How climate warming could disrupt a deep-rooted relationship

Researchers from Syracuse University and the University of Minnesota find that warming trends will likely result in major disturbances of networks of fungi potentially harming forest resilience

Peer-Reviewed Publication

SYRACUSE UNIVERSITY

 

IMAGE: AMANITA MUSCARIA, AN ECTOMYCORRHIZAL FUNGUS, FROM THE B4WARMED EXPERIMENT. THESE TYPES OF FUNGI PLAY AN IMPORTANT ROLE IN FOREST HEALTH AND MAY BE IN DANGER UNDER CURRENT LEVELS OF CLIMATE WARMING. view more 

CREDIT: LOUIS MIELKE

Children are taught to leave wild mushrooms alone because of their potential to be poisonous. But trees on the other hand depend on fungi for their well-being. Look no further than ectomycorrhizal fungi, which are organisms that colonize the roots of many tree species where the boreal ecosystem (zone encompassing Earth’s northernmost forests) and the temperate ecosystem (zone between the tropical and boreal regions) meet. This area features a mix of boreal trees including needle-leaved evergreens and temperate tree species including maple and oak.

Just like a healthy human relationship, trees and fungi work well together because they help one another. When the ectomycorrhizal fungi attach themselves to tree roots, they acquire carbon in the form of sugars from their tree hosts and in turn provide the trees with important nutrients like nitrogen and phosphorous. It’s an important symbiotic relationship that drives ecosystem function and resilience.

But as climate change and global warming cause higher temperatures and amplified drought, little is known about how these important fungi will respond. Additionally, there are lingering questions about how climate warming will impact the underground threads – known as ectomycorrhizal networks - formed by fungi that connects trees and facilitates the transfer of water, nitrogen and other minerals.

To investigate this issue, a research team from Syracuse University and the University of Minnesota conducted a climate change experiment where they exposed boreal and temperate tree species to warming and drought treatments to better understand how fungi and their tree hosts respond to environmental changes.

The study, led by Christopher W. Fernandez, assistant professor of biology in Syracuse University’s College of Arts and Sciences, was recently published in the journal Proceedings of the National Academy of Sciences (PNAS). Their findings revealed that the combined effects of warming and water stress will likely result in major disturbances of ectomycorrhizal networks and may harm forest resilience and function.

The team conducted their work at a long-term climate change experiment called B4WARMED (Boreal Forest Warming at an Ecotone in Danger) in Minnesota. The experiment features plots where both boreal and temperate tree species have been planted and exposed to warming and drought treatments. This allows researchers to explore how the ectomycorrhizal fungi and the networks they form with their tree hosts respond to environmental stressors.

Fernandez, whose research aims to understand processes involving plant, microbial and ecosystem ecology, says their study revealed that composition of ectomycorrhizal fungal species changes dramatically with climate change. Specifically, they saw a shift from species commonly found in mature forests that have high biomass mycelium (the thread-like body of the fungus that explores the soil and that is likely important for network formation) towards low biomass species that are generally found in highly disturbed ecosystems.

“There is a supported hypothesis that these low biomass species probably do not provide the host much benefit in terms of nutrition compared to high biomass species,” says Fernandez. “We found that the networks formed by these fungi that ‘connect’ the trees shifted from relatively complex and well-connected networks to ones that are simpler with less connections.”

Fungal mycelium is a network of thread-like tissue filaments that help plants and trees share nutrients. (Credit: Christopher Fernandez)

The authors say these shifts were significantly related to the performance of the tree hosts and their ability to convert carbon dioxide into oxygen and sugars through photosynthesis. “Climate change is reducing the amount of carbon the trees fix and likely has cascading effects on how much carbon they can provide to their ectomycorrhizal fungi,” continues Fernandez. “This is likely causing a shift towards low biomass species, resulting in the breakdown of networks between trees.”

The research team believes this to be the first study examining the response of ectomycorrhizal networks to climate change and their results should generate new research focusing on other ecosystems. Building on this work, they say the next step will be to link the changes in ectomycorrhizal networks to ecosystem level processes such as nutrient and carbon cycling to better understand how resilient they are to changing climate.

