact of the famine extended well beyond the immediate loss of life. Dr Mubin Syed, a radiologist specialising in vascular and obesity medicine, emphasises that these famines have left a lasting mark on the health of future generations. Dr Syed explains that South Asians, having endured numerous famines, have inherited "starvation-adapted" traits. These traits are characterised by increased fat storage. As a result, the risk of cardiovascular diseases, diabetes, and obesity is heightened in their descendants. This tendency towards fat storage is believed to be closely tied to epigenetic factors, which play a crucial role in how these traits are passed down through generations. Epigenetic mechanisms and their impact These inherited traits are shaped by complex epigenetic mechanisms, which regulate gene expression in response to environmental stressors like famines without altering the underlying DNA sequence. DNA methylation, a process involving the addition of small chemical groups to DNA, plays a crucial role in regulating gene expression. When a gene is 'on,' it is actively transcribed into messenger RNA (mRNA), resulting in the synthesis of proteins such as enzymes that regulate energy metabolism or hormones like insulin that manage blood sugar levels. Conversely, when a gene is 'off,' it is not transcribed, leading to a deficiency of these essential proteins. During periods of famine, increased DNA methylation can enhance the body's ability to conserve and store energy by altering the activity of metabolism-related genes. Epigenetic inheritance, a phenomenon where some epigenetic tags escape the usual reprogramming process and persist across generations, plays a crucial role in how famine-induced traits are passed down. Typically, reproductive cells undergo a reprogramming phase where most epigenetic tags are erased to reset the genetic blueprint. However, certain DNA methylation patterns can evade this erasure and remain attached to specific genes in the germ cells, the cells that develop into sperm and egg cells. These persistent modifications can influence gene expression in the next generation, affecting metabolic traits and responses to environmental stressors. This means the metabolic adaptations seen in famine survivors, such as increased fat storage and altered hormone levels, can be transmitted to their descendants, predisposing them to similar health risks. Research has highlighted how these inherited traits manifest in distinct hormone profiles across different ethnic groups. A study published in Diabetes Care found that South Asians had higher leptin levels (11.82 ng/mL) and lower adiponectin levels (9.35 µg/mL) compared to Europeans, whose leptin levels were 9.21 ng/mL and adiponectin levels were 12.96 µg/mL. Leptin, encoded by the LEP gene, is a hormone that reduces appetite and encourages fat storage. Adiponectin, encoded by the ADIPOQ gene, improves insulin sensitivity and supports fat metabolism. Epigenetic changes, such as DNA methylation in the LEP and ADIPOQ genes, have led to these imbalances which were advantageous for South Asian populations during times of famine. Elevated leptin levels helped ensure the body could maintain energy reserves for survival, while lower adiponectin levels slowed fat breakdown, preserving stored fat for future use. This energy-conservation mechanism allowed individuals to endure long periods of food scarcity. Remarkably, these epigenetic changes can be passed down to subsequent generations. As a result, descendants continue to exhibit these metabolic traits, even in the absence of famine conditions. This inherited imbalance—higher leptin levels and lower adiponectin—leads to a higher predisposition to metabolic disorders. Increased leptin levels can cause leptin resistance, where the body no longer responds properly to leptin’s signals, driving overeating and fat accumulation. Simultaneously, reduced adiponectin weakens the body’s ability to regulate insulin and break down fats efficiently, resulting in higher blood sugar levels and greater fat storage. These combined effects heighten the risk of obesity and Type 2 diabetes in South Asian populations today. Integrating cultural awareness in health strategies Understanding famine-induced epigenetic changes provides a compelling case for rethinking public health strategies in affected populations. While current medicine cannot reverse famine-induced epigenetic changes in South Asians, culturally tailored interventions and preventive measures are crucial to reducing metabolic risks. These should include personalised dietary plans, preventive screenings, and targeted healthcare programmes. For example, the Indian Diabetes Prevention Programme showed that lifestyle changes reduced diabetes risk by 28.5% among high-risk individuals. Equally, policymakers must consider the broader societal factors that contribute to these health risks, and qualitative studies highlight challenges in shifting cultural attitudes. Expectations that women prepare meals in line with traditional norms often limit healthier dietary options.Differing perceptions of physical activity can complicate efforts to promote healthier lifestyles. For example, a study in East London found that some communities consider prayer sufficient