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The endowment effect Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Behavioural Economics II 31/10/25, 12:46 Last updated: Published: 22/03/24, 19:51 The endowment effect This is article no. 2 in a series on behavioural economics. Next article: Loss aversion . Previous article: The role of honesty . In microeconomics, we say preferences are reversible. If you would pay £2 for a bar of chocolate, then you would be happy to sell a bar of chocolate for £2, especially if I gave it to you for free. Sounds reasonable? Well, in fact, this is not the case. Once again, consumers, just like you and me, are irrational, and thanks to what’s known as the endowment effect, classical economics falls flat once again. The endowment effect In an experiment conducted by Knetsch, participants were randomly allocated into three different categories. The first were given a coffee mug, the second were given some candy, and the third were given nothing. We say that the first two groups were endowed; they were given an item for free at no cost to them. Then the participants in the first two groups were given the option to either swap their item for either the mug or the candy or keep the item they were endowed with. The third group, treated as a control, was given the option to choose between the two and keep which they preferred the most. In the control group, we saw that about half of the participants chose the mug and half chose the candy. But in the endowed groups, an overwhelming majority decided to keep the item they were given rather than swapping! Therefore, as we can clearly see, when someone is endowed with an item, their perception of its utility (or benefit) seems to increase, so when given the opportunity to switch items, they often decline. Clearly, from an economic perspective, when endowed with an item, your utility curve for that item differs from when given the opportunity to choose. But why might that be the case? When you are endowed with an item, you own that item and, in a sense, hold responsibility over it. You become possessive, and this sense of ownership seems to have its own psychological value; therefore, the act of giving it up for something of equal worth is no longer treated as a fair trade-off. Whereas when not endowed, you have no sentiment value attached to the items, and for the most part, people are indifferent between them! A good example of this could be an old, run-down car. Buyers of this car see it for what it is—something that is barely functional. But owners of the car who have driven it for 20 years see it as more than that. There is an emotional attachment to the car that makes it more valuable in their eyes. Is the endowment effect always true? List conducted a similar experiment. A survey was undertaken by both unexperienced and experienced 'traders', and then after the survey, they were given trading cards as a reward. They were then given the opportunity to trade their cards if they wanted to. Non-experienced traders were subject to the endowment effect, so they kept the cards they worked hard for, but experienced traders knew that some cards may be more valuable, even if only slightly, which meant that they were able to overcome this effect. Additionally, what was found was that when participants were aware and went into the experiment knowing that there would be a trade, they had the intention to trade, which also managed to remove the endowment effect. In essence, the endowment effect serves as a reminder of the complexities inherent in human psychology and decision-making. There are many limitations in traditional economic models, which emphasises the need for behavioural economics and the inclusion of multidisciplinary thinking. To discover more about behavioural economics and in particular how honesty plays a big role in restructuring economic thinking, click here to read my prior article, and be sure to look out for more articles to come in the future! Written by George Chant Related articles: Explaining altruism / Mathematical models in cognitive decision-making References: Knetsch, Jack L. “The Endowment Effect and Evidence of Nonreversible Indifference Curves.” The American Economic Review 79, no. 5 (1989): 1277–84. John A. List, Does Market Experience Eliminate Market Anomalies?, The Quarterly Journal of Economics , Volume 118, Issue 1, February 2003, Pages 41–71,33 Project Gallery

Research shows that insomnia does have a hereditary side Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Does insomnia run in families? Here's what genetics tells us Last updated: 10/07/25, 18:25 Published: 10/07/25, 18:11 Research shows that insomnia does have a hereditary side Have you ever noticed restless nights affecting more than one relative? Maybe your sister tosses and turns, or your brother wakes up before dawn, wide awake and anxious. It might feel like poor sleep is passed down from parents to kids, and science suggests that feeling isn’t just in your head. In one study, nearly 40% of people with insomnia had a close family member with it, compared to 29% of those without; making them 1.57 times more likely to share the struggle. So is that inherited, or just a string of bad luck? Here’s what science has to say. Your DNA can affect sleep Research shows that insomnia does have a hereditary side. If someone in your family, say a parent, sibling or even a grandparent, struggles night after night, you’re more likely to face similar problems. That doesn’t guarantee you’ll wake up at 3 a.m. every night, but it does raise your baseline risk: studies estimate that around one-third of insomnia liability is genetic. In practical terms, inheriting certain gene variants can make the brain’s sleep-promoting signals weaker or the wake-promoting signals stronger. Think of those genes as nudging you toward more restless nights rather than pushing you entirely into insomnia. So if genes only lay the groundwork, what else determines whether someone actually stays awake counting sheep? That’s where life’s daily stresses come into play. How genes shape your sleep Scientists have identified a handful of genes that guide our body’s natural clock. Our circadian rhythm influences how deeply and how long we sleep. For instance, variants in the PER3 or CLOCK genes can shift your internal timing. This makes it harder to feel sleepy at a conventional hour. Picture the circadian clock as an orchestra conductor: if the conductor’s timing fluctuates, the entire performance, your sleep cycle, can fall out of sync. Other inherited factors affect the brain’s “volume knobs” for alertness. Certain gene differences can heighten sensitivity to minor disturbances; like a creaky floorboard or an ambulance siren, so that you jitter awake even when there’s no real threat. Over