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A hereditary neurodegenerative disorder Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Huntington's disease 27/09/25, 11:04 Last updated: Published: 18/10/23, 16:12 A hereditary neurodegenerative disorder Huntington’s disease (HD) is a neurodegenerative disorder causing cognitive decline, behavioural difficulties, and uncontrollable movements. It is a hereditary disease that has a devastating effect on the individual’s life and unfortunately is incurable. Genetic component What may come as a surprise, is that in everyone’s genetics there are two copies (one from each parent) of the Huntingtin’s gene coding for the Huntingtin protein. This gene is coded by CAG repeats. In healthy genes, the CAG sequence is repeated between 10 and 26 times. However, if the gene is faulty, CAG repeats over 40 times resulting in a dysfunctional Huntingtin protein. The disease is autosomal dominant meaning regardless of gender, if either parent is a carrier, their child has a 50% chance of inheriting the faulty gene. REMINDER: because the gene is dominant, it means those who inherit even one copy will develop the disease Effect on the brain The faulty Huntingtin protein accumulates in cells, leading to cell death and damage to the brain. If you were to look at the brains of individuals with Huntington’s Disease, you would see a reduction in volume of the caudate and putamen. These areas are part of the striatum, which is a subdivision of the basal ganglia, involved in fine tuning our voluntary movements, i.e., reaching out to grab a cup. As the disease progresses, this atrophy can extend to other areas of the brain including the thalamus, frontal lobe, and cerebellum. Symptoms The symptoms normally manifest in three categories: motor, cognitive and psychiatric. We know that the basal ganglia is involved in our voluntary movement, so the damage causes one of the most visible symptoms in HD- uncontrollable and jerky movements. Cognitive symptoms include personality changes, difficulties with planning and attention. There can also be impairments to how those with HD recognise emotions- all these symptoms can interact to make social interaction more difficult. Finally, the psychiatric symptoms often seen include irritability and aggression, depression, anxiety, and apathy. Impact on life and family At the age when diagnosis usually occurs (around 30 years old), patients are often buying houses, getting married and either having children or deciding to start a family. The diagnosis may change peoples outlook on having children and can put a great psychological burden on them if they have unknowingly passed it along to those already born. Diagnosis also brings consequences to seemingly mundane, but incredibly important issues such as gaining life insurance, with some companies not covering individuals with an official diagnosis. Subsequently this makes life harder for their families, as the patient will eventually be unable to work and there could be associated costs with the need for care facilities as the disease progresses. Unfortunately, this is a progressive neurodegenerative condition with no cure. The only treatment options available at present, are interventions which aim to alleviate the patients’ symptoms. Whilst these treatments will reduce the motor and psychiatric symptoms, they cannot stop the progression of Huntington’s disease. We have only scratched the surface on the impact Huntington’s disease has on a patient and their families. It is so important to understand ways in which everyone that is affected can be best supported during the disease progression, to give all those involved a better quality of life. Written by Alice Jayne Greenan Related articles: A potential gene therapy for HD / Epilepsy Project Gallery

Exploring the distinctive features that define and disrupt the brain Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A deep dive into the hallmarks defining Alzheimer’s disease 08/07/25, 14:39 Last updated: Published: 06/11/24, 12:02 Exploring the distinctive features that define and disrupt the brain The progressive decline in neurocognition, resulting in a detrimental effect on one’s activities of daily living, is referred to as dementia. It typically affects people over the age of 65. Multiple theories have been proposed to explain the pathogenesis of Alzheimer’s disease (AD), including the buildup of amyloid plaques in the brain and the formation of neurofibrillary tangles (NFT) in cells. Understanding the pathophysiology of AD is imperative to the development of therapeutic strategies. Therefore, this article will outline the major hallmarks and mechanisms of AD. Hallmark 1: amyloid plaques One of the most widely accepted hypotheses for AD is the accumulation of amyloid beta protein (Aβ) in the brain. Aβ is a 4.2 kDa peptide consisting of approximately 40–42 amino acids, originating from a precursor molecule called amyloid precursor protein. This process, defined as amyloidosis, is strongly linked to brain aging and neurocognitive decline. How do the amyloid plaques form? See Figure 1 . Reasons for the accumulation of amyloid plaques: Decreased autophagy: Amyloid proteins are abnormally folded proteins. Autophagy in the brain is primarily carried out by neuronal and glial cells, involving key structures known as autophagosomes and lysosomes. When autophagy becomes downregulated, the metabolism of Aβ is impaired, eventually resulting in plaque buildup. Overproduction of acetylcholinesterase (AChE): Acetylcholine (Ach) is the primary neurotransmitter involved in memory, awareness, and learning. Overproduction of ACHE by astrocytes into the synaptic cleft can lead to excessive breakdown of Ach, with detrimental effects on cognition. Reduced brain perfusion: Blood flow delivers necessary nutrients and oxygen for cellular function. Reduced perfusion can lead to “intracerebral starvation”, depriving cells of the energy needed to clear Aβ. Reduced expression of low-density lipoprotein receptor-related protein 1: Low-density lipoprotein receptor-related protein 1 (LRP1) receptors are abundant in the central nervous system under normal conditions. They are involved in speeding up the metabolic pathway of