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<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">PsyPost – Psychology News</span></td>
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<td><a href="https://www.psypost.org/new-research-show-how-tobacco-may-worsen-brain-related-outcomes-in-cannabis-users/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">New research show how tobacco may worsen brain-related outcomes in cannabis users</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 24th 2025, 10:00</div>
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<p><p>A new study suggests that people who use both cannabis and tobacco have elevated levels of a key enzyme in their brain compared to people who only use cannabis. This finding may offer a biological explanation for why combining these substances is often linked to more severe mental health symptoms and greater difficulty quitting. The research was published in the journal <em><a href="https://doi.org/10.1016/j.dadr.2025.100369" target="_blank">Drug and Alcohol Dependence Reports</a></em>.</p>
<p>The high rate of co-use between cannabis and tobacco products has long been a concern for public health experts. Studies have shown that individuals who use both substances often report worse clinical outcomes, including higher rates of depression and anxiety, when compared to those who use cannabis alone. Researchers from McGill University sought to understand the potential brain mechanisms that could be driving this difference.</p>
<p>The scientific team focused on the body’s endocannabinoid system, a complex cell-signaling network that helps regulate mood, appetite, and memory. A key component of this system is a naturally produced compound called anandamide. Lower levels of anandamide have been associated with poorer mental health, including increased symptoms of anxiety and depression.</p>
<p>The amount of anandamide in the brain is controlled by an enzyme called fatty acid amide hydrolase, or FAAH. The job of FAAH is to break down anandamide. When FAAH levels are high, more anandamide is broken down, leading to lower overall levels of this beneficial compound. The researchers proposed that tobacco use might increase FAAH levels, providing a reason for the negative outcomes observed in people who co-use cannabis and tobacco.</p>
<p>To investigate this possibility, the researchers recruited 13 participants who were regular cannabis users. They then divided these individuals into two groups based on their tobacco use. The first group consisted of five people who used both cannabis and at least one cigarette daily. The second group was made up of eight people who used cannabis but had no current tobacco use.</p>
<p>The two groups were closely matched on several characteristics, including age, sex, and patterns of cannabis consumption, such as how long they had been using and how much they used per week. This matching was done to help ensure that any observed differences in the brain were more likely related to tobacco use rather than other factors.</p>
<p>Each participant underwent a sophisticated brain imaging procedure known as positron emission tomography. This technique allows scientists to visualize and measure the activity of specific molecules in the living human brain. To measure FAAH levels, the researchers injected participants with a special imaging agent called [11C]CURB, which is designed to bind directly to the FAAH enzyme.</p>
<p>By tracking this imaging agent, the scanner could produce a map showing the concentration of FAAH in different parts of the brain. The researchers focused their analysis on six brain regions known to be rich in both cannabinoid and nicotine receptors, including the prefrontal cortex, hippocampus, and cerebellum. They also accounted for each participant’s sex and a common genetic variation that is known to influence FAAH levels.</p>
<p>The results of the brain scans revealed a distinct difference between the two groups. The individuals who used both cannabis and tobacco had consistently higher levels of the FAAH enzyme across all brain regions examined. The difference was statistically significant in two areas: the substantia nigra, a region involved in reward and movement, and the cerebellum, an area critical for motor control and cognitive functions.</p>
<p>A similar, though not statistically significant, trend was observed in the sensorimotor striatum. The magnitude of the difference in the substantia nigra and cerebellum was considered large, indicating a substantial biological effect. These findings provide the first direct evidence in humans that co-using tobacco is associated with higher FAAH activity than using cannabis alone.</p>
<p>The researchers also explored whether the amount of substance use was related to FAAH levels. They found a positive correlation between the number of cigarettes smoked per day and the level of FAAH in the cerebellum. This means that individuals who smoked more cigarettes tended to have higher concentrations of the enzyme in that brain region. In contrast, the team found no significant association between the amount of cannabis used and FAAH levels.</p>