time, those tiny awakenings add up, preventing you from reaching the deep, restorative stages of sleep. Yet, these genes don’t act in isolation. The brain remains remarkably adaptable through epigenetic changes; chemical tags that turn genes on or off. Experiences such as stress, illness, or a drastically changed schedule can strengthen or weaken those genetic susceptibilities. Sleep isn’t just genetic; here’s why Even if you inherit gene variants linked to insomnia, your environment and habits often decide the end result. High-pressure jobs, financial worries, or family conflicts can ignite sleep troubles in someone without a family history of insomnia. Conversely, someone with a strong genetic vulnerability might sleep soundly if life stays relatively stress-free and routines remain consistent. Everyday choices, like scrolling through social media until the last minute, drinking coffee late afternoon, or keeping wildly shifting bedtimes, further fuel the problem. For example, evening exposure to bright screens suppresses melatonin, the hormone that signals your brain it’s time to sleep. That means even if your “insomnia genes” are mild, you’re still creating obstacles to a good night’s rest. On the other hand, regular exercise (aim for at least 30 minutes most days), a balanced diet, and a calm, screen-free wind-down routine signal the brain that it’s safe to switch off. Over months, those good habits can overwrite the nudge from your genes, steering you towards deep, uninterrupted rest. Can you change your genetic destiny? Knowing that insomnia has a genetic component can feel validating. It clarifies that tossing and turning isn’t simply an unexplained routine. That awareness reduces shame and makes it easier to adopt practical solutions. If you suspect poor sleep runs in your family, watch for early warning signs: difficulty falling asleep, waking often, or waking too early. Catching these patterns early means you can experiment with sleep hygiene tweaks before the problem becomes chronic. Actionable steps include setting a consistent bedtime, dimming lights an hour before sleep, avoiding caffeine after mid-afternoon, and practising relaxation techniques, such as deep breathing or progressive muscle relaxation. If these changes don’t help, cognitive behavioural therapy for insomnia (CBT-I) targets both the thoughts and behaviours that perpetuate sleeplessness, effectively retraining the brain’s response to the bedroom. Those inherited sleep tendencies might suggest insomnia is written in your DNA; but by keeping a consistent bedtime, cutting down on late-night screens and being kind to yourself, you can rewrite that genetic script and finally enjoy the deep rest you’ve earned. Written by Rand Alanazi Related articles: Does anxiety run in families? / Link between sleep and memory loss / The chronotypes REFERENCES Beaulieu-Bonneau S, LeBlanc M, Mérette C, Dauvilliers Y, Morin CM. Family History of Insomnia in a Population-Based Sample. Sleep. 2007 Dec;30(12):1739–45. Pacheco D. Is Insomnia Genetic? [Internet]. Sleep Foundation. 2021. Available from: https://www.sleepfoundation.org/insomnia/is-insomnia-genetic PER3 [Internet]. Wikipedia. 2023. Available from: https://en.wikipedia.org/wiki/PER3 Dashti HS, Jones SE, Wood AR, Lane JM, van Hees VT, Wang H, et al. Genome-wide association study identifies genetic loci for self-reported habitual sleep duration supported by accelerometer-derived estimates. Nature Communications [Internet]. 2019 Mar 7;10(1):1–12. Available from: https://www.nature.com/articles/s41467-019-08917-4 Halperin D. Environmental noise and sleep disturbances: A threat to health? Sleep Science [Internet]. 2014 Dec;7(4):209–12. Available from: https://www.sciencedirect.com/science/article/pii/S1984006314000601 www.ushealthconnect.com H. Unraveling the Impact of Environmental Factors on Sleep Quality and Parkinson Disease [Internet]. Practicalneurology.com . 2025. Available from: https://practicalneurology.com/diseases-diagnoses/movement-disorders/unraveling-the-impact-of-environmental-factors-on-sleep-quality-and-parkinson-disease/32197/ Levenson JC, Kay DB, Buysse DJ. The Pathophysiology of Insomnia. Chest [Internet]. 2015 Apr;147(4):1179–92. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC4388122/ Spielman AJ, Caruso LS, Glovinsky PB. A Behavioral Perspective on Insomnia Treatment. Psychiatric Clinics of North America [Internet]. 1987 Dec 1;10(4):541–53. Available from: https://www.sciencedirect.com/science/article/pii/S0193953X1830532X the I. amBX [Internet]. amBX. 2020 [cited 2025 Jun 6]. Available from: https://www.ambx.com/news/what-is-the-natural-circadian-rhythm Hassell K, Reiter RJ, Robertson NJ. MELATONIN AND ITS ROLE IN NEURODEVELOPMENT DURING THE PERINATAL PERIOD: A REVIEW. Fetal and Maternal Medicine Review. 2013 May 1;24(2):76–107. Wang J, Liu J, Xie H, Gao X. Effects of Work Stress and Period3 Gene Polymorphism and Their Interaction on Sleep Quality of Non-Manual Workers in Xinjiang, China: A Cross-Sectional Study. International Journal of Environmental Research and Public Health. 2022 Jun 3;19(11):6843–3. Project Gallery

How diseases start and spread, the body’s defence system, vaccines, policies, and public opinion: unravel the maze of infection and immunity with these articles. Immunology Articles How diseases start and spread, the body’s defence system, vaccines, policies, and public opinion: unravel the maze of infection and immunity with these articles. You may also like: Biology , Medicine , Neuroscience , Chemistry COVID-19 misconceptions Common misconceptions during the COVID-19 pandemic Glossary of COVID-19 terms Key terms used during the COVID-19 pandemic A vaccine for malaria? A new hope for a vaccine for malaria The world vs. the next pandemic Can we see it coming? What steps do we need to take? Are pandemics becoming more severe? Arguments for and against Natural substances And how they can tackle infectious diseases A treatment for HIV? Can the CRISPR-Cas9 system be used as a potential treatment? The mast cell Key cells in the immune system Origins of COVID -19 How COVID-19 caused a pandemic Mechanisms of pathogen invasion How pathogens avoid detection by the immune system Astronauts in space How does little gravity affect the immune system? Ageing and immunity Ageing and its association with immune decline The impacts of global warming on dengue fever Dengue fever is a mosquito-borne Neglected Tropical Disease (NTD) Is the immune system 'selfish'? 'Selfish' genes from a Dawkins perspective, and the Modern Evolutionary Synthesis