Aβ by binding to its precursor and transporting them from the central nervous system into the blood, thereby reducing buildup. Reduced LRP1 expression can hinder this process, leading to amyloid buildup. Increased expression of the receptor for advanced glycation end products (RAGE): RAGE is expressed on the endothelial cells of the BBB, and its interaction with Aβ facilitates the entry of Aβ into the brain. Hallmark 2: neurofibrillary tangles See Figure 2 Neurofibrillary tangles are excessive accumulations of tau protein. Microtubules typically support neurons by guiding nutrients from the soma (cell body) to the axons. Furthermore, tau proteins stabilise these microtubules. In AD, signalling pathways involving phosphorylation and dephosphorylation cause tau proteins to detach from microtubules and stick to each other, eventually forming tangles. This results in a disruption in synaptic communication of action potentials. However, the exact mechanism remains unclear. Recent studies suggest an interaction between Aβ and tau, where Aβ can cause tau to misfold and aggregate, forming neurofibrillary tangles inside brain cells. Both Aβ and tau can self-propagate, spreading their toxic effects throughout the brain. This creates a vicious cycle, where Aβ promotes tau toxicity, and toxic tau can further exacerbate the harmful effects of Aβ, ultimately causing significant damage to synapses and neurons in AD. Hallmark 3: neuroinflammation Microglia are the primary phagocytes in the central nervous system. They can be activated by dead cells and protein plaques, where they initiate the innate immune response. This involves the release of chemokines to attract other white blood cells and the activation of the complement system which is a group of proteins involved in initiating inflammatory pathways to fight pathogens. In AD, microglia bind to Aβ via various receptors. Due to the substantial accumulation of Aβ, microglia are chronically activated, leading to sustained immune responses and neuroinflammation. Conclusion The contributions of amyloid beta plaques, neurofibrillary tangles and chronic neuroinflammation provide a framework for understanding the pathophysiology of AD. AD is a highly complex condition with unclear mechanisms. This calls for the need of continued research in the area as it is crucial for the development of effective treatments. Written by Blessing Amo-Konadu Related articles: Alzheimer's disease (an overview) / CRISPR-Cas9 to potentially treat AD / Sleep and memory loss REFERENCES 2024 Alzheimer’s Disease Facts and Figures. (2024). Alzheimer’s & dementia, 20(5). doi:https://doi.org/10.1002/alz.13809. A, C., Travers, P., Walport, M. and Shlomchik, M.J. (2001). The complement system and innate immunity. [online] Nih.gov. Available at: https://www.ncbi.nlm.nih.gov/books/NBK27100/ . Bloom, G.S. (2014). Amyloid-β and tau: the Trigger and Bullet in Alzheimer Disease Pathogenesis. JAMA neurology, [online] 71(4), pp.505–8. doi:https://doi.org/10.1001/jamaneurol.2013.5847. Braithwaite, S.P., Stock, J.B., Lombroso, P.J. and Nairn, A.C. (2012). Protein Phosphatases and Alzheimer’s Disease. Progress in molecular biology and translational science, [online] 106, pp.343–379. doi:https://doi.org/10.1016/B978-0-12-396456-4.00012-2. Heneka, M.T., Carson, M.J., El Khoury, J., Landreth, G.E., Brosseron, F., Feinstein, D.L., Jacobs, A.H., Wyss-Coray, T., Vitorica, J., Ransohoff, R.M., Herrup, K., Frautschy, S.A., Finsen, B., Brown, G.C., Verkhratsky, A., Yamanaka, K., Koistinaho, J., Latz, E., Halle, A. and Petzold, G.C. (2015). Neuroinflammation in Alzheimer’s disease. The Lancet. Neurology, 14(4), pp.388–405. doi:https://doi.org/10.1016/S1474-4422(15)70016-5. Kempf, S. and Metaxas, A. (2016). Neurofibrillary Tangles in Alzheimer′s disease: Elucidation of the Molecular Mechanism by Immunohistochemistry and Tau Protein phospho- proteomics. Neural Regeneration Research, 11(10), p.1579. doi:https://doi.org/10.4103/1673-5374.193234. Kumar, A., Tsao, J.W., Sidhu, J. and Goyal, A. (2022). Alzheimer disease. [online] National Library of Medicine. Available at: https://www.ncbi.nlm.nih.gov/books/NBK499922/. Ma, C., Hong, F. and Yang, S. (2022). Amyloidosis in Alzheimer’s Disease: Pathogeny, Etiology, and Related Therapeutic Directions. Molecules, 27(4), p.1210. doi:https://doi.org/10.3390/molecules27041210. National Institute on Aging (2024). What Happens to the Brain in Alzheimer’s Disease? [online] National Institute on Aging. Available at: https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/what-happens-brain- alzheimers-disease. Stavoe, A.K.H. and Holzbaur, E.L.F. (2019). Autophagy in Neurons. Annual Review of Cell and Developmental Biology, 35(1), pp.477–500. doi: https://doi.org/10.1146/annurev-cellbio-100818-125242 . Project Gallery

The emperor penguin's life cycle is intertwined with sea ice freezing and melting over the year Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Emperor penguins, the kings of the ice Last updated: 29/05/25, 10:38 Published: 24/04/25, 07:00 The emperor penguin's life cycle is intertwined with sea ice freezing and melting over the year This is article no. 6 in a series on animal conservation. Next article: Protecting rock-wallabies in Australia . Previous article: Gorongosa National Park . In November 2024, a malnourished emperor penguin was spotted in Australia, over 2000 miles from its home in Antarctica. It is said to be the furthest north a wild emperor has ever been seen. While scientists do not know why or how the penguin ended up there, it sparked conversations about climate change and the survival of this fascinating species. This article will describe the characteristics of the emperor penguin, and how climate change could affect it. Introduction to emperor penguins Emperor penguins ( Aptenodytes forsteri ) are the largest living penguin species, weighing 20-40 kilograms and standing about 1 metre tall. It is estimated that there are 256,000 breeding pairs of emperor penguins across 54 colonies, which are spread out along the entire coast of Antarctica. Their diet consists of krill, fish, and squid - and they can dive over 500m deep to find food. Emperor penguins are the only warm-blooded animal to breed during the Antarctic