Full publication citation: Christopher W. Fernandez, Louis Mielke, Artur Stefanski, Raimundo Bermudez, Sarah E. Hobbie, Rebecca A. Montgomery, Peter B. Reich, Peter G. Kennedy; Climate change–induced stress disrupts ectomycorrhizal interaction networks at the boreal–temperate ecotone. PNAS August 2023; 120 (34): e2221619120. doi: https://doi.org/10.1073/pnas.2221619120

The B4WARMED experiment features forest plots warmed with infrared lamps and soil heating cables allowing researchers to study the effects of climate warming.

CREDIT

Louis Mielke

Fungal mycelium is a network of thread-like tissue filaments that help plants and trees share nutrients.

CREDIT

Christopher Fernandez, Syracuse University

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JOURNAL

Proceedings of the National Academy of Sciences

DOI

10.1073/pnas.2221619120 

ARTICLE TITLE

Climate change–induced stress disrupts ectomycorrhizal interaction networks at the boreal–temperate ecotone

 

Researchers reveal novel AI-based camera alert system to promote coexistence between tigers and humans

Peer-Reviewed Publication

AMERICAN INSTITUTE OF BIOLOGICAL SCIENCES

 

IMAGE: THE TRAILGUARD AI CAMERA SYSTEM (LEFT, US QUARTER FOR SCALE) CAN BE WELL CAMOUFLAGED NEAR A TRAIL SUCH AS THIS ONE IN DUDHWA TIGER RESERVE, AS SEEN FROM THE TRAIL, THAT SENT MULTIPLE REAL-TIME NOTIFICATIONS OF POACHERS WITHOUT BEING DETECTED (RIGHT). view more 

CREDIT: TRAILGUARD AI

For decades, wildlife biologists have dreamt of a “smart” camera alerting system capable of detecting tigers and other endangered species on the prowl. Legacy camera-trap technology, while valuable for many research applications, has historically been hindered by false positives and an inability to facilitate rapid responses.

            Writing in BioScience, Jeremy Dertien of Clemson University and colleagues announce that for the first time ever, wild tigers and elephants have been detected by an artificial intelligence (AI)-powered, cryptic camera-alert system, TrailGuard AI, that transmits images to the cell phones and computers of park managers and other concerned entities in real time.

            The technology, originally developed to detect poachers, limits false positives, and its fast alert times permit "park managers the chance for rapid response to intrusion by poachers or to alert villagers to the nearby presence of tigers," according to the authors. Dertien and colleagues describe the first months of field deployment in India during the monsoon period of 2022, when TrailGuard AI was immediately useful in detecting tigers moving close to villages and using the same trails as wildlife poachers.

            Such technology is expected to be a valuable tool in mitigating human–wildlife conflict and furthering conservation efforts, report the authors. However, cautions coauthor Hrishita Negi, “integrating communities is essential for coexistence to work." Efforts are under way to educate those who may use the system and foster greater uptake of this and other valuable technologies.

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This work was supported by the Global Tiger Forum, National Tiger Conservation Authority, Clemson University, and the nongovernmental organization RESOLVE.

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JOURNAL

BioScience

DOI

10.1093/biosci/biad076/7261057 

METHOD OF RESEARCH

Experimental study

SUBJECT OF RESEARCH

Animals

ARTICLE TITLE

Mitigating human–wildlife conflict and monitoring endangered tigers using a real-time camera-based alert system

The Tyger 

BY WILLIAM BLAKE

Tyger Tyger, burning bright, 

In the forests of the night; 

What immortal hand or eye, 

Could frame thy fearful symmetry?

In what distant deeps or skies. 

Burnt the fire of thine eyes?

On what wings dare he aspire?

What the hand, dare seize the fire?

And what shoulder, & what art,

Could twist the sinews of thy heart?

And when thy heart began to beat.

What dread hand? & what dread feet?

What the hammer? what the chain,

In what furnace was thy brain?

What the anvil? what dread grasp.

Dare its deadly terrors clasp?

When the stars threw down their spears 

And water'd heaven with their tears:

Did he smile his work to see?

