An extensive collection of insightful reviews on the best STEM books available. Whether you're a student looking to deepen your knowledge or something to aid your revision and research, an educator seeking great resources for your classroom, or simply a curious mind passionate about science, technology, engineering, mathematics, medicine and more, you'll find something here to inspire and inform you.  Discover Your Next Great Read Deep Dive into STEM Books Here you can explore an extensive collection of insightful reviews on the best STEM books available. Whether you're a student looking to deepen your knowledge or something to aid or complement your revision and research, an educator seeking great resources for your classroom, or simply a curious mind passionate about science, technology, engineering, mathematics, medicine and more, you'll find something here to inspire and inform you. Our Curated Selections: Intern Blues by Robert Marion, M.D. The Emperor of All Maladies by Siddhartha Mukherjee The Molecule by Dr Rick Sax and Marta New

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What is it and what does it do? Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link The role of dopamine in the movement and the reward pathway 25/08/26, 14:06 Last updated: Published: 21/09/24, 16:59 What is it and what does it do? Dopamine is a neurotransmitter produced mainly in the ventral tegmental area (VTA) and the substantia nigra pars compacta (SNPC) in the brain, exhibiting both excitatory and inhibitory effects in different brain pathways. ( About 50% of the body’s dopamine is also produced in the gut). Dopamine is important in mediating the mesolimbic and nigrostriatal pathways for reward and movement, respectively. Therefore, damage to dopaminergic neurones affects dopamine levels in the brain and can consequently result in diseases associated with abnormal dopamine levels. Movement The role of dopamine is vital in modulating the initiation of movement through both the direct and indirect pathways of the basal ganglia ( Figure 1 ). In the direct pathway, dopamine produced from the SNPC binds to the D1 Gs-coupled receptors in the striatum resulting in the activation of the intracellular signalling cascade. Activation of these receptors results in increased intracellular cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA) levels, which control the modulation of ion channels, including calcium channels for further depolarisation of the striatal cells. The excitation of the striatum results in GABAergic inhibition of the globus pallidus internal segment (GPI) and the substantia nigra pars reticulata (SNPR). Hence, this results in the disinhibition of the thalamus, allowing for excitatory glutamatergic transmission to the motor cortex for the facilitation of movement. The activation of the striatum via D1 receptor stimulation can be supported by a study conducted by Gerfen et al. 2012 in which they concluded that PKA activates calcium voltage-gated 1 L-type calcium channels, resulting in depolarisation of striatal cells, which causes the enablement of movement via the direct pathway. However, in the indirect pathway, dopamine binds to D2 Gi-coupled receptors with a higher affinity than D1 receptors, causing inhibition of these receptors and their intracellular signalling cascades. Consequently, there is decreased inhibition of potassium channels by the second messengers, resulting in hyperpolarisation due to potassium efflux from the striatal cells. As the striatum is inactivated, this reduces the overall inhibitory effect of the indirect pathway on the thalamus, allowing for movement. Therefore, dopamine is critical for the normal functioning of humans by allowing them to control their movements for survival, for example, by pushing a ball away when it is about to hit them. Reward pathway The mesolimbic dopaminergic pathway ( Figure 2 ) is the most recognised reward pathway in the brain. This pathway contains the VTA, located in the midbrain, the nucleus accumbens (NA) and the tuberculum olfactorium (TO), located in the basal forebrain. The lateral regions of the VTA are the most abundant in A10 dopaminergic neurones in comparison to other regions of the VTA. These A10 neurones are activated in association with reward anticipation, for example, after exercising. The medial VTA dopaminergic neurones project to the core and medial shell regions of the NA, and the lateral VTA project towards the lateral shell region of the NA (figure 3). Thus, increasing dopamine levels in the NA and inducing the processing of the reward. Moreover, dopaminergic inputs from the VTA to the TO allow the individual to develop an odour preference for a specific