<p>The study’s authors suggest that these elevated FAAH levels could be the mechanism underlying the poorer clinical outcomes seen in people who co-use. Higher FAAH would lead to lower anandamide, which in turn is linked to mood and anxiety problems. This offers a neurobiological pathway that could explain why this group often experiences greater mental health challenges and more severe withdrawal symptoms.</p>
<p>The researchers acknowledged several limitations to their study. First and foremost, the sample size was very small, meaning the results should be considered preliminary. Larger studies are needed to confirm these findings and to determine if the same pattern holds true in other brain regions.</p>
<p>Additionally, the study did not include a group of people who only used tobacco or a control group of non-users. Without these comparison groups, it is difficult to determine if the increased FAAH is due to tobacco use itself or a specific interaction between tobacco and cannabis. The study also did not directly measure participants’ levels of depression or anxiety, so it could not draw a direct line between FAAH levels and clinical symptoms.</p>
<p>Future research is needed to address these points. Scientists recommend conducting larger studies that include groups of tobacco-only users and healthy controls. Such studies could clarify the independent and combined effects of cannabis and tobacco on the endocannabinoid system. Connecting these brain measurements with clinical assessments of mood and anxiety would also be an important next step.</p>
<p>Despite its preliminary nature, this research opens up a new avenue for understanding the risks of combining cannabis and tobacco. If confirmed, the findings could point toward new therapeutic strategies. Medications that inhibit the FAAH enzyme are already under development, and this work suggests they might one day be a useful tool for treating cannabis use disorder, especially for the large number of individuals who also use tobacco.</p>
<p>The study, “<a href="https://www.sciencedirect.com/science/article/pii/S2772724625000526" target="_blank">A preliminary investigation of tobacco co-use on endocannabinoid activity in people with cannabis use</a>,” was authored by Rachel A. Rabin, Joseph Farrugia, Ranjini Garani, Romina Mizrahi, and Pablo Rusjan.</p></p>
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<td><a href="https://www.psypost.org/contrary-to-common-belief-research-reveals-some-brain-areas-expand-with-age/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Contrary to common belief, research reveals some brain areas expand with age</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 24th 2025, 08:00</div>
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<p><p>I recently asked myself if I’ll still have a healthy brain as I get older. I hold a professorship at a neurology department. Nevertheless, it is difficult for me to judge if a particular brain, including my own, suffers from early neurodegeneration.</p>
<p>My <a href="https://www.nature.com/articles/s41593-025-02013-1">new study</a>, however, shows that part of your brain increases in size with age rather than degenerating.</p>
<p>The reason it’s so hard to measure neurodegeneration is because of how complicated it is to measure small structures in our brain.</p>
<p>Modern neuroimaging technology allows us to <a href="https://pubmed.ncbi.nlm.nih.gov/14625465/">detect a brain tumour</a> or to identify an epileptic lesion. These abnormalities are several millimetres in size and can be depicted by a magnetic resonance imaging (MRI) scanner, which operates at around <a href="https://koppdevelopment.com/articels/MRI%20Safety%20at%203T%20VS%201-5T.pdf">30,000-60,000 times</a> stronger than the natural magnetic field of the Earth. The problem is that human thinking and perception operate at an even smaller scale.</p>
<p>Our <a href="https://www.annualreviews.org/content/journals/10.1146/annurev-cellbio-112122-032521">thinking and perception happens</a> in the neocortex. This <a href="https://www.sciencedirect.com/science/article/pii/S1053811917306821">outer part of our brain</a> consists of six layers. When you feel touch to your body, layer four of your sensory cortex gets activated. This layer is the width of a grain of sand – much smaller than what MRI scanners at hospitals can usually depict. When you modulate your body sensation, for example by trying to read this text rather than feeling the pain from your bad back, layers five and six of your sensory cortex get activated – which are even smaller than layer four.</p>
<p>For my study, published in the journal Nature Neuroscience, I had access to a 7 Tesla MRI scanner which offers five times better image resolution <a href="https://cdn0.scrvt.com/39b415fb07de4d9656c7b516d8e2d907/1800000003537381/2fb6832f1137/Magnetom-Flash-66_Clinical-Neuroimaging-at-7T-compared-to-Lower-Field-a-Photo-Essay_Jones_1800000003537381.pdf">than standard MRI scanners</a>. It makes snapshots of the fine-scale brain networks during perception and thought visible.</p>