Did he who made the Lamb make thee?

Tyger Tyger burning bright,

In the forests of the night:

What immortal hand or eye,

Dare frame thy fearful symmetry?

Blake, William. "The Tyger." ​​​​​​​​​​​​​​Songs of Experience. ​​​​​​​Facsimile reproduction of the 1794 illuminated manuscript, published by The William Blake Trust and the Tate Gallery, 2009, in ​​​​​​​William Blake: The Complete Illuminated Books.

 

How to tackle the global deforestation crisis

Vital forest is cleared every day, with major climate effects. Satellites have revolutionized measurement of the problem, but what can we do about it?

Peer-Reviewed Publication

MASSACHUSETTS INSTITUTE OF TECHNOLOGY

Imagine if France, Germany, and Spain were completely blanketed in forests — and then all those trees were quickly chopped down. That’s nearly the amount of deforestation that occurred globally between 2001 and 2020, with profound consequences. 

Deforestation is a major contributor to climate change, producing between 6 and 17 percent of global greenhouse gas emissions, according to a 2009 study. Meanwhile, because trees also absorb carbon dioxide, removing it from the atmosphere, they help keep the Earth cooler. And climate change aside, forests protect biodiversity. 

“Climate change and biodiversity make this a global problem, not a local problem,” says MIT economist Ben Olken. “Deciding to cut down trees or not has huge implications for the world.” 

But deforestation is often financially profitable, so it continues at a rapid rate. Researchers can now measure this trend closely: In the last quarter-century, satellite-based technology has led to a paradigm change in charting deforestation. New deforestation datasets, based on the Landsat satellites, for instance, track forest change since 2000 with resolution at 30 meters, while many other products now offer frequent imaging at close resolution. 

“Part of this revolution in measurement is accuracy, and the other part is coverage,” says Clare Balboni, an assistant professor of economics at the London School of Economics (LSE). “On-site observation is very expensive and logistically challenging, and you’re talking about case studies. These satellite-based data sets just open up opportunities to see deforestation at scale, systematically, across the globe.”

Balboni and Olken have now helped write a new paper providing a road map for thinking about this crisis. The open-access article, “The Economics of Tropical Deforestation,” appears this month in the Annual Review of Economics. The co-authors are Balboni, a former MIT faculty member; Aaron Berman, a PhD candidate in MIT’s Department of Economics; Robin Burgess, an LSE professor; and Olken, MIT’s Jane Berkowitz Carlton and Dennis William Carlton Professor of Microeconomics. Balboni and Olken have also conducted primary research in this area, along with Burgess.

So, how can the world tackle deforestation? It starts with understanding the problem. 

Replacing forests with farms

Several decades ago, some thinkers, including the famous MIT economist Paul Samuelson in the 1970s, built models to study forests as a renewable resource; Samuelson calculated the “maximum sustained yield” at which a forest could be cleared while being regrown. These frameworks were designed to think about tree farms or the U.S. national forest system, where a fraction of trees would be cut each year, and then new trees would be grown over time to take their place.

But deforestation today, particularly in tropical areas, often looks very different, and forest regeneration is not common. 

Indeed, as Balboni and Olken emphasize, deforestation is now rampant partly because the profits from chopping down trees come not just from timber, but from replacing forests with agriculture. In Brazil, deforestation has increased along with agricultural prices; in Indonesia, clearing trees accelerated as the global price of palm oil went up, leading companies to replace forests with palm tree orchards. 

All this tree-clearing creates a familiar situation: The globally shared costs of climate change from deforestation are “externalities,” as economists say, imposed on everyone else by the people removing forest land. It is akin to a company that pollutes into a river, affecting the water quality of residents. 

“Economics has changed the way it thinks about this over the last 50 years, and two things are central,” Olken says. “The relevance of global externalities is very important, and the conceptualization of alternate land uses is very important.” This also means traditional forest-management guidance about regrowth is not enough. With the economic dynamics in mind, which policies might work, and why? 