Conservation, diseases, animal behaviour, adaptation and survival. Expand your knowledge on the incredible diversity of life on Earth with these articles. Zoology Articles Conservation, diseases, animal behaviour, adaptation and survival. Expand your knowledge on the incredible diversity of life on Earth with these articles. You may also like: Biology , and Ecology Deception by African birds The species Dicrurus adsimilis uses deception by flexible alarm mimicry to target and carry out food-theft attempts An experiment on ochre stars Investigating the relative fitness of the species Pisaster ocharceus Orcinus orca A species report Rare zoonotic diseases We all know about COVID-19. But what about the other zoonotic diseases? Article #1 in a series on Rare diseases. Marine iguanas Their conservation The cost of coats 55 years of vicuna conservation in South America. Article #1 in a series on animal conservation around the world. Conserving the California condor These birds live on the west coast of North America. Article #2 in a series on animal conservation around the world. Emperor penguins Kings of ice. Article #6 in a series on animal conservation around the world. Protecting rock-wallabies in Australia A group of 25 animal species, and subspecies related to kangaroos. Article #7 in a series on animal conservation around the world. Do other animals get periods? Looking at menstruation in non-human animals e.g. monkeys, bats Same-sex attraction in non-human animals SSSB in birds, mammals, and invertebrates Changing sex in fish Why some fish change sex during their lifetimes

From foe to ally Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Herpes vs devastating skin disease 09/07/25, 14:16 Last updated: Published: 06/01/24, 11:14 From foe to ally This is article no. 3 in a series on rare diseases. Next article: Epitheliod hemangioendothelioma . Previous article: Breast cancer in males . Have you ever plucked loose skin near your nail, ripping off a tiny strip of good skin too? Albeit very small, that wound can be painful. Now imagine that it is not just a little strip that peels off, but an entire sheet. And it does not detach only when pulled, but at the slightest touch. Even a hug opens wounds, even a caress brings you pain. This is life with recessive dystrophic epidermolysis bullosa (RDEB), the most severe form of dystrophic pidermolysis bullosa (DEB). Herpes becomes a therapy DEB is a rare genetic disease of the skin that affects 3 to 10 individuals per million people (prevalence is hard to nail down for rare diseases). A cure is still far off, but there is good news for patients. Last May, the US Food and Drug Administration (FDA) approved Vyjuvek (beremagen geperparvec) to treat skin wounds in DEB. Clinical studies showed that it speeds up healing and reduces pain. Vyjuvek is the first gene therapy for DEB. It is manufactured by Krystal Biotech and - get this- it is a tweaked version of the herpes virus. Yes, you got that right, the virus causing blisters and scabs has become the primary ally against a devastating skin disease. This approval is a milestone for gene therapies, as Vyjuvek is the first gene therapy - based on the herpes virus, - to apply on the skin as a gel, - approved for repeated use. This article describes how DEB, and especially RDEB, affects the skin and wreaks havoc on the body; the following article will explain how Vyjuvek works. DEB disrupts skin integrity We carry around six to nine pounds of skin. Yet we often forget its importance: it stops germs and UVs, softens blows, regulates body temperature and makes us sensitive to touch. Diseases that compromise the skin are therefore devastating. These essential functions rely on the organisation of the skin in three layers: epidermis, dermis and hypodermis ( Figure 1 ). Typically, a Velcro strap of the protein collagen VII firmly anchors the epidermis to the dermis. The gene COL7A1 contains the instructions on how to produce collagen VII. In DEB, mutations in COL7A1 result in the production of a faulty collagen VII. As the Velcro strap is weakened, the epidermis becomes loosely attached to the dermis. Mutations in one copy of COL7A1 cause the dominant form of the disease (DDEB), mutations in both copies cause RDEB. With one copy of the gene still functional, the skin still produces some collagen VII, when both copies are mutated, little to no collagen VII is left. Therefore, RDEB is more severe than DDEB. In people with RDEB, the skin can slide off at the slightest touch and even gentle rubs can cause blisters and tears ( Figure 2 ). Living with RDEB Life with RDEB is gruelling and life expectancy doesn't exceed 30 years old. Wounds are very painful, slow to heal and get infected easily. The risk of developing an aggressive skin cancer is higher. The constant scarring can cause limb deformities. In addition, blisters can appear in the mouth, oesophagus, eyes and other organs. There is no cure for DEB for now; treatments can only improve the quality of life. Careful dressing of wounds promotes healing and prevents infections. Painkillers are used to ease pain. Special diets are required. And, to no one's surprise, physical activities must be avoided. Treating RDEB Over the past decade, cell and genetic engineering advances have sparked the search for a cure. Scientists have explored two main alternatives to restore the production of collagen VII in the skin. The first approach is based on transferring skin cells able to produce collagen VII. Despite promising results, this approach treats only tinyl patches of skin, requires treatments in highly specialised centres and it may cause cancer. The second approach is the one Vyjuvek followed. Scientists place the genetic information to make collagen VII in a modified virus and apply it to a wound. There, the virus infects skin cells, providing them with a new COL7A1 gene to use. These cells now produce a functional collagen VII and can patch the damage up. We already know which approach came up on top. Vyjuvek speeds up the healing of wounds as big as a smartphone. Professionals can apply it in hospitals, clinics or even at the patient’s home. And it uses a technology that does not cause cancer. But how does Vyjuvek work? And why did scientists choose the herpes virus to build Vyjuvek? We will find the answer in the following article. And since perfection does not belong to biology, we will also discuss the limitations of this remarkable gene therapy. NOTES: 1. DEB is part of a group of four inherited conditions, collectively named epidermolysis bullosa (EB), where the skin loses integrity. EB is also known as “Butterfly syndrome” because the skin becomes as fragile as a butterfly’s wing. These conditions are EB simplex, junction EB, dystrophic EB and Kindler EB. 2. Most gene therapies are based on modified, or recombinant in science jargon, adenoassociated viruses, which I reviewed for Scientia News. 3. Over 700 mutations have been reported. They disrupt collagen VII and its function with various degrees of severity. Consequently, RDEB and DDEB display several clinical phenotypes. 4. Two studies have adopted this approach: in the first study, Siprashvili and colleagues (2016) grafted ex vivo retrovirally-modified keratinocytes, the main cell type in the epidermis, over the skin of people with RDEB; in the second study, Lwin and colleagues (2019) injected ex vivo lentivirally-modified fibroblasts in the dermis of people with RDEB. Written by Matteo Cortese, PhD Related article: Ehlers-Danlos syndrome Project Gallery