<p>Using a 7 Tesla scanner, my team and I investigated the sensory cortex in healthy younger adults (around 25 years old) and healthy older adults (around 65 years old) to better understand brain ageing. We found that only layers five and six, which <a href="https://pubmed.ncbi.nlm.nih.gov/19277215/">modulate body perception</a>, showed signs of age-related degeneration.</p>
<p>Layer four, <a href="https://pubmed.ncbi.nlm.nih.gov/21047937/">needed to feel touch</a> to your body, was enlarged in healthy older adults in my study. We also did a comparative study with mice. We found similar results in the older mice, in that they also had a more pronounced layer four than the younger mice. However evidence from our study of mice, which included a third group of very old mice, showed this part of the brain may degenerate in more advanced old age.</p>
<p><a href="https://pubmed.ncbi.nlm.nih.gov/34096114/">Current theories</a> assume our brain gets smaller as we grow older. But my team’s findings contradict these theories in part. It is the first evidence that some parts of the brain get bigger with age in normal older adults.</p>
<p>Older adults with a thicker layer four would be expected to be more sensitive to touch and pain, and (due to the reduced deep layers) have difficulties modulating such sensations.</p>
<p>To understand this effect better, we studied a middle-aged patient who was born without one arm. This patient had a smaller layer four. This suggests their brain received fewer impulses in comparison to a person with two arms and therefore developed less mass in layer four. Parts of the brain that are used more <a href="https://www.science.org/doi/10.1126/science.1085423?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%20%200pubmed">develop more synapses</a>, hence more mass.</p>
<p>Rather than systematically degenerating, older adults’ brains seem to preserve what they use, at least in part. Brain ageing may be compared with a complex machinery in which some often used parts are well oiled, while others less frequently used get roasted. From that perspective, brain ageing is individual, shaped by our lifestyle, including our sensory experiences, reading habits, and cognitive challenges that we take on in everyday life.</p>
<p>In addition, it shows that the brains of healthy older adults preserve their capacity to stay in tune with their surroundings.</p>
<h2>A lifetime of experiences</h2>
<p>There is another interesting aspect about the results. The pattern of brain changes that we found in older adults – a stronger sensory processing region and a reduced modulatory region – shows similarities to neurodivergent disorders such as the autism spectrum disorder or attention deficit hyperactivity disorder.</p>
<p>Neurodivergent disorders are characterised by enhanced <a href="https://pubmed.ncbi.nlm.nih.gov/39515075/">sensory sensitivity</a> and reduced filtering abilities, leading to problems in concentration and cognitive flexibility.</p>
<p>Do our findings indicate that ageing drives the brain in the direction of neurodivergent disorders? Older adults brains have been formed by a lifetime of experiences whereas neurodivergent people are born with these brain patterns. So it would be hard to know what other effects building brain mass with age might have.</p>
<p>Yet, our findings give us some us clues about why older adults sometimes have difficulties adapting to new sensory environments. In such situations, for example being confronted with a new technical device or visiting a new city, the reduced modulatory abilities of layers five and six may become particularly evident, and may increase the likelihood for disorientation or confusion. It may also explain reduced abilities for multitasking with age, such as using a mobile phone while walking. Sensory information needs to be modulated to avoid interference when you’re doing more than one thing.</p>
<p>Both the middle and the deep layers had more myelin, a fatty protective layer that is crucial for nerve function and communication, in the older mice as well as humans. This suggests that in people over the age of 65, there is a compensatory mechanism for the loss of modulatory function. This effect seemed to be breaking down in the very old mice though.</p>
<p>Our results provide evidence for the power of a person’s lifestyle for shaping the ageing brain.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/257156/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/part-of-your-brain-gets-bigger-as-you-get-older-here-is-what-that-means-for-you-257156">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/parkinsons-linked-protein-clumps-destroy-brains-primary-energy-molecule/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Parkinson’s-linked protein clumps destroy brain’s primary energy molecule</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 24th 2025, 06:00</div>