The search for solutions

As Balboni and Olken note, economists often recommend “Pigouvian” taxes (named after the British economist Arthur Pigou) in these cases, levied against people imposing externalities on others. And yet, it can be hard to identify who is doing the deforesting. 

Instead of taxing people for clearing forests, governments can pay people to keep forests intact. The UN uses Payments for Environmental Services (PES) as part of its REDD+ (Reducing Emissions from Deforestation and forest Degradation) program. However, it is similarly tough to identify the optimal landowners to subsidize, and these payments may not match the quick cash-in of deforestation. A 2017 study in Uganda showed PES reduced deforestation somewhat; a 2022 study in Indonesia found no reduction; another 2022 study, in Brazil, showed again that some forest protection resulted. 

“There’s mixed evidence from many of these [studies],” Balboni says. These policies, she notes, must reach people who would otherwise clear forests, and a key question is, “How can we assess their success compared to what would have happened anyway?” 

Some places have tried cash transfer programs for larger populations. In Indonesia, a 2020 study found such subsidies reduced deforestation near villages by 30 percent. But in Mexico, a similar program meant more people could afford milk and meat, again creating demand for more agriculture and thus leading to more forest-clearing. 

At this point, it might seem that laws simply banning deforestation in key areas would work best — indeed, about 16 percent of the world’s land overall is protected in some way. Yet the dynamics of protection are tricky. Even with protected areas in place, there is still “leakage” of deforestation into other regions.  

Still more approaches exist, including “nonstate agreements,” such as the Amazon Soy Moratorium in Brazil, in which grain traders pledged not to buy soy from deforested lands, and reduced deforestation without “leakage.” 

Also, intriguingly, a 2008 policy change in the Brazilian Amazon made agricultural credit harder to obtain by requiring recipients to comply with environmental and land registration rules. The result? Deforestation dropped by up to 60 percent over nearly a decade.  

Politics and pulp

Overall, Balboni and Olken observe, beyond “externalities,” two major challenges exist. One, it is often unclear who holds property rights in forests. In these circumstances, deforestation seems to increase. Two, deforestation is subject to political battles. 

For instance, as economist Bard Harstad of Stanford University has observed, environmental lobbying is asymmetric. Balboni and Olken write: “The conservationist lobby must pay the government in perpetuity … while the deforestation-oriented lobby need pay only once to deforest in the present.” And political instability leads to more deforestation because “the current administration places lower value on future conservation payments.”

Even so, national political measures can work. In the Amazon from 2001 to 2005, Brazilian deforestation rates were three to four times higher than on similar land across the border, but that imbalance vanished once the country passed conservation measures in 2006. However, deforestation ramped up again after a 2014 change in government. Looking at particular monitoring approaches, a study of Brazil’s satellite-based Real-Time System for Detection of Deforestation (DETER), launched in 2004, suggests that a 50 percent annual increase in its use in municipalities created a 25 percent reduction in deforestation from 2006 to 2016.

How precisely politics matters may depend on the context. In a 2021 paper, Balboni and Olken (with three colleagues) found that deforestation actually decreased around elections in Indonesia. Conversely, in Brazil, one study found that deforestation rates were 8 to 10 percent higher where mayors were running for re-election between 2002 and 2012, suggesting incumbents had deforestation industry support. 

“The research there is aiming to understand what the political economy drivers are,” Olken says, “with the idea that if you understand those things, reform in those countries is more likely.”

Looking ahead, Balboni and Olken also suggest that new research estimating the value of intact forest land intact could influence public debates. And while many scholars have studied deforestation in Brazil and Indonesia, fewer have examined the Democratic Republic of Congo, another deforestation leader, and sub-Saharan Africa. 

Deforestation is an ongoing crisis. But thanks to satellites and many recent studies, experts know vastly more about the problem than they did a decade or two ago, and with an economics toolkit, can evaluate the incentives and dynamics at play. 

“To the extent that there’s ambuiguity across different contexts with different findings, part of the point of our review piece is to draw out common themes — the important considerations in determining which policy levers can [work] in different circumstances,” Balboni says. “That’s a fast-evolving area. We don’t have all the answers, but part of the process is bringing together growing evidence about [everything] that affects how successful those choices can be.” 