Uncovering the truth behind the origins of the virus Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Origins of COVID-19 10/07/25, 10:27 Last updated: Published: 08/10/23, 16:07 Uncovering the truth behind the origins of the virus The quest for the crime of the century begins now! Suspicion of the Wuhan Institute of Virology Since the early epidemic reports in Wuhan, the origin of COVID-19 has been a matter of contention. Was SARS-CoV-2 the outcome of spontaneous transmission from animals to humans or scientific experimentation? Although most of the recorded initial cases occurred near a seafood market, Western Intelligence Agencies knew that the Wuhan Institute of Virology (WIV) was situated nine miles to the south. Researchers at the biosafety centre combed Yunnan caves for bats harbouring SARS-like viruses. They have been extracting genetic material from their saliva, urine, and faeces. Additionally, bat coronavirus RaTG13 (BatCoV RaTG13) shared 96% of its genome with SARS-CoV-2. Suspicion increased when it was discovered that WIV researchers dealt with chimeric versions of SARS-like viruses capable of infecting human cells. However, similar "gain-of-function" studies in Western biosecurity institutions have shown that such slow virulence increases may occur naturally. The coincidence that the pandemic began in the same city as the WIV outbreak was too obvious to ignore. According to two Chinese specialists , "the likelihood of bats flying to the market was quite remote". Chan and Ridley's "Quest for the Origin of COVID-19" Chan and Ridley have created a viral whodunit titled "Quest for the origin of COVID-19" to excite the curiosity of armchair detectives and scientific sceptics. Both need clarification as to why a virus of unknown origin was detected in Wuhan and not in Yunnan, 900 kilometres to the south. The stakes could not be more significant; if the virus were deliberately developed and spread by a Chinese laboratory, it would be the crime of the century. They are prudent in not going that far. They are, however, within their rights to cast doubt on the findings since their concerns were shared by numerous coronavirus experts who openly discounted the possibility of a non-natural origin and declared that the virus displayed no evidence of design at the time. Is this the impartial and fair probe the world has been waiting for? They present no evidence for the development of SARS-CoV-2. For example, Chan asserts that it seemed pre-adapted to human transmission " to an extent comparable to the late SARS-CoV-2 outbreak ". This statement is based on a single spike protein mutation that appears to "substantially enhance" its potential to connect to human receptor cells, meaning it had "apparently stabilised genetically" when identified in Wuhan. Nonetheless, this is a staggeringly misleading statement. As seen by the alphabet soup of mutations, the coronavirus has undergone multiple alterations that have consistently increased its suitability. Additionally, viruses isolated from pangolins attach to human receptor cells more efficiently than SARS-CoV-2, indicating the possibility of additional adaptation. According to two virologists, although the SARS-CoV-2 virus was not wholly adapted to humans, it was "merely enough". Evidence for design of SARS-CoV-2 and possible natural origins of the virus Another concerning feature of SARS-CoV-2 is a furin cleavage site, which enables it to infect human cells by interfering with the receptor protein. The identical sequence is present in highly pathogenic influenza viruses and was previously utilised to modify the spike protein of COVID-19. Chan and Ridley explain that this is the kind of insertion that would occur in a laboratory-modified bat virus. As a result, 21 leading experts have concluded that the furin sequence is insufficient. Coronaviruses have been shown to possess " near identical " genomes that often can infect humans and animals. Because the furin cleavage site characteristic is not seen in known bat coronaviruses, it is possible that it evolved naturally. Surprisingly, Chan and Ridley do not suggest that the SARS virus's high human infectivity feature was inserted on purpose since "there is no way to determine". There is also no way to determine if a RaTG13 is the pandemic virus's progenitor since history is replete with pandemics that began with zoonotic jumps. This argument is based on the strange fact that WIV researchers retrieved the bat isolate in 2013 from a decommissioned mine shaft in Yunnan. Six people were removing bat guano from the cave that year when they suffered an unexplained respiratory ailment. As a consequence, half of them perished. The 4% genetic diversity between RaTG13 and SARS-CoV-2, on the other hand, is similar to 40 years of evolutionary change. While exploring caves in northern Laos, researchers discovered three more closely related bat coronaviruses, which have a higher affinity to attach to human cells than the early SARS-CoV-2 strains. This indicates an organic origin, either through another animal host or directly from a bat, maybe when a farmer went into a cave. This is arguably the most reasonable explanation since it is consistent with forensic and epidemiological data. The food sample isolates collected from the Wuhan seafood market are similar to human isolates, and the majority of original human cases had a history of market exposure, in contrast to the absence of an epidemiological connection to the WIV or any other Wuhan research institution. Lack of evidence for a laboratory origin If scientists could demonstrate prior infection at the Wuhan market or other Chinese wildlife markets that sell the most likely intermediary species, including pangolins, civet cats, and raccoon dogs, the case for a natural origin would be strengthened. Although multiple animals tested positive for sister human viruses during the SARS epidemic, scientists have yet to find evidence of earlier infections in animals in the instance of Sars-CoV-2. Nonetheless, the absence of evidence does not confirm the absence and may indicate that samples were not taken from the appropriate animal. The same may be said of the lab leak argument's lack of evidence. However, even though history is littered with pandemics, no significant pandemic has ever been