A climate shock that unfolded about 304 million years ago is offering scientists a dramatic warning about how quickly Earth’s climate system can amplify an initial temperature rise. During the Late Paleozoic Ice Age, a relatively modest increase in global temperatures appears to have triggered a much larger episode of warming, as methane released from thawing permafrost intensified the greenhouse effect. Researchers say the ancient event provides a powerful geological parallel for the climate changes occurring today.

The study, led by Le Yao of the Nanjing Institute of Geology and Paleontology with contributions from University of Cincinnati geosciences professor Thomas Algeo and international colleagues, examined a short-lived warming episode during Earth’s penultimate ice age. Their findings suggest that global sea surface temperatures eventually increased by more than 7 degrees Celsius, or approximately 12 degrees Fahrenheit. The rise was not necessarily caused by one enormous initial pulse of carbon. Instead, it may have developed through a chain reaction in which warming activated additional natural sources of greenhouse gases.

The Late Paleozoic Ice Age extended across a vast span of geological time, when large ice sheets covered parts of the supercontinent Gondwana. Although the planet was in an “icehouse” state, atmospheric carbon dioxide and methane still had the power to destabilize the climate. The newly analyzed warming event is particularly significant because it occurred under ice-age conditions rather than during an already warm greenhouse world. That makes it a valuable analog for the modern Earth, which still contains continent-scale ice masses in Greenland and Antarctica.

According to the researchers, the initial climate disturbance may have been linked to volcanic activity. Volcanic emissions can inject carbon dioxide and other gases into the atmosphere, where they absorb outgoing infrared radiation and prevent some heat from escaping into space. The warming may also have been assisted by changes in Earth’s orbit. Over long cycles, variations in orbital shape alter the distribution of sunlight across the planet, influencing the growth and retreat of ice sheets and changing the seasonal balance of solar energy.

At first, the additional carbon may have produced only a limited temperature increase. But once warming crossed a critical threshold, frozen ground in high-latitude regions began to thaw. Permafrost contains large quantities of organic carbon preserved in frozen soils. When that material becomes available to microbes, decomposition can release carbon dioxide and methane. Methane is especially powerful over shorter atmospheric timescales because, molecule for molecule, it absorbs considerably more infrared radiation than carbon dioxide, even though it remains in the atmosphere for less time.

This process can create a positive climate feedback. An initial warming causes permafrost to thaw, thawing releases greenhouse gases, and the additional gases produce further warming. That extra heat can accelerate more thawing, allowing the cycle to reinforce itself. The researchers describe the ancient event as a transient global warming episode in which a comparatively modest carbon release appears to have crossed a climatic tipping point and initiated much more extensive carbon emissions from natural reservoirs.

The geological timescale of the ancient warming is also central to the study’s relevance. Algeo said the temperature change unfolded over tens of thousands of years, with warming occurring at an average rate of roughly one-tenth of a degree Celsius per 1,000 years. Modern warming is progressing far more rapidly. Researchers have observed an increase of nearly 1 degree Celsius in global sea surface temperature over approximately the past century, a rate many times faster than the average change reconstructed for the ancient event.

The comparison does not mean that Earth is destined to repeat the precise conditions of 304 million years ago. Continents, ecosystems, atmospheric composition and ice-sheet geometry were all different in the Late Paleozoic. However, the physics of greenhouse warming and the existence of carbon feedbacks remain relevant. Ancient climate records reveal how a system that appears stable can respond nonlinearly when warming activates processes capable of releasing additional greenhouse gases.

The findings also place human history in a broader planetary context. All recorded human civilization has developed during the most recent ice age, despite the fact that the term can sound incompatible with today’s climate. In scientific usage, Earth remains in an ice age because substantial permanent ice sheets still exist in Greenland and Antarctica. The ancient warming episode matters precisely because it demonstrates that an ice age does not guarantee a permanently cold or stable climate. Even within an icehouse world, a small disturbance can trigger rapid and substantial changes when reinforcing feedbacks are engaged.

The research, published in the Proceedings of the National Academy of Sciences, underscores why scientists closely monitor permafrost, polar ice and other climate-sensitive carbon stores. The ancient record cannot provide an exact forecast of future warming, but it shows that Earth’s climate has repeatedly responded to carbon disturbances with amplifying feedbacks. As modern emissions continue to raise temperatures at an exceptional rate, the geological evidence offers a clear message: the danger lies not only in the carbon released directly by human activity, but also in the natural carbon sources that warming can unlock.

Subject of Research: Ancient global warming, permafrost methane feedbacks, and climate tipping points during the Late Paleozoic Ice Age

Article Title: A transient global warming event during Earth’s penultimate icehouse

Web References: https://doi.org/10.1073/pnas.2601643123

References: Proceedings of the National Academy of Sciences, DOI: 10.1073/pnas.2601643123

Image Credits: Andrew Higley, University of Cincinnati

Keywords: climate change, global warming, ice age, Late Paleozoic Ice Age, permafrost, methane, climate feedback, tipping point, paleoclimate, geology, volcanic activity, Earth’s climate history

A new study has brought scientists closer to observing how inflammation during pregnancy may alter the earliest stages of human brain development. Using three-dimensional tissue models made from human fetal brain samples, researchers modeled maternal immune activation and identified the signaling molecule interleukin-17A, or IL-17A, as a major driver of abnormal cortical development. The findings, published in Nature Neuroscience, offer a human-based experimental system for investigating how immune signals outside the brain can influence the formation of neural circuits before birth.