###

Written by Peter Dizikes, MIT News

Paper: “The Economics of Tropical Deforestation”

https://www.annualreviews.org/doi/abs/10.1146/annurev-economics-090622-024705

 

 

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JOURNAL

Annual Review of Economics

DOI

10.1146/annurev-economics-090622-024705 

ARTICLE TITLE

"The Economics of Tropical Deforestation"

 

Genetic biomarker may predict severity of food allergy

Offers potential for determining the risk of severe reactions for patients and families with food allergies

Peer-Reviewed Publication

ANN & ROBERT H. LURIE CHILDREN'S HOSPITAL OF CHICAGO

Researchers from Ann & Robert H. Lurie Children’s Hospital of Chicago and colleagues reported for the first time that a genetic biomarker may be able to help predict the severity of food allergy reactions. Currently there is no reliable or readily available clinical biomarker that accurately distinguishes patients with food allergies who are at risk for severe life-threatening reactions versus more mild symptoms. Findings were published in the Journal of Allergy and Clinical Immunology.

Dr. Lang and colleagues found that the presence of an enzyme isoform called α-tryptase, which is encoded by the TPSAB1 gene, correlates with increased prevalence of anaphylaxis or severe reaction to food as compared to subjects without any α-tryptase.

“Determining whether or not a patient with food allergies has α-tryptase can easily be done in clinical practice using a commercially available test to perform genetic sequencing from cheek swabs,” said lead author Abigail Lang, MD, MSc, attending physician and researcher at Lurie Children’s and Assistant Professor of Pediatrics at Northwestern University Feinberg School of Medicine. “If the biomarker is detected, this may help us understand that the child is at a higher risk for a severe reaction or anaphylaxis from their food allergy and should use their epinephrine auto-injector if exposed to the allergen. Our findings also open the door to developing an entirely new treatment strategy for food allergies that would target or block α-tryptase. This is an exciting first step and more research is needed.”

Tryptase is found mainly in mast cells, which are white blood cells that are part of the immune system. Mast cells become activated during allergic reactions. Increased TPSAB1 copy number which leads to increased α-tryptase is already known to be associated with severe reactions in adults with Hymenoptera venom allergy (or anaphylaxis following a bee sting).

Dr. Lang’s study included 119 participants who underwent TPSAB1 genotyping, 82 from an observational food allergy cohort at the National Institute of Allergy and Infectious Diseases (NIAID) and 37 from a cohort of children who reacted to peanut oral food challenge at Lurie Children’s.

“We need to validate our preliminary findings in a much larger study, but these initial results are promising,” says Dr. Lang. “We also still need a better understanding of why and how α-tryptase makes food allergy reactions more severe in order to pursue this avenue for potential treatment.”

Rajesh Kumar, MD, MSc, from Lurie Children’s is the co-senior author on the study. Dr. Kumar is the Interim Division Head of Allergy and Immunology and Professor of Pediatrics at Northwestern University Feinberg School of Medicine.

This work was supported in part by the Midwest Allergy Research Institute (MARI) Food Allergy Pilot Research Award and NIAID-sponsored T32 grant AI083216. This project was funded in part with federal funds from the Division of Intramural Research of the National Institute of Allergy and Infectious Diseases, NIH. This project has also been funded in whole or in part with federal funds from the National Cancer Institute, National Institutes of Health, under Contract No. 75N91019D00024.

Research at Ann & Robert H. Lurie Children’s Hospital of Chicago is conducted through Stanley Manne Children’s Research Institute. The Manne Research Institute is focused on improving child health, transforming pediatric medicine and ensuring healthier futures through the relentless pursuit of knowledge. Lurie Children’s is a nonprofit organization committed to providing access to exceptional care for every child. It is ranked as one of the nation’s top children’s hospitals by U.S. News & World Report. Lurie Children’s is the pediatric training ground for Northwestern University Feinberg School of Medicine.