traced back to a laboratory. In other words, the null hypothesis is a zoonotic occurrence; Chan and Ridley must demonstrate otherwise. The irony is their drive to construct a compelling case for a laboratory accident. They are oblivious to the much more pressing story of how the commerce in wild animals, global warming, and habitat degradation increase the likelihood of pandemic viral development. This is the most plausible origin story that should concern us. Summary Although Chan and Ridley's "Quest for the Origin of COVID-19" has cast suspicion on the Wuhan Institute of Virology, there is still insufficient evidence to support the lab leak theory. There is, however, growing evidence for a natural origin of SARS-CoV-2, with multiple animals testing positive for sister human viruses during the SARS epidemic and the discovery of more closely related bat coronaviruses in northern Laos. As such, we should be more concerned with the increasing likelihood of pandemic viral development due to the commerce in wild animals, global warming, and habitat degradation. Written by Sara Maria Majernikova Project Gallery

Using the new technology AI to develop drugs Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Artificial Intelligence in Drug Research and Discovery 09/07/25, 10:56 Last updated: Published: 24/05/23, 10:20 Using the new technology AI to develop drugs Drug research has been transformed by artificial intelligence (AI), which has become a game-changing technology in several industries. Only a small portion of potential drugs make it to the market after the lengthy and expensive traditional drug discovery process. A drug's discovery and development can take over ten years and cost an average of US$2.8 billion. Even then, nine out of 10 medicinal compounds fall short of passing regulatory approval and Phase II clinical trials. The use of AI in this process, however, has the potential to greatly improve effectiveness, accuracy, and success rates. Given that AI can help with rational drug design, support decision-making, identify the best course of treatment for a patient, including personalised medicines, manage the clinical data generated, and use it for future drug development, it is reasonable to assume that it will play a role in the development of pharmaceutical products from the laboratory bench to bedside table. There are several ways in which AI is currently being used to enhance the drug discovery process. One of the primary applications is virtual screening ( Figure 2 ), which involves using machine learning algorithms to analyse large libraries of chemical compounds and predict which ones are likely to be effective against a specific disease target. This can significantly reduce the time and cost required for drug discovery by narrowing down the number of compounds that need to be tested in the lab. Another way AI is being used in drug discovery is through generative models, which use deep learning algorithms to design molecules that are optimised for specific therapeutic targets. This approach can be used to design molecules that are effective against a specific target while also minimising toxicity or other undesirable properties. Data analysis is another area where AI can be applied in drug discovery. By analysing large datasets of biological and chemical information, AI can help researchers identify patterns and relationships that may be relevant to drug discovery. For example, AI can be used to analyse genomic data to identify potential drug targets or to analyse drug-drug interactions to identify potential safety issues. However, one of the main challenges is the need for high-quality data, as AI models rely on large amounts of data to make accurate predictions. Additionally, there is a risk that AI models may miss important insights or make incorrect predictions if the data used to train them is biased or incomplete. Nevertheless, the continued development of AI and its amazing tools seeks to lessen the difficulties experienced by pharmaceutical firms, impacting both the medication development process and the full lifecycle of the product, which may account for the rise in the number of start-ups in this industry. The importance of automation will increase as a result of using the most up-to-date AI-based technologies, which will not only shorten the time needed for products to reach the market but also enhance product quality, increase overall production process safety, and make better use of available resources while also being cost-effective. In conclusion, the use of AI in drug discovery has the potential to revolutionize the field and significantly improve the success rate of potential drug candidates. Despite the challenges and limitations, the continued research and development of AI in drug discovery will undoubtedly lead to faster, cheaper, and more accurate drug development. Written by Navnidhi Sharma Related articles: A breakthrough procedure in efficient drug discovery / AI in medicinal chemistry / AI advancing genetic disease diagnosis Project Gallery

Understanding what goes wrong in the brain Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Epilepsy 101 29/04/25, 16:10 Last updated: Published: 09/10/24, 11:32 Understanding what goes wrong in the brain Epilepsy is a condition that affects millions of people worldwide, often causing unprovoked seizures due to irregular brain activity. But what exactly happens in the brain when someone has epilepsy? It is important to establish that not everyone with seizures has epilepsy. While epilepsy can start at any age, it often begins in childhood, or in people over the age of 60. Epilepsy can be due to genetic factors - 1 in 3 people with epilepsy have family history- or brain damage from causes like stroke, infection, severe head injury or a brain tumour. However, around half of epilepsy cases have an unknown cause. Now, imagine your brain as a big city with lots of lights. Each light represents a part of your brain that controls things like movement, feelings, and thoughts. Epilepsy is like when the lights in the city start flickering or shut completely. There are three main types of epilepsy, and each affects the lights in different ways: 1) Generalized epilepsy: when all the lights in the city flicker or go out at once, affecting the whole brain. There are two main kinds: Generalized Motor (Grand Mal) Seizures: Imagine the lights in the city going wild, making everything shake. This is like the shaking or jerking movements during myoclonic or tonic-clonic seizures. Generalized Non-Motor (Absence) Seizures: Picture the lights suddenly pausing, making everything freeze. During these seizures, a person might stare into space or make small, repeated movements, like lip-smacking. 