stimulus due to motivation-oriented behaviour. Hence, this could be a reason why the anticipation of eating one's favourite food by evoking the memory of its smell is associated with the feeling of reward. Experiments conducted by FitzGerald et al. 2014 support my points regarding the role of the TO in the mesolimbic pathway. In their study, mice were given a choice of two different odours to choose from. The team noted activation of c-Fos neurones in the forebrain, indicating neuronal activity in this region, which is involved in reward motivation behaviour. Hence, allowing them to support the importance of the TO in odour processing and reward behaviour in the mice when choosing a more pleasurable odour. Eventually, projections from the TO and NA converge at the ventral pallidum, where the enrichment of reward-related learning occurs. Therefore, dopamine is essential for the initiation of the reward pathway in ensuring the continuation of reward behaviour when exposed to a specific stimulus and for survival due to the association of reproduction with reward. Furthermore, recent research from the University of Colorado suggests that dopamine's role extends beyond its well-established involvement in the brain's reward pathway. The study found that dopamine also plays a key role in motivating individuals to move more quickly when a reward is anticipated, highlighting its influence on both motivation and movement. Conclusion In conclusion, dopamine is essential for the initiation of movement and in the reward pathway for normal human functioning and survival. Studies into aldehyde-dehydrogenase 1 in the SNPC have found that it protects dopaminergic neurones against neurodegeneration. Further studies will aid in understanding the mechanisms by which this enzyme is regulated and the actions by which it protects dopaminergic neurones in the SNPC. Written by Maria Z Kahloon Related articles: The dopamine connection between the gut and the brain / Interplay of hormones and microbiome / Types of movement Project Gallery

A potential gene therapy: oligonucleotides are inserted into cells and bind to the target huntingtin mRNA Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Antisense oligonucleotide gene therapy for treating Huntington's disease 25/08/26, 14:10 Last updated: Published: 25/02/24, 14:38 A potential gene therapy: oligonucleotides are inserted into cells and bind to the target huntingtin mRNA Huntington’s disease (HD) is an inherited neurodegenerative disease caused by a CAG extension in exon 1 of the huntingtin gene. An extended polyglutamine tract in the huntingtin protein is developed due to the expanded alleles, resulting in intracellular signalling defects. Antisense Oligonucleotide (ASO) gene therapy is currently being pioneered to treat HD. In this therapy, oligonucleotides are inserted into cells and bind to the target huntingtin mRNA. Thus, inhibiting the formation of the huntingtin protein by either physically blocking the translation of mRNA (figure 1) or by utilising RNase H to degrade the mRNA. Previous ASO gene therapy experiments conducted on R6/2 mice that express the human huntingtin gene have been successful. In HD research, the R6/2 mouse model is commonly used to replicate HD symptoms and is therefore useful for testing potential treatments. The transgenic R6/2 mouse has an N-terminally mutant Huntingtin gene with a CAG repeat expansion within exon 1. In this successful experiment, scientists treated one group of R6/2 mice with the ASO treatment that suppresses the production of human huntingtin mRNA, and saline solution was administered to the control group of mice. This experiment aimed to confirm if ASO therapy improves the survival rate in the R6/2 mice. The results showed that human huntingtin mRNA levels of the mice treated with ASO therapy were lower than the control group. Furthermore, the mice treated with ASO therapy had a higher percentage of survival and lived longer (21 weeks), in comparison to the control group mice that survived until 19 weeks. Thus, it could be concluded that if less human huntingtin mRNA was present in the ASO group, then less human huntingtin mRNA would be translated, and so there would be less synthesis of the huntingtin protein, in contrast to the control group. The results of this study are enormously informative in understanding how gene therapy can be used in the future to treat other neurological diseases. However, before ASO therapy is approved for clinical use, further trials will need to be conducted in humans to verify the same successful outcomes as the R6/2 mice. If approved, then the symptoms of HD, including dystonia could be safely controlled with ASO