exercise, which adds complexity to changing attitudes. Facing our past to secure a healthier future As we uncover the long-term effects of environmental stressors like historical famines, it becomes clear that our past is not just a distant memory but an active force shaping our present and future health. Epigenetic changes inherited from South Asian ancestors who endured famine have heightened the risk of metabolic disorders in their descendants. For instance, UK South Asian men have been found to have nearly double the risk of coronary heart disease (CHD) compared to White Europeans. Consultant cardiologist Dr Sonya Babu-Narayan has stated, “Coronary heart disease is the world’s biggest killer and the most common cause of premature death in the UK.” With over 5 million South Asians in the UK alone, this stark reality requires immediate action. We must not only address the glaring gaps in scientific research but also develop targeted public health policies to tackle these inherited health risks. These traits are not relics of the past; they are living legacies that, without swift intervention, will continue to affect generations to come. To truly address the inherited health risks South Asians face, we must go beyond surface-level awareness and commit to long-term, systemic change. Increasing funding for research that directly focuses on the unique health challenges within this population is non-negotiable. Equally crucial are culturally tailored public health initiatives that resonate with the affected communities, alongside comprehensive education programmes that empower individuals to take control of their health. These steps are not just about improving outcomes—they’re about breaking a cycle. The question, therefore, is not simply whether we understand these epigenetic changes, but whether we have the resolve to confront their full implications. Can we muster the political will needed to confront these inherited risks? Can we unite our efforts to stop these risks from affecting the health of entire communities? The cost of inaction is not just measured in statistics—it will be felt in the lives lost and the potential unrealised. The time to act is now. Written by Naziba Sheikh Related articles: Epigenetics / Food deserts and malnutrition / Mental health in South Asian communities / Global health injustices- Kashmir , Bangladesh REFERENCES Safi, M. (2019). Churchill’s policies contributed to 1943 Bengal famine – study. [online] the Guardian. Available at: https://www.theguardian.com/world/2019/mar/29/winston-churchill-policies-contributed-to-1943-bengal-famine-study . Bakar, F. (2022). How History Still Weighs Heavy on South Asian Bodies Today. [online] HuffPost UK. Available at: https://www.huffingtonpost.co.uk/entry/south-asian-health-colonial-history_uk_620e74fee4b055057aac0e9f . Sayed, M., Deek, F. and Shaikh, A. (2022). The Susceptibility of South Asians to Cardiometabolic Disease as a Result of Starvation Adaptation Exacerbated During the Colonial Famines. [online] Research Gate. Available at: https://www.researchgate.net/publication/366596806_The_Susceptibility_of_South_Asians_to_Cardiometabolic_Disease_as_a_Result_of_Starvation_Adaptation_Exacerbated_During_the_Colonial_Famines#:~:text=This%20crisis%20could%20be%20the,adapted%20physiology%20can%20become%20harmful . Utah.edu . (2009). Epigenetics & Inheritance. [online] Available at: https://learn.genetics.utah.edu/content/epigenetics/inheritance/ . Palaniappan, L., Garg, A., Enas, E., Lewis, H., Bari, S., Gulati, M., Flores, C., Mathur, A., Molina, C., Narula, J., Rahman, S., Leng, J. and Gany, F. (2018). South Asian Cardiovascular Disease & Cancer Risk: Genetics & Pathophysiology. Journal of Community Health, 43(6), pp.1100–1114. doi: https://doi.org/10.1007/s10900-018-0527-8 . Diabetes UK (2022). Risk of Type 2 Diabetes in the South Asian Community. [online] Diabetes UK. Available at: https://www.diabetes.org.uk/node/12895 . King, M. (2024). South Asian Heritage Month: A Journey Through History and Culture . [online] Wearehomesforstudents.com . Available at: https://wearehomesforstudents.com/blog/south-asian-heritage-month-a-journey-through-history-and-culture . Project Gallery

The utilisation of Stonehenge as an astronomical calculator Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The celestial blueprint of time: Stonehenge, United Kingdom Last updated: 08/10/25, 16:22 Published: 09/10/25, 07:00 The utilisation of Stonehenge as an astronomical calculator This is Article 3 in a series about astro-archaeology. Next article coming soon. Previous article: The astronomical symbolism of the Giza Pyramids . Stonehenge, located within the south-west of England, is one of the UK’s most notable man-made structures, built during the neolithic period around 3100BC. Not only is this famous UNESCO heritage site a breakthrough in engineering, but the sandstone architecture also holds an enigmatic connection between the land and the sky. Its location and stone arrangement mirrors a blueprint that can be analysed to predict the timings of astronomical phenomena. The utilisation of Stonehenge as an astronomical calculator was established by astronomer Gerald Hawkins in 1965. Using computer software, Hawkins discovered that the location of Stonehenge