2) Focal epilepsy: when only the lights in one part of the city flicker or go out. This means only one part of the brain is affected: Focal Aware Seizures: The lights flicker, but people in that part of the city know what’s happening. The person stays aware during the seizure. Focal Impaired Awareness Seizures: The lights flicker, and people lose track of what’s going on. The person might not remember the seizure. Focal Motor Seizures: Some lights flicker, causing strange movements, like twitching, rubbing hands, or walking around. Focal Non-Motor Seizures: The lights stay on, but everything feels strange, like sudden change in mood or temperature. The person might feel odd sensations without moving in unusual ways. 3) ‘Unknown’ epilepsy: ‘Unknown’ epilepsy is like a power outage where no one knows where it happened because the person was alone or asleep during the seizure. Doctors might later figure out if it's more like generalized or focal epilepsy. Some people can even have both types. But how do doctors find out if someone has epilepsy? A range of tests could be used to look at the brain’s activity and structure, including: Electroencephalogram (EEG): detects abnormal electrical activities in the brain using electrodes. This procedure can be utilised in Stereoelectroencephalography (SEEG), a more invasive method where the electrodes are placed directly on or within the brain to locate the abnormal electrical activities more precisely. Computerized Tomography (CT) and Magnetic Resonance Imaging (MRI): form images of the brain to detect abnormal brain structures such as brain scarring, tumours or damage that may cause seizures. Blood tests: test for genetic or metabolic disorders, or health conditions such as anaemia, infections or diabetes that can trigger seizures. Magnetoencephalogram (MEG): measures magnetic signals generated by nerve cells to identify the specific area where seizures are starting, to diagnose focal epilepsy. Positron emission tomography (PET): detects biochemical changes in the brain, detecting regions of the brain with lower-than-normal metabolism linked to seizures. Single-photon emission computed tomography (SPECT): identifies seizure focus by measuring changes in blood flow in the brain during or between seizures, using a tracer injected into the patient. The seizure focus in this scan is seen by an increase in blood flow to that region. So, how does epilepsy affect the brain? For most people, especially those with infrequent or primarily generalised seizures, cognitive issues are less likely compared to those with focal seizures, particularly in the temporal lobe. The following cognitive functions can be affected: Memory : seizures can disrupt the hippocampus in the temporal lobe, responsible for storing and receiving new information. This can lead to difficulties in remembering words, concepts, names and other information. Language : seizures can affect areas of the brain responsible for speaking, understanding and storing words, which can lead to difficulties in finding familiar words. Executive function: seizures can impact the frontal lobe of the brain which is responsible for planning, decision making and social behaviour, leading to challenges in interacting, organising thoughts and controlling unwanted behaviour. While epilepsy itself cannot be cured, treatments exist to control seizures including: Anti-Epileptic Drugs (AEDs): suppress the brain’s ability of sending abnormal electrical signals - effective in 70% of patients. Diet: ketogenic diets can reduce seizures in some medication- resistant epilepsies and in children as they alter the chemical activity in the brain. Surgery: 1) Resective Surgery: removal of the part of the brain causing the seizures, such as temporal lobe resection, mainly for focal epilepsy. 2) Disconnective Surgery: cutting the connections between the nerves through which the seizure signals travel in the brain, such as in corpus callosotomy, mainly for generalised epilepsy. 3) Neurostimulation device implantation (NDI): insertion of devices in the body to control seizures by stimulating brain regions to control the electrical impulses causing the seizures. This includes vagus nerve stimulation and Deep Brain Stimulation (DBS). Even though epilepsy can be challenging, many people manage it successfully with the right treatment. Continued research offers hope for even better, long lasting treatments in the future. Written by Hanin Salem Related articles: Different types of epilepsy seizures / Alzheimer's disease / Parkinson's disease / Autism REFERENCES D’Arrigo, T. (n.d.). What Are the Types of Epilepsy? [online] WebMD. Available at: https://www.webmd.com/epilepsy/types-epilepsy [Accessed 5 Aug. 2024]. Epilepsy Foundation. (n.d.). Thinking and Memory. [online] Available at: https://www.epilepsy.com/complications-risks/thinking-and-memory [Accessed 10 Aug. 2024]. GOSH Hospital site. (n.d.). Invasive EEG monitoring. [online] Available at: https://www.gosh.nhs.uk/conditions-and-treatments/procedures-and- treatments/invasive-monitoring/ [Accessed 9 Aug. 2024]. My Epilepsy Team.com. (2016). Epilepsy: What People Don’t See (Infographic) | MyEpilepsyTeam. [online] Available at: https://www.myepilepsyteam.com/resources/epilepsy-what-people-dont-see- infographic [Accessed 29 Aug. 2024]. National institute of Neurological Disorders and stroke (2023). Epilepsy and Seizures | National Institute of Neurological Disorders and Stroke. [online] www.ninds.nih.gov . Available at: https://www.ninds.nih.gov/health- information/disorders/epilepsy-and-seizures [Accessed 10 Aug. 2024]. NHS (2020). Epilepsy. [online] NHS. Available at: https://www.nhs.uk/conditions/epilepsy/ [Accessed 10 Aug. 2024]. Project Gallery

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

An introductory and comprehensive review of complex diseases and their environmental influences. Using schizophrenia as an example, we are interested in exploring one of the biggest questions that underlie complex diseases. Go Back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The environment on complex diseases: schizophrenia Last updated: 01/03/26 Published: 08/05/23 An introductory and comprehensive review of complex diseases and their environmental influences. Using schizophrenia as an example, we are interested in exploring one of the biggest questions that underlie complex diseases. Introduction: Not Exactly a Yes or No Question Many things in science revolve around questions. It is remarkable to find the number of questions left for scientists to answer or those that will remain unanswered. Indeed, one of the most daunting tasks for any scientist would be to see through every detail of a piece of information, even if everyone has seen it, but with different sets of lenses and asking different sets of questions. After all, “why did the apple fall from its tree?”