therapy. Furthermore, scientists need to consider that an increased survival rate of only an additional two weeks, as shown in the experiment does not always correlate to an increased quality of life for the patient. Therefore, it needs to be established if the benefits of ASO gene therapy will outweigh the risks associated with it. Furthermore, the drug PBT2, which influences copper interactions between abnormal proteins, has been investigated as a potential treatment option for Huntington's disease (HD). Some studies have suggested that the aggregation of mutant huntingtin proteins may be influenced by interactions with metals, including copper. Therefore, PBT2 was designed to chelate metals and consequently reduce abnormal protein aggregation in the body. Preclinical studies demonstrated improvements in motor performance and increased lifespan in R6/2 mouse models. However, clinical trials in humans have produced mixed results, and the development of PBT2 is currently paused because of inconsistent efficacy findings and regulatory challenges. As a result, further research is needed to identify more effective disease-modifying therapies for HD. Written by Maria Z Kahloon Related article: Overview of Huntington's disease REFERENCES Kordasiewicz HB, Stanek LM, Wancewicz EV, Mazur C, McAlonis MM, Pytel KA, et al. Sustained therapeutic reversal of Huntington’s disease by transient repression of huntingtin synthesis. Neuron. 2012;74(6):1031–44. Valcárcel-Ocete L, Alkorta-Aranburu G, Iriondo M, Fullaondo A, García-Barcina M, Fernández-García JM, et al. Exploring genetic factors involved in Huntington disease age of onset: E2F2 as a new potential modifier gene. PLoS One. 2015;10(7):e0131573. Liou S. Antisense gene therapy [Internet]. Stanford.edu . 2010 [cited 2021 Aug 6]. Available from: https://hopes.stanford.edu/antisense-gene-therapy/ Huntington's disease research study in R6/2 MOUSE model: Charles River [Internet]. Charles River Labs. [cited 2021 Aug 26]. Available from: https://www.criver.com/products-services/discovery-services/pharmacology-studies/neuroscience-models-assays/huntingtons-disease-studies/r62-mouse?region=3696 Frank S. Treatment of Huntington's disease. Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics. Springer US; 2014;11(1):153-160. Potkin KT, Potkin SG. New directions in therapeutics for HUNTINGTON DISEASE. Future neurology. 2018;13(2):101-121. Project Gallery

Cultural beliefs, stigma, family values and more, inhibit open discussion of mental health Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Addressing mental health within the South Asian community Last updated: 05/03/26, 14:56 Published: 22/05/25, 08:00 Cultural beliefs, stigma, family values and more, inhibit open discussion of mental health Mental health is a critical aspect of human life, yet it remains a deeply taboo subject within the South Asian community. Despite the growing awareness in mainstream discourse, many South Asians—especially those living in diasporic communities such as the UK, the US, and Canada—continue to face significant barriers when it comes to recognising, understanding, and seeking help for mental health concerns. But why does this silence continue? The answer lies in a combination of cultural beliefs, stigma, family values, societal expectations, and a general lack of education, especially among the older generations. Unlike Western cultures, which tend to emphasise individualism, South Asian societies often focus on collectivism, where the success and well-being of the family take precedence over the individual. This cultural foundation has both strengths and challenges. While it preaches community and support, it also discourages expressions of emotional vulnerability, especially when that vulnerability may be perceived as bringing shame or dishonour to the family. Mental health is often viewed as a personal weakness, a spiritual failing, or something that reflects poorly on one’s upbringing or family reputation. A survey conducted by the NHS in the UK revealed that 35% of South Asian youth aged 18–24 reported experiencing some form of mental health issue, compared to 30% of White British youth. While these figures suggest a slightly higher incidence, what is more alarming is the disparity in access to care and treatment. Many South Asians are less likely to seek help due to fears of being perceived as 'crazy' or weak. In some cases, mental health symptoms are dismissed as temporary mood swings, spiritual crises, or simply a lack of willpower. A study published by the Mental Health Foundation (2020) found that only 32% of South Asians surveyed had a functional understanding of mental health, compared to 60% of the general UK