aligned with several solar and lunar positions. He theorised that Stonehenge was built to predict astronomical events, such as eclipses, and to determine the position of summer and winter solstices. From the shape and positions of the 19 stones that comprise Stonehenge, its ‘horseshoe’ shape could predict the lunar eclipses. A booklet titled Stonehenge: Sun, Moon, Wandering Stars , written by M.W. Postins further detailed the significance of Stonehenge in archaeoastronomy. Postins suggested two scale models, the ‘Temple model’ and the ‘Enclosure model’, which detailed the significance of each stone and its relation to different events. For example, the booklet notes that the Altar Stone, a large sandstone located in the centre of Stonehenge, was placed across the solstice axis and represents the ‘Summer solstice sunrise’. Additionally, Postins hypothesised that the five trilithons, which are the vertical stones that form the structure of Stonehenge, represented planets that can be viewed with the naked eye. These include the two lowest trilithons on the East and Northern sides of the structure, representing Mercury and Venus. There has been new research, currently underway by the universities of Oxford, Leicester and Bournemouth in collaboration with the Royal Astronomical Society, linking the Stonehenge monument to a unique lunar phenomenon, called the ‘Major Lunar Standstill’. Right from the early construction of Stonehenge, researchers note that the major lunar standstill may have influenced the design of the monument. Four of the stones at Stonehenge align with two of the Moon’s positions, which aid to indicate moonrise and moonset. This would have allowed individuals to use the moonlight for longer periods of activity, such as night time hunting, as well as visualise the cycle of the lunar phases as a method of time watching for farming and celebratory purposes. Potentially, there is speculation that this made the positioning and construction of Stonehenge intentional. The timeless effect of the Stonehenge landmark, which shaped life in the past and continues to be of astronomical interest to determine the future, is a remarkable example of the functions of built structures for the analysis of astronomical events. It truly is a celestial blueprint for the relationship between the earth and cosmology. Written by Shiksha Teeluck Related article: Astro-geography of Lonar Lake REFERENCES English Heritage. (2024). Stonehenge: Major Lunar Standstill . https://www.english-heritage.org.uk/visit/places/stonehenge/things-to-do/major-lunar-standstill/ OSR. (2009). Stonehenge: An Astronomical Calculator . https://osr.org/blog/astronomy/stonehenge-an-astronomical-calculator/?srsltid=AfmBOopNQnJ-XUZSyLY_Aqu3L2nOJgSoAceRzQJIVZbsIsFhW6s3U_NT Tiverton & Mid Devon Astronomy Society. (n.d.). Astro-Archaeology at Stonehenge . http://www.tivas.org.uk/stonehenge/stone_ast.html 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, 07:00 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 Out of gallery

​Dive into the latest biological research! Learn about the regulation and policy of stem cell research, health inequalities and other public health news. Biology Articles Dive into the latest biological research! Learn about the regulation and policy of stem cell research, health inequalities and other public health news. You may also like: Cancer , Ecology , Genetics , Immunology , Neuroscience , Zoology , and Medicine Regulation and policy of stem cell research The 14-day rule and stem cell-based embryo models Maveerar Naal Health, trauma, and resilience amid decades of war in Sri Lanka What are health inequalities? Unequal access to healthcare. Article #1 in a series on health inequalities. Socioeconomic health inequalities Unequal access to healthcare due to social and financial factors. Article #2 in a series on health inequalities. Ethnic health inequalities Unequal access to healthcare due to ethnicity and race. Article #3 in a series on health inequalities. Addressing health inequalities Addressing these inequalities due to various reasons. Article #4 in a series on health inequalities. Dessert deception How junk food advertising affects public health Previous

Read articles delving into the universal genetic code: from CRISPR-Cas9 and epigenetics, to AI diagnosis, schizophrenia, and ancestry. Genetics Articles Read articles delving into the universal genetic code: from CRISPR-Cas9 and epigenetics, to AI diagnosis, schizophrenia, and ancestry. You may also like: Biology The CRISPR- CAS9 system Who were the Nobel Prize winners of Chemistry in 2020? What did they discover? Micro-chimerism, and George Floyd's death A Publett collaboration Schizophrenia Complex disease series: the influence of the environment on complex diseases. Article #1 Genetically-engineered bacteria decompose plastic A solution to plastic pollution Gene therapy by rAAVs rAAVs- recombinant adeno-associated viruses An introduction to epigenetics Interactions between genes and the environment Are aliens on Earth? Applications of ancient DNA analysis New horizons in Alzheimer's Reaching new potential in research The Y chromosome unveiled A remarkable discovery Decoding p53 A fundamental tumour supressor protein Epigenetics and queen bees What distinguishes queen bees from worker bees? Genetics of excessive smoking and drinking What are their contribution? SNPs and haplogroups Solving the mystery of ancestry Germline gene therapy A Scientia News Biology and Genetics collaboration Chimeras A genetic phenomenon Unfolding prion diseases What happens when proteins don't fold properly? Article #5 in a series on Rare diseases. Diagnosing genetic diseases with AI The advancements made by AI in diagnosis Breaking down Tay-Sachs A rare inherited disease caused by a missing enzyme. Article #6 in a series on Rare diseases. Genetics of ageing and longevity What genes and transcription factors are involved in these processes? Ehlers-Danlos syndrome How it's caused. Article #7 in a series on Rare diseases. Next