. However, asking questions is one thing. Finding answers and, more importantly, the evidence or proof that supports them does not always yield conclusive results. Nevertheless, perhaps some findings may shine a new light on a previously unanswered question. We can categorise the study of genetics into two questions: “What happens if everything goes well?” and “What happens if it goes wrong?”. Whilst there are virtually limitless potential causes of any genetic disease, most genetic diseases are known to be heritable. A mutation in one gene that causes a disease can be inherited from the parents to their offspring. Often, genetic diseases are associated with a fault in one gene, known as a single-gene disorder, with notorious names including Huntington’s disease, cystic fibrosis, sickle cell anaemia, and familial hypercholesterolaemia. These diseases have different mechanisms, and the causes are also diverse. But all these diseases have one thing in common: they are all caused by a mutation or fault in one gene, and inheriting any specific genes may lead to disease development. In other words, “either you have it, or you do not”. The role of DNA and mutations in complex diseases. Image/ craiyon.com Multifactorial or complex diseases are a classification geneticists give to diseases caused by factors, faults or mutations in more than one gene. In other words, a polygenic disease. As a result, the research, diagnosis, and identification of complex diseases may not always produce a clear “black-and-white” conclusion. Furthermore, complex diseases make up most non-infectious diseases known. The diseases associated with leading causes of mortality are, in their respective ways, complex. Household names include heart diseases, Alzheimer’s and dementia, cancer, diabetes, and stroke. All of these diseases may employ many mechanisms of action, involving multiple risk factors instead of direct cause and effect, using environmental and genetic interactions or factors to their advantage, and in contrast to single-gene disorders, do not always follow clear or specific patterns of inheritance and always involve more than one problematic genes before the complete symptoms manifest. For these reasons, complex diseases are infamously more common and even more challenging to study and treat than many other non-infectious diseases. No longer the easy “yes or no” question. The Complex Disease Conundrum: Schizophrenia Here we look at the case of a particularly infamous and, arguably, notorious complex disease, schizophrenia (SCZ). SCZ is a severely debilitating and chronic neurodevelopmental disorder that affects around 1% of the world’s population. Like many other complex diseases, SCZ is highly polygenic. The NHS characterise SCZ as a “disease that tends to run in families, but no single gene is known to be directly responsible…having these genes does not necessarily mean one will develop SCZ”. As previously mentioned, many intricate factors are at play behind complex diseases. In contrast, there is neither a single known cause for SCZ nor a cure. Additionally, despite its discovery a century ago, SCZ is arguably not well understood, giving a clue to the sophisticated mechanisms that underlie SCZ. To further illustrate how such complexities may pose a challenge to future medical treatments, we shall consider a conundrum that diseases like SCZ may impose. The highly elaborate nature of complex diseases means that it is impossible to predict disease outcomes or inheritance with absolute certainty nor rule out potential specific causes of diseases. One of the most crucial aspects of research on complex diseases is their genetic architecture, just as a house is arguably only as good as its blueprint. Therefore, a fundamental understanding of the genes behind diseases can lead to a better knowledge of diseases’ pathogenesis, epidemiology, and potential drug target, and hopefully, one day bridge our current healthcare with predictive and personalised medicine. However, as mentioned by the NHS, one of the intricacies behind SCZ is that possessing variants of diseased genes does not translate to certainty in disease development or symptom manifestation. Our conundrum, and perhaps the biggest question on complex diseases like SCZ is: “Why, even when an individual possesses characteristic genes of a complex disease, they may not necessarily exhibit symptoms or have the disease?”. The enigma surrounding complex diseases lies in the elegant interactions between our genes, the blueprint of life, and “everything else”. Understanding the interplay of factors behind complex diseases may finally explain many of the intricacies behind diseases like SCZ. Genes and Environment: an Obvious Interaction? The gene-environment important implications on complex disease development were demonstrated using twin studies. A twin study, as its name suggests, is the study of twins by their similarities, differences, and many other traits that twins may exhibit to provide clues to the influences of genetic and external factors. Monozygotic (MZ) twins each share the same genome and, therefore, are genetically identical. Therefore, if one twin shows a phenotype, the other twin would theoretically also have said genes and should exhibit the corresponding trait. Experimentally, we calculate the concordance rate, which means the probability of both twins expressing a phenotype or characteristic, given that one twin has said characteristic. Furthermore, the heritability score may be mathematically approximated using MZ concordance and the concordance between dizygotic twins (twins that share around half a genome). These studies are and have been particularly useful in demonstrating the exact implications genetic factors have on phenotypes and how the expression of traits may have been influenced by confounding factors. In the case of SCZ, scientists have seen, over decades, a relatively low concordance rate but high heritability score. A recent study (published in 2018) through the Danish SCZ research cohort involved the analysis of around 31,500 twins born between the years 1951 and 2000, where researchers reported a concordance rate of 33% and estimated heritability score of 79%, with other older studies reporting a concordance rate up to and around 50%. The percentages suggest that SCZ is likely to be passed down. In other words, a genetically identical twin only has approximately 1 in 2 risks of also developing symptoms of SCZ if its opposite twin also displays SCZ. The scientists concluded that although genetic predisposition significantly affects one’s susceptibility or vulnerability against SCZ, it is not the single cause of SCZ. Demographically, there have been studies that directly link environmental risks to SCZ. Some risk factors, such as famines and malnutrition, are