population. This suggests that stigma is caused by a lack of knowledge, which prevents early intervention and exacerbates untreated conditions. Among those who recognise they have a problem, there is often a reluctance to seek professional help, particularly from psychologists or psychiatrists. Instead, some may turn to spiritual leaders or rely solely on familial support, both of which, while culturally significant, may not always offer the necessary therapeutic intervention. One of the major mental health concerns within the South Asian community is depression and anxiety, and these conditions often go undiagnosed. Research from the Centre for Mental Health has indicated that South Asian individuals are more likely to report symptoms of depression and anxiety than their White counterparts, but are less likely to receive treatment. According to a 2022 study by Public Health England, South Asian women are 1.5 times more likely to suffer from common mental health disorders, such as anxiety and depression, but only 13% accessed mental health services compared to 25% of White British women. Many culturally specific factors contribute to higher rates of anxiety and depression in South Asian communities. These include intergenerational trauma, immigration stress, identity conflict, and pressures related to marriage, family reputation, and academic or career success. Young South Asians often find themselves navigating between traditional family expectations and Western societal norms, leading to identity struggles that can trigger chronic stress and anxiety. Additionally, gender roles in South Asian cultures often impose strict expectations on behaviour. Women may be discouraged from voicing emotional distress, as they are expected to be nurturing and self-sacrificing. Men, on the other hand, are often pressured to appear strong and unemotional, which leads to a culture where expressing vulnerability is equated with failure. These rigid expectations prevent both genders from openly discussing their struggles or seeking help. Barriers to accessing mental health services are not only cultural but also structural. Many South Asians, particularly first-generation immigrants, may face language barriers when communicating with healthcare providers. There is also a lack of culturally competent therapists who understand the nuances of South Asian traditions, values, and family structures. Without representation or relatability, individuals may feel misunderstood or alienated by the mental healthcare system. Despite these challenges, there is hope. The rise of South Asian mental health advocates, community-based initiatives, and culturally tailored therapy programs is slowly helping to dismantle stigma. Social media has also played a vital role in bringing these conversations to the forefront, especially among Gen Z and Millennials. Many people are now speaking out and sharing their stories and experiences, which helps shift the narrative within the South Asian Community. We can help break the stigma surrounding mental health in the South Asian community by raising awareness, educating others, and normalising conversations around emotional wellbeing. It starts at the grassroots level: in homes, schools, religious institutions, and workplaces. Encouraging open dialogue and fostering environments where individuals feel safe to share their experiences without judgment is key. More importantly, we must validate the struggles of those suffering from mental health issues—telling them that it is okay to not be okay, and that seeking help is a sign of strength, not weakness. Furthermore, the government and health services can do more! They should invest in culturally sensitive mental health resources, including multilingual therapy options and outreach programs tailored specifically for South Asian populations. In conclusion, addressing mental health within the South Asian community requires a collective effort to challenge outdated norms, educate people across all age groups, and improve access to inclusive and empathetic mental healthcare. Depression, anxiety, and other mental illnesses are not signs of weakness; they are real, treatable conditions that deserve compassion and support. Only by acknowledging this and working together can we begin to transform the narrative and create a healthier, more open future for the South Asian community, letting the future generation have a safe and open space to talk and get help for their mental health! Written by Rajeevan Sinnathurai ------- Scientia News thanks Rajeevan of Open Talk, for this enlightening piece on mental health in the South Asian Community. Connect with Open Talk on Instagram and TikTok . ------- Related articles: Mental health awareness / Imposter syndrome / Anxiety / South Asian epigenetics / Global health injustices- Kashmir , Bangladesh , Sri Lankan Tamils / Ethnic health inequalities REFERENCES NHS Digital. (2021). Mental Health of Children and Young People in England . Mental Health Foundation. (2020). Mental Health in the South Asian Community . Centre for Mental Health. (2022). Race and Mental Health Inequalities . Public Health England. (2022). Mental Health Services Use by Ethnic Groups in the UK . 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, 15:39 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