Jennifer Doudna and Emmanuelle Charpentier were jointly awarded the Nobel Prize in Chemistry in the year 2020, for their major contributions in reducing the number of components in the CRISPR-Cas9 system. An outline of their discovery CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats) can be used, by removing, adding, or altering particular DNA sequences and may edit specific parts of the genome. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Who were the winners of the Nobel Prize in Chemistry in 2020? Last updated: 26/04/26 Published: 02/02/23 Jennifer Doudna and Emmanuelle Charpentier were jointly awarded the Nobel Prize in Chemistry in the year 2020, for their major contributions in assembling and demonstrating Cas9 gene editing capabilities in vitro. An outline of their discovery Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR-Cas9) can be used, by removing, adding, or altering particular DNA sequences and may edit specific parts of the genome. A four-part mechanism called the Cas9 endonuclease consists of two small molecules. Charpentier discovered the tracrRNA, which, when combined with the crRNA (discovered in 2007 by a different group), they could assemble and demonstrate Cas9 gene editing capabilities in vitro. The two types of sequences were later combined to the now well-known "single-guide RNA" (sgRNA)- done in collaboration with Doudna in 2012. By combining these two RNA molecules into a sgRNA, the Cas9 endonuclease was redesigned into a more manageable two-component system that could locate and cut the DNA target defined by the guide RNA- CRISPR/Cas9 ‘genetic scissors’. It can silence or activate genes as well as add or remove others. The Nobel Prize in Chemistry was awarded in 2020 in recognition of this contribution. Some advantages of this technology: quick easy adaptable innovative, unique Disadvantages: distribution challenges extremely conservative ethical issues some off-target effects some negative outcomes Significance of this discovery This discovery is important in preventing disease and is such a revolutionary tool. It does not just help humans but also animals, plants and even bacteria. CRISPR has already been applied to various disorders, such as cancer and infectious diseases. By making it possible to make changes to the target cells' genomes, which were previously challenging to do, the procedure offers a new perspective on biological treatment and demonstrates how important this tool is. But since this technology is still recent, scientists must develop straightforward processes and techniques to monitor and test its progress, performance, and outcomes. Jennifer Doudna Hailing from Washington DC., USA, Jennifer Doudna was born in 1964. As a professor of biochemistry, biophysics, and structural biology, Doudna’s main research focus is on RNA, and its variety of structures and functions. It was her research lab’s work that led to the discovery of CRISPR-Cas9 as an extraordinarily powerful tool to cut and edit the human genome to treat disease. This remarkable discovery was a decade ago in 2012, when Doudna and others were able to copy a bacterial system to create molecular scissors, in order to edit the genetic code. In October 2020, at the time of her being awarded the Nobel Prize in Chemistry, Doudna was affiliated to the University of Berkeley, in California. Emmanuelle Charpentier Coming from a French background, Emmanuelle Charpentier is a professor and researcher in microbiology, genetics, and biochemistry. Born in 1968, researcher Charpentier has made tremendous progress in her respective field. From being the director at the Berlin Max Planck Institute for Infection Biology in 2015, to founding her own independent research institute- the Max Planck Unit for the Science of Pathogens in the year 2018, and of course being jointly awarded the Nobel Prize in Chemistry in 2020; it is true that Charpentier has added new, valuable research in her work and has come a long way in her career. Why the CRISPR/ Cas9 system fascinates us We find CRISPR fascinating because as biological science students, we know this tool is vital for genetics and can help cure present incurable diseases such as sickle cell disease as well as cancer, showing what a revolutionary tool this is. It does not just help humans but also animals, plants and even bacteria showing how broad biology is and different fields can be linked to one another. Researchers are constantly coming up with new ways to use CRISPR-Cas9 gene