winter, one of the world's coldest and darkest times of the year. Therefore, they are adapted to the cold days, harsh winds, and high water pressure in which they live. For example, they have over 20 kinds of feathers - some of which help with waterproofing while swimming, and others help with thermal insulation. Many penguin species huddle together as juveniles to conserve body heat, but emperors are the only species to do so as adults. Thus, emperor penguins are a unique and ecologically fascinating species. Life cycle and fast ice The emperor penguin's life cycle is intertwined with sea ice freezing and melting over the year ( Figure 1 ). For most of the year, emperors live on fast ice, which are ice sheets floating on the sea but attached to the coast. The first reason they need fast ice is moulting, when emperor penguins replace all their feathers in late summer. They moult on ice because they cannot swim until their new layer of waterproof feathers has grown. Emperor penguins return to fast ice at the onset of winter to mate, lay eggs, and raise chicks. While one parent stays on the fast ice to look after the chick, the other parent goes to sea to find food for the family. The chick grows waterproof adult feathers for fast ice to break up in summer. At this point, the penguins live at sea until moulting time. This way, emperor penguin survival is linked to fast ice availability. Threat from climate change Because emperor penguins are so heavily dependent on fast ice, scientists are concerned about the potential impacts of global warming. Rising sea surface temperatures mean fast ice may not form long enough in the year for emperor penguins to complete their life cycle. In late 2022, sea ice was dramatically reduced in the Bellingshausen Sea in Antarctica, and 4 of the 5 nearby emperor penguin colonies had a failed breeding season. These failed seasons may become more common in the future with climate change. A 2020 study predicted that in the worst case climate scenario, 80% of penguin colonies will see population declines of over 90% by 2100. If international climate targets are met, only 19% of colonies are expected to decline that badly ( Figure 2 ). Because the International Union for Conservation of Nature classified emperors as Near Threatened, they do not meet Antarctica's criteria for being a protected species. Scientists have requested this conservation status be upgraded to better reflect the inability of emperor penguins to adapt or disperse away from the effects of climate change. Emperor penguins face no threats from humans other than global warming, so reducing greenhouse gas emissions is crucial to protect them. Conclusion Emperor penguins are charismatic creatures with unique adaptations to live during the cold Antarctic winter. Their survival is strongly linked to the availability of sea ice because they moult, breed, and care for their offspring on ice sheets. Global warming is making these ice sheets disappear, so emperor penguins must be monitored and protected to ensure survival through a changing climate. Written by Simran Patel Related articles: The Arctic Springtail / California Condors / Brain-climate connection REFERENCES CBS News. (2024) Malnourished emperor penguin that swam ashore in Australia 2,000 miles from home a quandary for rescuers. CBS News . Available from: https://www.cbsnews.com/news/emperor-penguin-australia-2000-miles-from-antarctic-ice-melting-climate-change/ (Accessed 11th November 2024). Fretwell, P.T., Boutet, A. & Ratcliffe, N. (2023) Record low 2022 Antarctic sea ice led to catastrophic breeding failure of emperor penguins. Communications Earth & Environment . 4 (1): 1–6. Garnier, J., Clucas, G., Younger, J., Sen, B., Barbraud, C., Larue, M., Fraser, A.D., Labrousse, S. & Jenouvrier, S. (2023) Massive and infrequent informed emigration events in a species threatened by climate change: the emperor penguins . Available from: https://hal.science/hal-03822288 (Accessed 10th November 2024). Hooper, S. (11th November 2024) Experts baffled after penguin shows up on beach 2,200 miles away from home Metro . Available from: https://metro.co.uk/2024/11/11/experts-baffled-penguin-shows-beach-2-200-miles-away-home-21970144/ (Accessed 11th November 2024). Jenouvrier, S. et al. (2020) The Paris Agreement objectives will likely halt future declines of emperor penguins. Global Change Biology . 26 (3): 1170–1184. Labrousse, S., Nerini, D., Fraser, A.D., Salas, L., Sumner, M., Le Manach, F., Jenouvrier, S., Iles, D. & LaRue, M. (2023) Where to live? Landfast sea ice shapes emperor penguin habitat around Antarctica. Science Advances . 9 (39): eadg8340. LaRue, M. et al. (2024) Advances in remote sensing of emperor penguins: first multi-year time series documenting trends in the global population. Proceedings of the Royal Society B: Biological Sciences . 291 (2018): 20232067. Le Maho, Y. (1977) The Emperor Penguin: A Strategy to Live and Breed in the Cold: Morphology, physiology, ecology, and behavior distinguish the polar emperor penguin from other penguin species, particularly from its close relative, the king penguin. American Scientist . 65 (6): 680–693. Trathan, P.N. et al. (2020) The emperor penguin - Vulnerable to projected rates of warming and sea ice loss. Biological Conservation . 241: 108216. Williams, C.L., Hagelin, J.C. & Kooyman, G.L. (2015) Hidden keys to survival: the type, density, pattern and functional role of emperor penguin body feathers. Proceedings of the Royal Society B: Biological Sciences . 282 (1817): 20152033. Project Gallery