more evident than others. However, some studies also associate higher SCZ risk among highly industrialised countries and first or second-generation migrants. For instance, few studies point out an increased risk of SCZ within ethnic minorities and Afro-Caribbean immigrants in the United Kingdom. Hypotheses that may explain such data include stress during migration, potential maternal malnutrition, and even exposure to diseases. With this example, hopefully, we all may appreciate how the aetiology of SCZ and other complex diseases are confounded by environmental factors. In addition, how such factors may profoundly influence an individual’s genome. SCZ is a clear example of how genetic predisposition, the presence of essential gene variants characteristic of a disease, may act as a blueprint to a terrible disease waiting to be “built” by certain factors as if they promote such development. It is remarkable how genetic elements and their interactions with many other factors may contribute almost collectively to disease pathogenesis. We can reflect this to a famous quote amongst clinical geneticists: “genetics loads the gun, and environment pulls the trigger.” Carrying high-risk genes may increase the susceptibility to a complex disease, and an environment that promotes such disease may tip the balance in favour of the disease. However, finding and understanding the “blueprints” of SCZ, what executes this “blueprint”, and how it works is still an area of ongoing research. Furthermore, how the interplay between genetics and external factors can lead to profound effects like disease outcomes is still a relatively new subject. The Epigenome: the Environment’s Playground To review, it is clear that genes are crucial in complex disease aetiology. In the case of SCZ, high-risk genes and variances are highly attributed to disease onset and pathogenesis. However, we also see with twin studies that genetics alone cannot explain the high degree of differences between twins, particularly when referring to SCZ concordance between identical twins. In other words, external factors are at play, influencing one’s susceptibility and predisposition to SCZ. These differences can be explained by the effects epigenetics have on our genome. Epigenetic mechanisms regulate gene expression by modifying the genome. In short, on top of the DNA double strands, the genome consists of additional proteins, factors, and even chemical compounds that all aid the genetic functions our body heavily relies on. The key to epigenetics lies in these external factors’ ability to regulate gene expression, where some factors may promote gene expression whilst others may prevent it. Epigenetic changes alter gene functions as they can turn gene expression “on” and “off”. Furthermore, many researchers have also shown how epigenetic changes may accumulate and be inherited somatically with cell division and even passed down through generations. Therefore, epigenetic changes may occur without the need to change any of the DNA codes, yet, they may cause a profound effect by controlling gene expression throughout many levels of the living system. These underlying mechanisms are crucial for the environment’s effect on complex diseases. Some external factors may directly cause variances or even damage to the genome (e.g. UV, ionising radiation), and other sources may indirectly change gene expression by manipulating epigenetic changes. The exact molecular genetics behind epigenetic mechanisms are elaborate. However, we can generally find three common epigenetic mechanisms: DNA Methylation, Histone Modification, and Non-coding RNA. Although each method works differently, they achieve a common goal of promoting or silencing gene expression. All of these are done by the many molecular components of epigenetics, altering the genome without editing the gene sequence. We refer to the epigenome, which translates to “above the genome”, the genome itself and all the epigenetic modifiers that regulates gene expression on many levels. Environmental factors and exposure may influence epigenetic mechanisms, affecting gene expression in the cell or throughout the body, sometimes permanently. Therefore, it is clear how the epigenome may change throughout life as different individuals are exposed to numerous environmental factors. Furthermore, each individual may also have a unique epigenome. Depending on which tissues or cells are affected by these mechanisms, tissues or cells may even have a distinct epigenome, unlike the genome, which is theoretically identical in all cells. One example of this is the potential effects of DNA methylation on schizophrenia epidemiology. DNA methylation can silence genes via the enzymes DNA methyltransferases (DNMT), a family of enzymes capable of catalysing the addition of methyl groups directly into the DNA. The DNMT enzymes may methylate specific nucleotides on the gene, which usually would silence said gene. Many researchers have found that the dysregulation of DNA methylation may increase the risk towards the aetiology of numerous early onset neuro-developmental disorders. However, SCZ later-onset development also points towards the influence of environmental risk factors that target DNA methylation mechanisms. Studies show links between famines and SCZ increased prevalence, as the DNMT enzymes heavily rely on nutrients to supply essential amino acids. Malnutrition is thought to play a considerable role in DNA methylation changes and, therefore, the risk of SCZ. Small Piece of a Changing Puzzle Hopefully, we can see a bigger picture of the highly intricate foundation beneath complex diseases. Bear in mind that SCZ is only one of many complex diseases known. SCZ is ultimately not a pristine and impartial model to study complex disorders. For instance, concordance rates of complex diseases change depending on their genetic background. In addition, they may involve different mutations, variance, or dysregulation of differing pathways and epigenetic mechanisms. After all, complex diseases are complex. Finally, this article aimed to give a rundown of the epigenetics behind complex diseases like SCZ. However, it is only a snapshot compared to the larger world of the epigenome. Furthermore, some questions remain unanswered: the genetic background and architecture of complex diseases, and ways to study, diagnose, and treat complex diseases. This Scientia article is one of the articles in Scientia on the theme of complex disease science and genetics. Hopefully, this introductory article is an insight and can be used to reflect upon, especially when tackling more complicated subjects of complex diseases and precision medicine. Written by Stephanus Steven Related articles: Schizophrenia, Inflammation, and Accelerated Ageing / An Introduction to Epigenetics