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JOURNAL

Journal of Allergy and Clinical Immunology

DOI

10.1016/j.jaci.2023.07.014 

 

Newly discovered bone stem cell causes premature skull fusion

Peer-Reviewed Publication

WEILL CORNELL MEDICINE

 

IMAGE: A CONCEPTUAL RENDERING OF HOW A NEW STEM CELL IN THE JOINTS BETWEEN THE FLAT BONES OF THE SKULL DRIVES SKULL GROWTH AND FUSION. view more 

CREDIT: AI IMAGE GENERATED USING MIDJOURNEY ON MAY 24, 2023; PROVIDED BY THE GREENBLATT LAB.

Craniosynostosis, the premature fusion of the top of the skull in infants, is caused by an abnormal excess of a previously unknown type of bone-forming stem cell, according to a preclinical study led by researchers at Weill Cornell Medicine.

Craniosynostosis arises from one of several possible gene mutations, and occurs in about one in 2,500 babies. By constricting brain growth, it can lead to abnormal brain development if not corrected surgically. In complex cases, multiple surgeries are needed.

In the study, which appears Sept. 20 in Nature, the researchers examined in detail what happens in the skull of mice with one of the most common mutations found in human craniosynostosis. They found that the mutation drives premature skull fusion by inducing the abnormal proliferation of a type of bone-making stem cell—the DDR2+ stem cell—that had never been described before.

“We can now start to think about treating craniosynostosis not just with surgery but also by blocking this abnormal stem cell activity,” said study co-senior author Dr. Matt Greenblatt, an associate professor of pathology and laboratory medicine at Weill Cornell Medicine and a pathologist at NewYork-Presbyterian/Weill Cornell Medical Center.

The other co-senior author of the study was Dr. Shawon Debnath, a research associate in the Greenblatt laboratory.

In a study published in Nature in 2018, Drs. Debnath and Greenblatt and their colleagues, described the discovery of a type of bone-forming stem cell they called the CTSK+ stem cell. Because this type of cell is present in the top of the skull, or “calvarium,” in mice, they suspected that it has a role in causing craniosynostosis.

In the new study, they investigated that possibility by engineering mice in which CTSK+ stem cells lack one of the genes whose loss of function causes craniosynostosis. They expected that the gene deletion somehow would induce these calvarial stem cells to go into bone-making overdrive. This new bone would fuse the flexible, fibrous material called sutures in the skull that normally allow it to expand in infants.

“We were surprised to find that, instead of the mutation in CTSK+ stem cells leading to these stem cells being activated to fuse the bony plates in the skull as we expected, mutations in the CTSK+ stem cells instead led to the depletion of these stem cells at the sutures—and the greater the depletion, the more complete the fusion of the sutures,” Dr. Debnath said.

The unexpected finding led the team to hypothesize that another type of bone-forming stem cell was driving the abnormal suture fusion. After further experiments, and a detailed analysis of the cells present at fusing sutures, they identified the culprit: the DDR2+ stem cell, whose daughter cells make bone using a different process than that utilized by CTSK+ cells.

The team found that CTSK+ stem cells normally suppress the production of the DDR2+ stem cells. But the craniosynostosis gene mutation causes the CTSK+ stem cells to die off, allowing the DDR2+ cells to proliferate abnormally.

To investigate these stem cells in human tissue, the team formed a collaboration with craniosynostosis surgeon Dr. Caitlin Hoffman, neurogeneticist Dr. Elizabeth Ross, and neuropathologist Dr. David Pisapia, all at Weill Cornell Medicine and NewYork-Presbyterian/Weill Cornell Medical Center; and craniosynostosis surgeon Dr. Thomas Imahiyerobo of Columbia University Vagelos College of Physicians and Surgeons and NewYork-Presbyterian/Columbia University Irving Medical Center.

The researchers found the human versions of DDR2+ stem cells and CTSK+ stem cells in calvarial samples from craniosynostosis surgeries—underscoring the likely clinical relevance of their findings in mice.

The findings suggest that inappropriate DDR2+ stem cell proliferation in the calvarium, in infants with craniosynostosis-linked gene mutations, could be treated by suppressing this stem cell population, through mimicking the methods that CTSK+ stem cells normally use to prevent expansion of DDR2+stem cells. The researchers found that the CTSK+ stem cells achieve this suppression by secreting a growth factor protein called IGF-1, and possibly other regulatory proteins.