Unmasking the complexities of the condition Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Crohn's disease 09/07/25, 14:01 Last updated: Published: 22/03/24, 20:16 Unmasking the complexities of the condition Introduction Crohn's disease is a chronic inflammatory condition that primarily targets the gastrointestinal tract. While it commonly afflicts individuals aged 20 to 50, it can also manifest in children and older adults, albeit less frequently. Symptoms of Crohn's disease vary widely and may include skin lesions spanning from the mouth to the anus, along with prevalent issues such as diarrhoea, abdominal pain, weight loss, rectal bleeding, fatigue, and fever. Diagnosis Diagnosing Crohn's disease can be challenging due to its similarity to other conditions. However, specific symptoms like bloody diarrhoea, iron deficiency, and unexplained weight loss are significant indicators that warrant further investigation by a gastroenterologist. Many tests that can confirm Crohn’s disease: Endoscopy: endoscopy, including procedures like colonoscopy and upper endoscopy, is a dependable method for diagnosing Crohn's disease and distinguishing it from other conditions with similar symptoms. During an endoscopy, a thin tube called an endoscope is inserted into the rectum to visually inspect the entire gastrointestinal tract and collect small tissue samples for further analysis. Imaging: Computed tomography (CT), magnetic resonance imaging (MRI), and ultrasonography are valuable tools for assessing disease activity and detecting complications associated with Crohn's disease. These imaging techniques can examine areas of the gastrointestinal tract that may not be accessible via endoscopy, providing comprehensive insights into the condition's progression and associated issues. Laboratory testing: various laboratory tests, including complete blood count, C-reactive protein levels, pregnancy tests, and stool samples, are conducted to screen for Crohn's disease. These tests are typically the initial step in diagnosis, helping to avoid the necessity for more invasive procedures like endoscopies and imaging. Additionally, laboratory testing may involve assessing inflammatory markers such as erythrocyte sedimentation rate (ESR) and faecal calprotectin to further aid in diagnosis and monitoring of the condition. Treatment and prevention While there is currently no cure for Crohn’s disease, numerous treatments have been developed over time to effectively manage symptoms and sometimes even induce remission. When determining a treatment plan for patients, factors such as age, specific symptoms, and the severity of inflammation are taken into careful consideration. Corticosteroids and immunomodulators are medications commonly used to manage Crohn’s disease. Corticosteroids work by reducing inflammation and suppressing the immune system, typically employed to address flare-ups due to their rapid action. However, they are not suitable for long-term use as they may lead to significant side effects. In contrast, maintenance therapy often involves immunomodulators such as azathioprine, methotrexate, or biologic agents like anti-TNF drugs (such as infliximab or adalimumab). These medications target specific immune pathways to enhance the effectiveness of the immune system. Research indicates that immunomodulators are associated with fewer adverse effects compared to corticosteroids and are effective in maintaining remission. Monoclonal antibody treatment is another approach used to manage symptoms and sustain remission in Crohn's disease. These therapies are categorised as biologic treatments, targeting precise molecules involved in inflammation and the immune response. Despite carrying certain risks, such as infections, the likelihood of developing cancer with these treatments is typically deemed low. Crohn’s disease frequently leads to complications that may necessitate surgical intervention. Gastrointestinal surgeries can greatly alleviate symptoms and enhance the quality of life for patients. However, surgery is usually considered only when medical therapy proves insufficient in controlling the disease or when complications arise. Although the exact cause of Crohn’s disease remains uncertain, factors such as genetics, immune system dysfunction, and environmental influences are believed to contribute to its development. While there is no definitive evidence pinpointing specific causative factors, numerous studies suggest potential links to an unhealthy diet and lifestyle, dysbiosis (imbalance of healthy and unhealthy gut bacteria), smoking, and a family history of the disease. Therefore, it is crucial to minimise exposure to these risk factors in order to decrease the likelihood of developing Crohn’s disease. Written by Sherine Abdul Latheef Related articles: the gut microbiome / the dopamine connection / Diverticular disease / Mesenchymal stem cells REFERENCES Veauthier B, Hornecker JR. Crohn's Disease: Diagnosis and Management. Am Fam Physician. 2018;98(11):661-669. Torres J, Mehandru S, Colombel JF, Peyrin-Biroulet L. Crohn's disease. Lancet. 2017;389(10080):1741-1755. doi:10.1016/S0140-6736(16)31711-1 Mills SC, von Roon AC, Tekkis PP, Orchard TR. Crohn's disease. BMJ Clin Evid. 2011;2011:0416. Published 2011 Apr 27. Sealife, A. (2024) Crohn’s disease, Parkland Natural Health. Available at: https://wellness-studio.co.uk/crohns-disease/ (Accessed: 09 March 2024). How to stop anxiety stomach pain & cramps (2022) Calm Clinic - Information about Anxiety, Stress and Panic. Available at: https://www.calmclinic.com/anxiety/symptoms/stomach-pain (Accessed: 09 March 2024). Project Gallery

When misfolded proteins lead to disease Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unfolding prion diseases and their inheritance 22/04/25, 14:11 Last updated: Published: 06/03/24, 11:32 When misfolded proteins lead to disease This is article no. 5 in a series on rare diseases. Next article: Neuromyelitis optica . Previous article: Epitheliod hemangioendothelioma . Prion proteins are found abundantly in the brain; their function is unclear, but they are involved in a multitude of physiological mechanisms, including myelin homeostasis and the circadian rhythm. Correctly folded prion proteins in the cellular form are termed PrP C , while their infectious isoform is called PrP Sc . As shown in Figure 1, the misfolded PrP Sc is largely made up of β-pleated sheets instead of α-helices; PrP Sc is prone to forming aggregates that cause transmissible spongiform encephalopathies (TSEs). Prion diseases can be categorised by their aetiology: acquired, sporadic, and hereditary. Acquired prion diseases are caused by the inadvertent introduction of PrP Sc prions into an individual. Sporadic prion diseases are the most common type, where PrP C misfolds into PrP Sc for an unknown reason and propagates this misfolding within other prion proteins. Hereditary prion diseases are caused by