editing technology to solve problems in the real world, such as epigenome editing, new cell and gene therapies, infectious disease research, and the conservation of endangered species. The advantages of this technology are that it is quick, easy and adaptable, but its disadvantages include distribution challenges, extremely conservative ethical issues, some off-target effects, and some negative outcomes. By making it possible to make changes to the target cells' genomes, which were previously challenging to do, the procedure offers a new perspective on biological treatment and demonstrates how important this tool is. Written by Jeevana Thavarajah, and Manisha Halkhoree Scientia News Founder and Managing Director Related articles: Female Nobel prize winners in Chemistry and in Physics

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Exploring the microscopic world of molecules Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Quantum Chemistry Last updated: 05/02/26, 10:12 Published: 06/02/25, 08:00 Exploring the microscopic world of molecules Quantum chemistry provides a glimpse into the strange and fascinating world of molecules and atoms, where the principles of traditional chemistry and physics no longer apply. While classical chemistry can explain molecular interactions and bonding, it cannot fully account for particles' unusual, frequently contradictory behaviour at the atomic and subatomic levels. Quantum mechanics provides scientists with a powerful framework for understanding the complicated behaviour of electrons and nuclei in molecules. The basics of quantum chemistry The notion of wave-particle duality, which states that particles, such as electrons, act not just like objects with mass but also like waves, is central to quantum chemistry. Because the exact position and momentum of an electron cannot be known at the same time (according to the Heisenberg Uncertainty Principle), probability distributions are used to describe electrons rather than accurate orbits. These distributions are represented by mathematical functions known as wave functions, which describe the probability of finding an electron in a specific location surrounding the nucleus. This fundamentally affects our understanding of chemical bonding. Instead of conceiving a bond as a solid connection between two atoms, quantum chemistry defines it as the overlap of electron wave functions, which can result in a variety of molecular topologies depending on their energy levels. Quantum mechanics and bonding theories Quantum mechanics has fundamentally altered our knowledge of chemical bonding. The classic Lewis structure model, which explains bonding as the sharing or transfer of electrons, is effective for simple molecules but fails to convey the complexities of real-world interactions. In contrast, quantum chemistry introduces the concept of molecular orbitals. In molecular orbital theory, electrons are not limited to individual atoms but can spread across a molecule in molecular orbitals, which are combinations of atomic orbitals from the participating atoms. These molecular orbitals provide a more detailed explanation for bonding, especially in compounds that do not match simple bonding models, such as delocalised systems like benzene or metals. For example, quantum chemistry explains why oxygen is paramagnetic (it possesses unpaired electrons), a characteristic that classical bonding theories cannot explain. Quantum chemistry and quantum computing One of the most interesting frontiers in quantum chemistry is its application to the development of quantum computers. Traditional computers, despite their enormous processing power, struggle to model the complicated behaviour of molecules, particularly large ones. This is because simulating molecules at the quantum level necessitates tracking all conceivable interactions between electrons and nuclei, which can quickly become computationally challenging. Quantum computers use fundamentally different ideas. They employ qubits, which, unlike classical bits, can exist in a state of both 0 and 1. This enables quantum computers to execute several calculations concurrently and manage the complexity of molecular systems considerably more effectively. This could lead to advancements in quantum chemistry, such as drug discovery, where precisely modelling molecular interactions is critical. Instead of depending on trial and error, scientists may utilise quantum computers to model how possible pharmaceuticals interact with biological molecules at the atomic level, thereby speeding up the creation of novel therapies. Similarly, quantum chemistry could help in the development of novel materials with desirable qualities, such as stronger alloys and more efficient energy storage devices. Why quantum chemistry matters The consequences of quantum chemistry go well beyond the lab. Understanding molecular behaviour at its most fundamental level allows us to create new technologies and materials that have an impact on everyday life. Nanotechnology, for example, relies largely on quantum principles to generate innovative materials with applications in medicine, electronics, and clean energy. Catalysis, the technique of speeding up reactions, also benefits from quantum chemistry insights, making