“We observed that we could partly prevent calvarial fusion by injecting IGF-1 over the calvarium,” said study first author Dr. Seoyeon Bok, a postdoctoral researcher in the Greenblatt laboratory.

“I can imagine DDR2+ stem cell-suppressing drug treatments being used along with surgical management, essentially to limit the number of surgeries needed or enhance outcomes,” Dr. Greenblatt said.

In addition to treatment-oriented research, he and his colleagues now are looking for other bone-forming stem cell populations in the skull.

“This work has uncovered much more complexity in the skull than we ever imagined, and we suspect the complexity doesn’t end with these two stem cell types,” Dr. Greenblatt said.

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JOURNAL

Nature

 

Scientists reveal how the effects of psychosis spread throughout the brain

Scientists detail new capacity to map and model the spread of brain changes in people with different stages of psychoses

Peer-Reviewed Publication

MONASH UNIVERSITY

 

IMAGE: PROFESSOR ALEX FORNITO view more 

CREDIT: MONASH UNIVERSITY

Psychoses like schizophrenia cost billions of dollars annually and derail the lives of people struggling with the disease. Now Monash University researchers have modelled how the effects of psychosis spread through the brain, allowing them to isolate areas where these changes may originate from and which could be targeted by therapies designed to reduce the disease’s progression.

The study, published today in the prestigious Journal of the American Medical Association Psychiatry, details how the scientists were able to map and model the spread of brain changes in people with different stages of psychoses such as schizophrenia,from people newly diagnosed to those who have experienced psychosis for years.

The study, led by  Dr Sid Chopra , from the Turner Institute for Brain and Mental Health and Monash University’s School of Psychological Sciences,  identified the hippocampus, which is important for memory, as a possible  early site of brain changes in psychosis. “This finding could potentially guide  therapies that can target this area of the brain, potentially limiting the impact of the illness or perhaps even reducing the risk of psychosis onset,” he said

The study looked at 534 individuals from four groups, spanning early and late stages of psychotic illness. The researchers used MRI to examine changes in grey matter that occur at the different illness stages

They found that the evolution of psychoses, as measured by changes in great matter, may originate in the hippocampus and gradually  spread  across the brain, over time, via the nerve or axonal connections. According to Dr Chopra, “we found that the pattern of grey matter change seen in psychosis is not randomly distributed across the brain, but is shaped by a complex network of structural connections – in a very similar way to how we see the progression of neurodegenerative diseases in the brain.”

The researchers used a mathematical model to predict  grey matter volume changes  in four different groups of people with schizophrenia, scanned at both early and late stages of illness. According to Professor Alex Fornito, who led the research team, “we found consistent evidence that the hippocampus, an area important for memory and which is known to play an important role in schizophrenia, is a candidate epicentre of brain changes in the illness,” he said.

Importantly the researchers were able to distinguish brain changes associated with disease from those linked to  the use of antipsychotic medication. “Most research has taken place with people who are already taking antipsychotic medications, making it difficult to disentangle the effects of medication from those of  illness,” said Dr Chopra. “Our network-based model was able to account for both medication-related and illness-related brain changes, meaning that brain network architecture represents a fundamental constraint on both types of brain changes in psychosis.” 

According to Dr Chopra, the new approach opens new possibilities for understanding the causes of brain changes in schizophrenia, and for forecasting how they might evolve in individual patients. “Our work demonstrates that it is possible to investigate promising mechanisms behind widespread brain changes in schizophrenia, using fairly simple models” he said. “We hope to further extend these models to identify possible treatment targets and predict how the illness might evolve in individual people.”

 

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JOURNAL

JAMA Psychiatry

DOI

10.1001/jamapsychiatry.2023.3293 

METHOD OF RESEARCH

Experimental study

SUBJECT OF RESEARCH

People

ARTICLE TITLE

Network-based spreading of grey matter changes across different stages of psychosis

ARTICLE PUBLICATION DATE

20-Sep-2023