genetic mutation of the human prion protein gene (PRNP), which causes misfolding into the infectious isoform. Consequently, these mutations can be passed to offspring, resulting in the same misfolding and disease. Interestingly, different types of PRNP mutations cause different types of prion diseases. Creutzfeldt-Jakob disease (CJD) is a type of TSE found in humans which causes mental deterioration and involuntary muscle movement; symptoms tend to worsen as the disease progresses, making it a degenerative disorder. Familial CJD (fCJD) is a rare type of hereditary prion disease and can sometimes result in a faster rate of disease progression compared to sporadic cases. Due to a dominant inheritance pattern, relatives of fCJD patients are often also affected by the disease. The most common mutation observed in familial CJD is an E200K mutation denoting the substitution of glutamic acid with lysine in the prion protein. Other common mutations resulting in fCJD include mutations at positions 178 and 210 on the prion protein. However, there are, less frequently, a multitude of other mutations correlated with familial CJD development. Familial CJD can be caused by STOP codon mutations, which result in a truncated protein, some of which show similar pathology to Alzheimer’s disease, such as Q16OX and Q227X. fCJD can also be caused by insertional mutations, possibly caused by unbalanced crossover and recombination. The prion protein consists of a nona-peptide (made up of nine amino acids) followed by four repeats of an octa-peptide (made up of eight amino acids). During insertion mutations, additional repeats of the octa-peptide are present in the prion protein. Interestingly, different numbers of inserts result in different pathological characteristics; patients with 1, 2 or 4 extra repeats show similarity to sporadic CJD, while those with 5-9 extra repeats show similarity to Gerstmann-Sträussler-Scheinker syndrome. Hereditary prion diseases are important to study in order to develop an understanding of not only prion misfolding diseases but also diseases associated with misfolding of other proteins, such as Alzheimer’s and Parkinson’s. Understanding the mechanisms of hereditary prion diseases will aid the development of treatments for such conditions. In particular, observing and investigating particular genetic mutations observed to play a part in prion misfolding is crucial alongside using genetic information to infer the risk of disease an individual may have. Written by Isobel Cunningham Project Gallery

The web of geopolitics surrounding the Rohingyas, and how this impacts their health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Addressing the health landscape of Bangladesh’s Rohingya community Last updated: 16/10/25, 10:19 Published: 18/09/25, 07:00 The web of geopolitics surrounding the Rohingyas, and how this impacts their health This is article no. 6 in a series about global health injustices. Previous article: Health gaps in conflict-affected Kashmir. Next article: A deep, critical reflection . Introduction Welcome to the sixth article of the Global Health Injustices Series, a collaboration with Nasif Mahmood . This article focuses on the ongoing injustices and health issues affecting the Rohingya refugees in Bangladesh. This community leads a vulnerable life and suffering that it is becoming one of the most significant South Asian crises in the 21st century. Due to Bangladesh's inadequate resources and geopolitical situation, the overall health and well-being of the country and the migratory population are severely hampered. A brief history of Bangladesh and the Rohingya population Bangladesh's history is intricate and has been influenced by many cultures. After India was divided in 1947, the area, previously part of ancient Bengal, was ruled by the British and became East Pakistan. Demands for autonomy resulted from tensions between West and East Pakistan. The Bangladesh Liberation War in 1971, culminating in these tensions, led to the country's independence. Bangladesh has made great strides in education, health, and economic growth since gaining its autonomy, despite facing economic hardship, political turmoil, and natural disasters. Rohingya, the Muslim ethnic minority from the state of Rakhine, were denied citizenship by the Myanmar Government, leaving them homeless. They endured years of persecution, discrimination, and violence. In 2017, an inhuman, violent crackdown by the military of the Myanmar government forced over 70,000 Rohingya to flee to Bangladesh. Over 1 million refugees live in Bangladesh, primarily in the Cox Bazar area. A lot of refugees cause overcrowding situations, and limited resources lead to a high rate of nutritional problems and spread of disease, specifically infectious diseases and mental health disorders in the refugee camp. Connecting geopolitics and health: impacts on the Rohingya population The Rohingya crisis is more than just a humanitarian issue; it is a tangled web of geopolitical challenges. The Myanmar government’s ongoing refusal to grant citizenship and fundamental rights to the Rohingya people not only deepens their suffering but also fuels instability in the region. They have not taken the necessary steps to ensure their safety, leaving the crisis unresolved. As refugees continue to pour into neighbouring countries, tensions have escalated, placing a heavy burden on host nations like Bangladesh. This crisis worsens existing socio-economic problems and stretches resources thin in areas struggling to care for their citizens. The international community has responded in various ways; some countries are pushing for tougher sanctions against Myanmar, while others are focused on delivering aid to those affected. However, the underlying issues driving this crisis will unlikely be resolved without a coordinated and sustained political effort ( Table 1, Figure 1 ). Addressing them can lead to improved outcomes for the Rohinyga population. On top of that, the health challenges faced by the Rohingya people go beyond just infectious diseases. The lack of access to essential health services has not only worsened physical health problems but has also led to a growing mental health crisis. Many Rohingya individuals are