industrial operations more efficient, such as cleaner fuel generation and more effective environmental remediation. Furthermore, quantum chemistry provides insights into biological processes. Enzymes, the proteins that catalyse processes in living organisms, work with a precision that frequently defies standard chemistry. Tunnelling, quantum phenomena in which particles slip past energy barriers, helps to explain these extraordinarily efficient biological processes. In brief, quantum chemistry provides the fundamental understanding required to push the limits of chemistry and physics by exposing how molecules interact and react in ways that traditional theories cannot fully explain. Quantum chemistry has the potential to radically alter our understanding of the microscopic world, whether through theoretical models, practical applications, or future technology advancements. Written by Laura K Related articles: Quantum computing / Topology / Computational organic chemistry Project Gallery

Since 2006 when the link between amyotrophic lateral sclerosis (ALS), frontotemporal degeneration and TDP-43 mutations was demonstrated by Arai et al., it has remained a focus in neurological academia. This is for good reason; the research boom around the role of TDP-43 in neurodegeneration has elucidated links between TDP-43, parkinsonism and frontotemporal dementia (FTD). Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link TDP-43 and Me: the Neurodegenerative Impact of Gene Misplacement in Parkinsonism Last updated: 08/03/26 Published: 06/04/23 Practice and Progress in Neurology Since 2006 when the link between amyotrophic lateral sclerosis (ALS), frontotemporal degeneration and TDP-43 mutations was demonstrated by Arai et al., it has remained a focus in neurological academia. This is for good reason; the research boo m around the role of TDP-43 in neurodegeneration has elucidated link s between TDP-43, parkinsonism and frontotemporal dementia (FTD). The link between point mutations, deletions and loss of gene function in PRKN has long been established, but has yet to lead to the development of a targeted therapeutic treatment. PRKN is involved in the tagging of excess or faulty proteins with ubiquitin, which leads to degradation of the proteins in the ubiquitin/proteasome system (UPS)- a system characterised in medical neurology by its potential to cause serious neurological disorders. This places parkinsonism in a domain of neurodegenerative disorders sharing a common root in UPS dysfunction, including Alzheimer’s Disease, multiple sclerosis and Huntington’s Disease. Panda et al. (2022) demonstrated how the dysfunction of the UPS due to PRKN aberration inhibits the breakdown of the damaging TDP-43 aggregates which develop in human brains in response to mutation or stress. In healthy people, autophagic granules would attack and kill off these TDP-43 aggregates as an end result of the UPS , but due to aberrations in PRKN the UPS is inhibited in those afflicted with parkinsonism, causing neurodegeneration. The discovery of how TDP-43 and parkinsonism are linked could lead to the development of a treatment mimicking the organic catalyst of the TDP-43 aggregate breakdown to replicate UPS, reducing TDP-43 aggregate volume and by proxy, inhibiting neurodegeneration. In 2007, research by Esper et al. catalysed recognition of drug-induced Parkinsonism as severely underdiagnosed, with evidence proving even neurologists fail to effectively remember which medications cause parkinsonism. Fast halting of the inciting agent is necessary for the reversal of all parkinsonism symptoms, but in some patients, cognitive symptoms may persist for a time after the medication is stopped. In response to the novel discoveries of Panda et al. (2022), it is likely due to the aggregation of TDP-43. Another possibility is that permanent cognitive symptoms after inciting agent cessation in DIP may be due to large TDP-43 aggregates unable to be destroyed by the UPS. Further research will demonstrate whether TDP-43 aggregates become more resistant to UPS or autophagy through the progression of DIP, whether due to size or other extraneous factors. As of late 2025, findings demonstrate that TDP-43-associated missplicing is common in Parkinson's disease brains, giving more weight to the theory. The implications of such a promising lead in neurotherapeutics for refractory parkinsonism cannot be understated. Surgical therapies have long since remained the industry standard in treating refractory parkinsonism, though this option remains prone to risk since many of those afflicted with parkinsonism are elderly, with drug-induced parkinsonism from treatment with antipsychotics, calcium channel blockers or other medications always heightening the number of the geriatric population requiring care for parkinsonism . Furthermore, the adequate treatment of those with parkinsonism in their youth could inhibit their progression to a refractory disease state in old age. Overall, the future looks very promising for those around the world suffering from all different forms of parkinsonism. Written by Aimee Wilson Related articles: A common diabetes drug treating Parkinson's disease / Lifestyle and PD risk

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