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<p><p>A new scientific report reveals that the protein aggregates associated with Parkinson’s disease are not inert clumps of cellular waste, but rather are chemically active structures that can systematically destroy the primary energy molecule used by brain cells. The research, published in the journal <em><a href="https://advanced.onlinelibrary.wiley.com/doi/10.1002/advs.202508441" target="_blank">Advanced Science</a></em>, demonstrates that these protein plaques can function like tiny, rogue enzymes, breaking down adenosine triphosphate and potentially starving neurons of the power they need to survive and function.</p>
<p>Scientists have long sought to understand how the accumulation of protein clumps, known as amyloids, leads to the devastating neuronal death seen in neurodegenerative conditions like Parkinson’s disease. These clumps are primarily made of a misfolded protein called alpha-synuclein. </p>
<p>The prevailing view has been that these aggregates cause harm by physically disrupting cellular processes, poking holes in membranes, or sequestering other important proteins. However, a team of researchers led by Pernilla Wittung-Stafshede at Rice University suspected there might be more to the story.</p>
<p>Previous work from the same group had shown that alpha-synuclein amyloids were not chemically inactive. They could facilitate certain chemical reactions on simple model compounds in a test tube. This led the researchers to question if these amyloids could also act on biologically significant molecules inside a cell. They focused on one of the most fundamental molecules in all of life: adenosine triphosphate, the universal energy currency that powers nearly every cellular activity. </p>
<p>Neurons have exceptionally high energy demands and cannot store fuel, making them particularly vulnerable to any disruption in their adenosine triphosphate supply. The team hypothesized that if amyloids could break down this vital molecule, it would represent a completely new way these pathological structures exert their toxicity.</p>
<p>To investigate this possibility, the scientists conducted a series of experiments. First, they needed to confirm that adenosine triphosphate even interacts with the alpha-synuclein amyloids. They used a chemical reaction they had previously studied, where the amyloids break down a substance called para-nitrophenyl orthophosphate. </p>
<p>When they added adenosine triphosphate to this mixture, the original reaction stopped. This competitive effect suggested that adenosine triphosphate was binding to the same active location on the amyloid surface, pushing the other substance out of the way.</p>
<p>Having established that adenosine triphosphate binds to the amyloids, the researchers then tested whether it was being broken down. They mixed prepared alpha-synuclein amyloids with a solution of adenosine triphosphate and used a diagnostic tool called the Malachite Green assay, which changes color in the presence of free phosphate, a byproduct of adenosine triphosphate breakdown. </p>
<p>They observed a steady increase in free phosphate over time, confirming that the amyloids were indeed cleaving the phosphate bonds in adenosine triphosphate. This activity was catalytic, meaning a single amyloid structure could process many molecules of adenosine triphosphate, one after another. The same experiment performed with individual, non-clumped alpha-synuclein proteins showed no such effect, indicating this energy-draining ability is a feature specific to the aggregated, amyloid form.</p>
<p>To understand the mechanism behind this chemical activity, the team used a powerful imaging technique known as cryogenic electron microscopy. This method allowed them to visualize the structure of the alpha-synuclein amyloid at a near-atomic level of detail while it was bound to adenosine triphosphate. </p>
<p>The resulting images revealed a remarkable transformation. The amyloid itself was formed from two intertwined filaments, creating a cavity between them. When adenosine triphosphate entered this cavity, a normally flexible and disordered segment of the alpha-synuclein protein, consisting of amino acids 16 through 22, folded into an ordered beta-strand. This newly formed structure acted like a lid, closing over the cavity and trapping the adenosine triphosphate molecule inside.</p>
<p>This enclosed pocket was lined with several positively charged amino acids called lysines. Since the phosphate tail of adenosine triphosphate is strongly negatively charged, these lysines likely serve to attract and hold the energy molecule in a specific orientation. The structure suggested that this induced-fit mechanism, where the amyloid changes its shape upon binding its target, was a key part of its chemical function.</p>
<p>To prove that these specific lysine residues were responsible for the activity, the researchers genetically engineered several mutant versions of the alpha-synuclein protein. In each version, they replaced one or more of the key lysines in the cavity with a neutral amino acid, alanine. These mutant proteins were still able to form amyloid clumps that looked similar to the original ones.</p>
<p>When they tested the mutant amyloids for their ability to break down adenosine triphosphate, they found the activity was almost completely gone. This result confirmed that the positively charged lysines are essential for the amyloid’s ability to perform the chemical reaction.</p>