grappling with post-traumatic stress disorder (PTSD), anxiety, and depression stemming from their traumatic experiences of violence, loss, trauma, isolation, and forced displacement. Yet, mental health services in the refugee camps are severely lacking. A study showed that the prevalence of emotional and behavioural disorders is high among forcefully migrated refugee children, because of traumatic exposure like the unexpected death of parents, forceful displacement, and the witnessing of family violence and abuse. The stigma surrounding mental health in many cultures, including in the Rohingya community, creates additional hurdles for those seeking help. Enhancing access to mental health support is crucial, not just for the immediate well-being of the refugees, but also for their long-term healing and successful integration into the societies that host them. Moreover, providing humanitarian aid and hosting such a large population in Bangladesh is becoming difficult. The national and international NGOs maintain healthcare for the Rohingya population. However, the funding shortage and inadequate infrastructure hinder the provision of adequate medical services. For this reason, the refugee camps have reported significant outbreaks of diphtheria, cholera, and COVID-19. Given the challenges, developing innovative solutions and working collaboratively on a global or regional scale is needed. By empowering local health workers and training them to offer basic healthcare and mental health support, to close the service delivery gaps. Additionally, building partnerships among NGOs, governments, and international organisations can help ensure that resources are allocated more effectively and that comprehensive health programs are created to meet the unique needs of the Rohingya population. It's crucial to engage the community; by listening to the voices and experiences of the Rohingya, we can develop interventions that truly respect their dignity and cultural context. Additionally, raising global awareness about the struggles faced by the Rohingya can lead to stronger advocacy efforts. Involving the media, educational institutions, and civil society can foster a deeper understanding of the interconnected issues of geopolitics and health. Initiatives that share personal stories and experiences can rally public support and drive meaningful change. Ultimately, tackling the Rohingya crisis calls for a multifaceted approach that blends immediate humanitarian aid with long-term strategies aimed at ending their statelessness and ensuring their rights as human beings are upheld and protected. Recommendations from NGOs National NGOs: Several national NGOs play an essential role in supporting the healthcare needs of the Rohingya population: Bangladesh Rural Advancement Committee (BRAC), one of the world's largest NGOs, provides comprehensive health care services, including maternal and child health, immunisation programmes, disease prevention initiatives, and arranges many health campaigns for refugees. Gonoshasthaya Kendra established a field hospital and free clinic in the Cox Bazar area near the refugee camp, focusing on primary health care and emergency medical support. International NGOs MedGlobal, an international NGO, responds to this global crisis by delivering medical assistance within the refugee camp. Support hospitals and clinics for affected refugees between 2017 and 2019. This organisation's volunteers contributed over 17,000 hours of aid, assisting more than 80,000 individuals. Medair is another international NGO offering health and nutritional support to the Rohingya refugees. Migrant Offshore Aid focuses on sea rescue operations and delivering medical aid and assistance to surfers. Together, these national and international organisations make meaningful contributions to the healthcare needs of the Rohingya population, handling both immediate medical concerns and long-term health support in a challenging environment. Their collaborative efforts help ensure that essential services reach those in critical need, facilitating better health outcomes for refugees. Although they address the healthcare needs of the Rohingya, several challenges can limit their effectiveness. For example, coordination issues may lead to overlapping efforts or service gaps, resulting in inequitable and unequal healthcare access. Also, limited resources and funding can slow extensive long-term support, leaving specific medical needs unaddressed. Additionally, the intricate political and social conditions restrict these organisations' capacity to operate effectively, impacting immediate care and sustainable health initiatives for the Rohingya population. Moving forward, it is crucial for host countries to: finance extra healthcare facilities in refugee camps to enhance access and reduce diseases, launch culturally appropriate mental health initiatives with locally trained workers to decrease stigma and provide community-based support, integrate nutrition programmes to address different forms of malnutrition in vulnerable communities and encourage further international support to maintain health initiatives among the Rohingya population. Conclusion The Rohingya crisis is an example of global health injustice exacerbated by geopolitical and humanitarian challenges. At the same time, Bangladesh is trying to provide temporary shelter for the refugees to minimise the crisis. However, this crisis also requires international cooperation, policy support, and increased funding. Solving this issue is essential for global public health and human rights. Notably, finding sustainable solutions will help the Rohingya people recover and thrive, and enhance stability and security in the region. Their future goes beyond humanitarian aid; it is about upholding inclusion, justice, and respect for human dignity, which should guide all efforts to link geopolitics with health outcomes. To truly tackle the health issues faced by the Rohingya community, we need to take a comprehensive approach that looks at the political, social, and economic factors at play. By adopting such all-encompassing systems, we can work towards a brighter and fairer future for the Rohingya community and other vulnerable groups around the globe who are facing similar challenges. The next article will be the final one reflecting on everything discussed in this series. Written by Nasif Mahmood and Sam Jarada Related articles: Health and well-being in- Palestine , Kashmir / South Asian famine / South Asian mental health REFERENCES Tinker HR. History of Bangladesh | Events, People, Dates, & Facts [Internet]. Encyclopedia Britannica. 