Maternal immune activation refers to the biological response triggered when a pregnant individual experiences infection or significant inflammation. Epidemiological studies have associated certain prenatal inflammatory exposures with an increased likelihood of neurodevelopmental conditions, including autism spectrum disorder, schizophrenia, and intellectual disability. Yet the mechanisms behind these associations have remained difficult to study. Animal models have provided important clues, but differences between species can limit their ability to reproduce the timing, cellular organization, and molecular environment of the developing human cortex.

The researchers addressed this challenge with “brain cerebroids,” three-dimensional, ex vivo models that preserve features of developing human fetal brain tissue. Unlike simplified cultures composed of a single cell type, these structures retain a more complex arrangement of neural progenitors, immature neurons, and supporting cells. Their three-dimensional architecture allows cells to communicate and organize in ways that more closely resemble the fetal cortex, including the production and movement of neurons that ultimately establish the layered structure of the brain’s outer region.

To recreate aspects of maternal immune activation, the team exposed the fetal brain cerebroids to inflammatory conditions associated with immune signaling during pregnancy. The central focus was IL-17A, a cytokine produced primarily by activated immune cells, particularly a subset of T cells known as T helper 17 cells. Cytokines are small signaling proteins that coordinate immune responses, but they can also affect tissues beyond the immune system. In the developing brain, inappropriate or excessive exposure to such signals may influence cell proliferation, migration, differentiation, and the formation of connections between neurons.

The study found that IL-17A exposure was linked to disruptions in cortical development within the human cerebroids. These effects are described as “IL-17A-driven,” indicating that the cytokine was not merely associated with the developmental changes but played a functionally important role in producing them. The disturbances affected the organization and behavior of developing neural cells, processes that are essential for building the cortex. During normal development, neural progenitor cells generate new neurons in tightly regulated sequences, while young neurons migrate to their appropriate positions. Interference with either process can alter the structure and connectivity of later-forming brain tissue.

The results are especially significant because they were observed in human fetal brain material rather than inferred only from animal studies. Previous research in mice has implicated maternal immune activation and IL-17A in changes to cortical organization and behavior in offspring. However, the human cerebroid model provides an opportunity to examine whether similar immune mechanisms operate in human tissue, where the timing of neurogenesis, cell-type composition, and cortical architecture differ from those of rodents. The approach may also help reveal human-specific responses that conventional laboratory animals cannot capture.

The findings do not mean that IL-17A exposure during pregnancy inevitably causes a neurodevelopmental condition, nor do they establish that prenatal inflammation is a single explanation for such conditions. Brain development is shaped by a combination of genetic factors, immune signals, environmental influences, and developmental timing. The experiments also took place in an ex vivo model, outside the full physiological environment of a living pregnancy. Cerebroids cannot reproduce the placenta, maternal circulation, hormonal changes, or the complete immune system, all of which influence how inflammatory signals reach the fetus and how long they remain active.

Nevertheless, the model could become a powerful platform for testing mechanisms and potential interventions. Researchers may use it to determine how IL-17A changes gene activity in neural progenitors, whether it alters communication between neurons and glial cells, and which molecular pathways make some developing cells more vulnerable than others. Because the tissue is human and three-dimensional, it may also support studies of patient-specific genetic risk, allowing investigators to compare how different backgrounds respond to the same inflammatory signal.

The work also highlights a broader shift in neuroscience toward experimental systems that combine human tissue with controlled laboratory manipulation. Understanding prenatal inflammation is difficult in clinical studies because immune exposure cannot be ethically assigned or precisely timed in pregnant people. Brain cerebroids offer a way to isolate individual components of that complex biology while preserving more of the developing tissue’s natural organization than conventional two-dimensional cell cultures. As these models improve, they may help distinguish temporary developmental changes from persistent alterations in cortical circuitry and identify when immune signaling is most consequential.

By showing that IL-17A can disrupt human cortical development in a three-dimensional ex vivo system, the study gives researchers a clearer biological target in the search for links between prenatal inflammation and later neurodevelopment. Its most immediate contribution is not a new diagnosis or treatment, but a more precise experimental framework: one that connects maternal immune signaling to cellular events in the developing human cortex. That connection could guide future work on prevention, therapeutic timing, and the complex origins of developmental differences long before the first symptoms become visible.

Subject of Research: Maternal immune activation and IL-17A-driven disruption of human fetal cortical development in 3D ex vivo brain cerebroids.

Article Title: Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development.

Article References: Assir, M.Z.K., Yanakiev, M., Gim, D.H. et al. Modeling maternal immune activation in 3D ex vivo human fetal brain cerebroids reveals IL-17A-driven disruption of cortical development. Nature Neuroscience (2026). https://doi.org/10.1038/s41593-026-02400-2

Image Credits: AI Generated

DOI: https://doi.org/10.1038/s41593-026-02400-2

Keywords: maternal immune activation, IL-17A, fetal brain development, cortical development, brain cerebroids, neurodevelopment, prenatal inflammation, human brain models, cytokines, neuroscience

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