<p>In a final step, the scientists solved the high-resolution structure of one of the inactive mutant amyloids (K21A) while it was bound to adenosine triphosphate. The images showed that the energy molecule could still sit in the cavity, but its orientation was different from that seen in the active, non-mutant amyloid. </p>
<p>More importantly, in this inactive complex, the flexible protein segment did not fold over to form the enclosing lid. This finding provided strong evidence that both the proper positioning of adenosine triphosphate by the lysines and the structural rearrangement that closes the cavity are necessary for the breakdown to occur.</p>
<p>The study does have some limitations. The experiments were conducted in a controlled laboratory setting, not in living cells or organisms. The specific structural form of the alpha-synuclein amyloid studied, known as polymorph type 1A, has not yet been identified in the brains of Parkinson’s patients, although similar structures exist. </p>
<p>Also, the rate at which the amyloids broke down adenosine triphosphate was slow compared to natural enzymes. Future research will need to determine if this process occurs within the complex environment of a neuron and if other, more clinically relevant amyloid forms share this toxic capability.</p>
<p>Despite these caveats, the findings introduce a new and potentially significant mechanism of neurodegeneration. The researchers suggest that even a slow reaction could have a profound local effect. An amyloid plaque contains a very high density of these active sites. This could create a zone of severe energy depletion in the immediate vicinity of the plaque, disabling essential cellular machinery. </p>
<p>For instance, cells use chaperone proteins that require adenosine triphosphate to try to break up these very amyloids. If the chaperones approach an amyloid plaque and enter an energy-depleted zone, their rescue function could be disabled, effectively allowing the plaque to protect itself and persist. This work transforms the view of amyloids from passive obstacles into active metabolic drains, opening new avenues for understanding and potentially treating Parkinson’s disease.</p>
<p>The study, “<a href="https://doi.org/10.1002/advs.202508441" target="_blank">ATP Hydrolysis by α-Synuclein Amyloids is Mediated by Enclosing β-Strand</a>,” was authored by Lukas Frey, Fiamma Ayelen Buratti, Istvan Horvath, Shraddha Parate, Ranjeet Kumar, Roland Riek, and Pernilla Wittung-Stafshede.</p></p>
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<td><a href="https://www.psypost.org/genetic-predisposition-for-inflammation-linked-to-a-distinct-metabolic-subtype-of-depression/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Genetic predisposition for inflammation linked to a distinct metabolic subtype of depression</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Oct 23rd 2025, 12:00</div>
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<p><p>A new study suggests that a person’s genetic predisposition for chronic inflammation helps define a specific subtype of depression linked to metabolic issues. The research also found this genetic liability is connected to antidepressant treatment outcomes in a complex, nonlinear pattern. The findings were published in the journal <em><a href="https://doi.org/10.61373/gp025r.0092" target="_blank">Genomic Psychiatry</a></em>.</p>
<p>Major depressive disorder is a condition with wide-ranging symptoms and variable responses to treatment. Many patients do not find relief from initial therapies, a reality that has pushed scientists to search for biological markers that could help explain this diversity and guide more personalized medical care. One area of growing interest is the connection between depression and the body’s immune system, specifically chronic low-grade inflammation. A key blood marker for inflammation is C-reactive protein, which is often found at elevated levels in people with depression.</p>
<p>However, measuring C-reactive protein directly from blood samples can be problematic for research because levels can fluctuate based on diet, infection, or stress. An international team of researchers, led by Alessandro Serretti of Kore University of Enna, Italy, sought a more stable way to investigate the link between inflammation and depression. They turned to genetics, using a tool known as a polygenic score. This score summarizes a person’s inherited, lifelong tendency to have higher or lower levels of C-reactive protein. While previous studies have connected this genetic score to specific depressive symptoms or to treatment outcomes separately, this new research aimed to examine both within the same large group of patients to build a more complete picture.</p>