2023 [cited 2025 Jul 15]. Available from: https://www.britannica.com/topic/history-of-Bangladesh Rahman MM, Bhuiyan MR, Ali MZ, Rahman MS, Hossain MA. Insecurity feelings and mental health status of Rohingya orphan children in BangladeshResearchGate; 2021 https://www.researchgate.net/publication/348521935_Insecurity_Feelings_and_Mental_Health_Status_of_Rohingya_Orphan_Children_in_Bangladesh UNHCR. Rohingya refugee crisis – Bangladesh. 2023. https://www.unhcr.org International Crisis Group (ICG). The health crisis in Rohingya refugee camps. 2022. https://www.crisisgroup.org Tay AK, Riley A, Islam R, Welton-Mitchell C, Duchesne B, Waters V, et al. The culture, mental health and psychosocial wellbeing of Rohingya refugees: a systematic review. Epidemiology and Psychiatric Sciences [Internet]. 2019 Apr 22 [cited 2025 Sep 10];28(5):489–94. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC6998923/ Human Rights Watch. The plight of Rohingya refugees in Bangladesh. 2023. https://www.hrw.org . Nivedita Sudheer, Banerjee D. The Rohingya refugees: a conceptual framework of their psychosocial adversities, cultural idioms of distress and social suffering. Cambridge Prisms Global Mental Health [Internet]. 2021 Jan 1 [cited 2025 Sep 10];8. Available from: https://www.cambridge.org/core/journals/global-mental-health/article/rohingya-refugees-a-conceptual-framework-of-their-psychosocial-adversities-cultural-idioms-of-distress-and-social-suffering/F4D229807D4ED7667EA16195FDF5C787 World Health Organization (WHO). Health challenges in Rohingya refugee camps. 2022. https://www.who.int Médecins Sans Frontières (MSF). Medical response in Rohingya refugee settlements. 2022. https://www.msf.org Project Gallery

Brush up on your mathematical knowledge with informative articles ranging from statistics and topology, to latent space transformations and Markov chain models. Maths Articles Brush up on your mathematical knowledge with informative articles ranging from statistics and topology, to latent space transformations and Markov chain models. You may also like: Economics , Physics , Engineering and Technology Unlocking the power of statistics What statistics are and its importance Latent spac e transformations Their hidden power in machine learning Topology In action Teaching maths How we can apply maths in our lives How to excel in maths A useful resource for students studying the subject Cognitive decision-making The maths involved Cross-curricular maths The game of life The maths behind trading A comprehensive guide to the Relative Strength Index (RSI) Markov chain models Named after the Russian mathematician, Andrei Markov, who had first studied them Proving causation Investigating why correlation doesn't necessarily mean causation, via Randomised Controlled Trials and Instrumental Variables

Why the fuss over a couple of km/s/Mpc? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Hubble Tension 09/07/25, 14:20 Last updated: Published: 25/11/23, 11:10 Why the fuss over a couple of km/s/Mpc? You have probably heard that the universe is expanding, and perhaps even that this expansion is accelerating. A consequent observation of this is that distant objects such as galaxies appear to recede from Earth faster if they are further away. Here is a helpful analogy: imagine a loaf of raisin bread that is rising as it is baked. A pair of raisins on opposite sides of the loaf will move away from one another at a greater rate than a pair of raisins near the center. The more dough (universe) there is between a pair of raisins (galaxies), the faster they recede from one another. See Figure 1 . This phenomenon is encapsulated in Hubble’s Law, which relates specifically to the recessional velocity due to the expansion of space. Hubble’s Law is given by the equation v = H0 D . Where: v is the recessional velocity D is the distance to the receding object H0 is the Hubble constant It is worth noting that distant objects will often have velocities of their own due to gravitational forces - so-called ‘peculiar velocities’. In order to clarify the meaning of the title of this article, we must explore the unit in which the Hubble constant H0 is most often quoted: km/s/Mpc. This describes the speed (in kilometers per second) at which a distant object, such as a galaxy, is receding for every megaparsec of distance that galaxy is from Earth. Edwin Hubble is the name most often associated with this cosmological paradigm shift; however, physicists Alexander Friedmann and Georges Lemaître worked independently on the notion of an expanding universe, deriving similar results before Hubble verified them experimentally in 1929 at the Mount Wilson Observatory, California. What is the Hubble Tension? Hopefully the above discussion of units and raisin bread convinced you that the Hubble constant H0 is linked to the expansion rate of the universe. The larger H0 is, the faster galaxies are receding at a given distance, thus indicating a more quickly expanding universe. Therefore, cosmologists wish to accurately measure H0 in order to draw conclusions about the age and size of the universe. The Hubble Tension arises from the contradicting measurements of H0 obtained from different experiments. See Figure 2 of Edwin Hubble. CMB measurement One of these experiments uses the Cosmic Microwave Background (CMB), which can be thought of as an afterglow of light from near the time of the Big Bang. The wavelength of this light has expanded with the universe ever since the period of recombination - which I mentioned in my previous article on the DESI instrument. Our current best model of the universe, called ΛCDM, can describe how the universe evolved from a hot, dense state to the universe we see today, subject to a specifically balanced energy budget between ordinary matter, dark matter, and dark energy. From fitting this ΛCDM model to CMB