When misfolded proteins lead to disease Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Unfolding prion diseases and their inheritance 22/04/25, 15:11 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

Recent prospects for carbon monoxide indicate so Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Can carbon monoxide unlock new pathways in inflammation therapy? 13/06/26, 16:25 Last updated: Published: 01/09/24, 11:31 Recent prospects for carbon monoxide indicate so Carbon monoxide (CO) is a colourless, odourless and tasteless gas which is a major product of the incomplete combustion of carbon-containing compounds. The toxic identity CO stems from its strong affinity for the haemoglobin in our blood which is around 300 times as strong as the affinity of oxygen. As a result, once the gas is inhaled, CO binds to the haemoglobin instead and reduces the amount of oxygen our blood can transport, which can cause hypoxia (low levels of oxygen in tissue) and dizziness, eventually leading to death. However, an intriguing fact is that CO is also endogenously produced in our body, due to the degradation of haem in the blood. Moreover, recent prospects for CO indicate that it may even be developed as an anti-inflammatory drug. How CO is produced in the body See Figure 1 Haem is a prosthetic (non-peptide) group in haemoglobin, where the oxygen binds to the iron in the molecule. When red blood cells reach the end of their lifespan of around 120 days, they are broken down in a reaction called haemolysis. This occurs in the bone marrow by macrophages that engulf the cells, which contain the necessary haem-oxygenase enzyme. Haem-oxygenase converts haem into CO, along with Fe2+ and biliverdin, the latter being converted to bilirubin for excretion. The breakdown of haem is crucial because the molecule is pro-oxidant. Therefore, free haem in the blood can lead to oxidative stress in cells, potentially resulting in cancers. Haem degradation also contributes to the recycling of iron for the synthesis of new haem molecules or proteins like myoglobin. This is crucial for maintaining iron homeostasis in the body. The flow map illustrates haemolysis and the products produced, which either protect cells from further stress or result in cell injury. CO can go on to induce anti-inflammatory effects- see Figure 2 . Protein kinases and CO Understanding protein kinases is crucial before exploring carbon monoxide (CO) reactions. Protein kinases phosphorylate (add a phosphate group to) proteins using ATP. Protein kinases are necessary to signal the release of a hormone or regulating cell growth. Each kinase has two regulatory (R) subunits and two catalytic (C) subunits. ATP as a reactant is usually sufficient for protein kinases. However, some kinases require additional mitogens – specific activating molecules like cytokines (proteins regulating immune cell growth), that are involved in regulating cell division and growth. Without the activating molecules, the R subunits bind tightly to the C subunits, preventing phosphorylation. Research on obese mice showed that CO binding to a Mitogen-Activated Protein Kinase (MAPK) called p38 inhibits inflammatory responses. This kinase pathway enhances insulin sensitivity, reducing obesity effects. The studies used gene therapy, modifying haem-oxygenase levels in mice. Mice with reduced haem-oxygenase levels had more adipocytes (fat-storing cells) and increased insulin resistance, suggesting CO treatment potential for chronic obstructive pulmonary disease (COPD), which causes persistent lung inflammation and results in 3 million deaths annually. Carbon-monoxide-releasing molecules As a result of these advancements, specific CO-releasing molecules (CORMs) have been developed to release carbon monoxide at specific doses. Researchers are particularly interested in the ability of CORMs to regulate oxidative stress and improve outcomes in conditions during organ transplantation, and cardiovascular diseases. Advances in the design of CORMs have focused on improving their stability, and targeted release to specific