<p>The investigation involved 1,059 individuals of Caucasian descent who were part of the European Group for the Study of Resistant Depression. All participants had a diagnosis of major depressive disorder and had been receiving antidepressant medication for at least four weeks. Researchers collected detailed clinical information, including the severity of depressive symptoms, which was assessed using the Montgomery–Åsberg Depression Rating Scale. Based on their response to medication, patients were categorized as responders, nonresponders, or as having treatment-resistant depression if they had not responded to two or more different antidepressants.</p>
<p>For each participant, the science team calculated a polygenic score for C-reactive protein. This was accomplished by analyzing each person’s genetic data and applying a statistical model developed from a massive genetic database, the UK Biobank. The resulting score provided a single, stable measure of each individual’s genetic likelihood of having high inflammation. The researchers then used statistical analyses to look for connections between these genetic scores and the patients’ symptoms, clinical characteristics, and their ultimate response to antidepressant treatment.</p>
<p>The results showed a clear link between a higher genetic score for C-reactive protein and a specific profile of symptoms and characteristics. Individuals with a greater genetic tendency for inflammation were more likely to have a higher body mass index and a lower employment status. They also reported less weight loss and appetite reduction during their depressive episodes, which are symptoms associated with metabolic function. The genetic score was not associated with the overall severity of depression or with core emotional symptoms like sadness or pessimism. This suggests that the genetic influence of inflammation is tied to a particular cluster of physical and metabolic symptoms, sometimes referred to as an immunometabolic subtype of depression.</p>
<p>When the researchers examined the connection to treatment outcomes, they discovered a more complicated relationship. The link was not a simple straight line where more inflammation meant a worse outcome. Instead, they observed what is described as a nonlinear or U-shaped pattern. Patients who did not respond to treatment tended to have the lowest genetic scores for C-reactive protein. In contrast, both patients who responded well to their medication and those with treatment-resistant depression had higher genetic scores. The very highest scores were observed in the group with treatment-resistant depression.</p>
<p>This complex finding remained significant even after the researchers statistically accounted for a range of other factors known to influence treatment success, such as the patient’s age, the duration of their illness, and the number of previous antidepressant trials. The genetic score for C-reactive protein independently explained an additional 1.9 percent of the variation in treatment outcomes. While a modest figure, it indicates that genetic information about inflammation provides a unique piece of the puzzle that is not captured by standard clinical measures. This U-shaped relationship echoes previous findings that used direct blood measurements of C-reactive protein, suggesting that both very high and very low levels of inflammation may be associated with different treatment pathways.</p>
<p>The researchers note some limitations of their work. The study’s design was cross-sectional, meaning it captures a single point in time and cannot prove that the genetic predisposition for inflammation causes certain symptoms or treatment outcomes. The participants were treated naturalistically with a variety of medications, which reflects real-world clinical practice but lacks the control of a randomized trial. Additionally, the sample consisted exclusively of individuals with European ancestry, so the findings may not be applicable to people from other backgrounds. The team also suggests that replication in other large studies is needed.</p>
<p>For future research, the authors propose integrating genetic scores with direct measurements of inflammatory biomarkers from blood tests. This combined approach could provide a more powerful tool for understanding both a person’s lifelong tendency and their current inflammatory state. Ultimately, this line of research could help refine psychiatric diagnosis and treatment. By identifying an immunometabolic subtype of depression, it may be possible to develop more targeted therapies. The findings contribute to a growing body of evidence supporting a move away from a “one-size-fits-all” approach to depression, opening the door for inflammation-guided strategies in personalized psychiatry.</p>
<p>The study, “<a href="https://doi.org/10.61373/gp025r.0092" target="_blank">Polygenic liability to C-reactive protein defines immunometabolic depression phenotypes and influences antidepressant therapeutic outcomes</a>,” was authored by Alessandro Serretti, Daniel Souery, Siegfried Kasper, Lucie Bartova, Joseph Zohar, Stuart Montgomery, Panagiotis Ferentinos, Dan Rujescu, Raffaele Ferri, Giuseppe Fanelli, Raffaella Zanardi, Francesco Benedetti, Bernhard T. Baune, and Julien Mendlewicz.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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