data from missions such as ESA’s Planck Mission, one can derive a value for the expansion rate of the universe, i.e., a value for H0 . The Planck Mission measured temperature variations (anisotropies) across the CMB with unprecedented angular resolution and sensitivity. The most recent estimate for the Hubble constant using this method gave H0 = 67.4 ± 0.5 km/s/Mpc . Local Distance Ladder measurement Another technique to determine the value of H0 uses the distance-redshift relation. This is a wholly observational approach. It relies on the fact that the faster an object recedes from Earth, the more the light from that object is shifted towards longer wavelengths (redshifted). Hubble’s Law relates this recessional velocity to a distance; therefore, one can expect a similar relation between distance and redshift. A ‘ladder’ is invoked since astronomers wish to use objects that are visible from a vast range of distances; the rungs of the ladder represent greater and greater distances to the astronomical light source. Each rung of the ladder contains a different kind of ‘standard candle’, which are sources with reliable, well-constrained luminosities that translate to an accurate distance from Earth. I encourage you to look into these different types; some examples are Cepheid variables, Type Ia Supernovae, and RR Lyrae variables. When this method was employed using the Hubble Space Telescope and SH0ES (Supernova H0 for the Equation of State), a value of H0 = 73.04 ± 1.04 km/s/Mpc was obtained. The disagreement Clearly, these two values for the Hubble constant do not agree, nor do their uncertainty ranges overlap. Figure 3 shows some of the 21st-century measurements of H0 ; an excellent illustration of how the uncertainty has decreased for both methods, therefore making their disagreement more statistically significant. Many sources of scientific engagement with the public cite this disagreement as the ‘Crisis in Cosmology!’. In the author’s opinion, this is unnecessarily hyperbolic and plays on the human instinct to pick a side between two opposing viewpoints. In fact, new methods to measure H0 have been implemented using the tip of the Red-Giant branch (TRGB) as a standard candle, which demonstrate closer agreement with the value derived from the CMB. Some cosmologists believe that eventually this Hubble Tension will dissipate as our calibration of astronomical distances improves with the next generation of telescopes. Constraining the value of the Hubble constant is by no means low-hanging fruit for cosmologists, nor is the field in crisis. To see the progress we have made, one has to look back in time to 1929 when Edwin Hubble’s first estimate using a trend line and 46 galaxies gave H0 = 500 km/s/Mpc ! We must remain hopeful that the future holds a consistent approximation for the expansion rate and, with it, the age of our universe. Written by Joseph Brennan 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

When we think of bacteria, we tend to focus on their pathogenicity and ability to cause diseases such as tuberculosis, which infects around one-quarter of the world’s population. However, whilst bacteria do have the potential to become parasitic, if the trillions of bacterial cells that make up the human microbiome ceased to exist, human health would experience a rapid decline. Go back Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Why bacteria are essential for human survival Last updated: 13/11/24 Published: 13/04/23 When we think of bacteria, we tend to focus on their pathogenicity and ability to cause diseases such as tuberculosis, which infects around one-quarter of the world’s population. However, whilst bacteria do have the potential to become parasitic, if the trillions of bacterial cells that make up the human microbiome ceased to exist, human health would experience a rapid decline. One reason for this is due to the critical role bacteria play in inducing the immune system against pathogenic threats. Upon viral infection, the interferon (IFN) defence system is initiated where the synthesis of antiviral cytokines is upregulated. Evidence suggests bacteria in the gut are capable of modulating the IFN system. They work by inducing macrophages and plasmacytoid dendritic cells to express type 1 IFN, which in turn primes natural killer cells and prepares cytotoxic CD8+ T cells for action. Erttmann et al (2022) demonstrate that a depletion of the gut microbiota diminishes the cell signalling pathways modulated by these commensal bacteria. This causes a reduction in type 1 IFN production, and thus an impairment in the activation of NK and CD8+ T cells. As a result, the body becomes more susceptible to attack by viral infections and less able to defend itself. This highlights just how vital the role bacteria in our microbiome play in providing us with innate immunity against viral pathogens and protecting our health. This also brings attention to our use of antibiotics, and the potential negative effects they may have on the commensal bacteria residing in our body. Erttmann et al (2022) further showed that mice treated with a variety of antibiotics exhibited a major reduction in gut microbiota diversity, thus severely comprising their ability to fight off viral infections. Research like this is important in informing doctors to be sensible in their administration of antibiotics, as well as informing patients to not self-medicate and unnecessarily ingest antibiotics. Ultimately, the commensal bacteria living in our bodies play essential roles in protecting human health, and it is, therefore, vital we take the necessary steps to also protect these remarkable microorganisms in return. Written by Bisma Butt Related article: The rising threat of antibiotic resistance REFERENCES Erttmann, S.F., Swacha, P., Aung, K.M., Brindefalk, B., Jiang, H., Härtlova, A., Uhlin, B.E., Wai, S.N. and Gekara, N.O., 2022. The gut microbiota prime systemic antiviral immunity via the cGAS-STING-IFN-I axis. Immunity, 55(5), pp.847-861. Ganal, S.C., Sanos, S.L., Kallfass, C., Oberle, K., Johner, C., Kirschning, C., Lienenklaus, S., Weiss, S., Staeheli, P., Aichele, P. and Diefenbach, A., 2012. Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota. Immunity, 37(1), pp.171-186.