tissues or cellular environments. For instance, CORMs based on transition metals like ruthenium, manganese, and iron have been developed to enhance their efficacy and minimize side effects. This is achieved through carbon monoxide forming a stable ‘ligand’ structure with metals to travel in the bloodstream. Under an exposure to light or a chemical, or even by natural breakdown, these structures can slowly distribute CO molecules. Although the current research did not find any notable side effects within mouse cells, this does not reflect the mechanisms in human organ systems, therefore there is still a major risk of incompatibility due to water insolubility and toxicity issues. These problems could lead to potentially lead to disruption in the cell cycle, which may promote neurodegenerative diseases. A proof-of-principle study explored the potential of CORM‐A1, boron‐based carboxylic acid acting as a CO-releasing molecule, to protect kidneys from warm ischemia and reperfusion (WI/R) injury in rat and swine models. It was found that intravenous administration of CORM‐A1 significantly increased blood carboxyhemoglobin (COHb) levels while facilitating CO accumulation in renal tissue. This confirmed its ability to deliver CO to peripheral organs. Conclusion: the future of carbon monoxide Carbon monoxide has transitioned from being a notorious toxin to a valuable therapeutic agent. Advances in CO-releasing molecules have enabled its safe and controlled use, elevating its anti-inflammatory and protective properties to treat various inflammatory conditions effectively. This shift underpins the potential of CO to revolutionise inflammation therapy. It is important to remember that while carbon monoxide-releasing molecules (CORMs) have potential in controlled therapeutic settings, carbon monoxide gas itself remains highly toxic and should be handled with extreme caution to avoid serious health risks. Written by Baraytuk Aydin Related articles: Schizophrenia, inflammation and ageing / Kawasaki disease REFERENCES Different Faces of the Heme-Heme Oxygenase System in Inflammation - Scientific Figure on ResearchGate. Available from: https://www.researchgate.net/figure/The-colorimetric-actions-of-the-heme-HO-system-heme-oxygenase-mediated-heme-degradation_fig3_6531826 (accessed 11 Jul, 2024). Nath, K.A. (2006) Heme oxygenase-1: A provenance for cytoprotective pathways in the kidney and other tissues, Kidney International. Available at: https://www.sciencedirect.com/science/article/pii/S0085253815519595 (Accessed: 12 July 2024). Gáll, T. et al. (2020) ‘Therapeutic potential of carbon monoxide (CO) and hydrogen sulfide (H2S) in hemolytic and hemorrhagic vascular disorders—interaction between the heme oxygenase and H2S-producing systems’, International Journal of Molecular Sciences, 22(1), p. 47. doi:10.3390/ijms22010047. Venkat, A. (2024) Protein kinase, Wikipedia. Available at: https://en.wikipedia.org/wiki/Protein_kinase (Accessed: 12 July 2024). Foresti, R., Shurey, S., Mao, Q., Kitagishi, H., Green, C. J., & Motterlini, R. (2025). CORM-A1 delivers carbon monoxide to the kidney and alleviates post-ischemic renal dysfunction in rat and swine models. Physiological reports , 13 (22), e70666. https://doi.org/10.14814/phy2.70666 Goebel, U. and Wollborn, J. (2020) Carbon monoxide in intensive care medicine-time to start the therapeutic application?! - intensive care medicine experimental, SpringerOpen. Available at: https://icm-experimental.springeropen.com/articles/10.1186/s40635-020-0292-8 (Accessed: 07 July 2024). Bansal, S. et al. (2024) ‘Carbon monoxide as a potential therapeutic agent: A molecular analysis of its safety profiles’, Journal of Medicinal Chemistry, 67(12), pp. 9789–9815. doi:10.1021/acs.jmedchem.4c00823. DeSimone, C.A., Naqvi, S.L. and Tasker, S.Z. (2022) ‘Thiocormates: Tunable and cost‐effective carbon monoxide‐releasing molecules’, Chemistry – A European Journal, 28(41). doi:10.1002/chem.202201326. Project Gallery

A hereditary neurodegenerative disorder Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Huntington's disease 25/03/26, 16:52 Last updated: Published: 18/10/23, 17:12 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 people's 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

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: 29/03/26, 16:57 Published: 24/04/25, 08:00 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 around 260,000 breeding pairs of emperor penguins across 61 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). Fretwell, P. (2024) Four unreported emperor penguin colonies discovered by satellite. Antarctic Science , 36(4), 277–279. 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