Artificial intelligence uses less energy by mimicking the human brain

 Artificial Intelligence (AI) can perform complex calculations and analyze data faster than any human, but to do so requires enormous amounts of energy. The human brain is also an incredibly powerful computer, yet it consumes very little energy.

As technology companies increasingly expand, a new approach to AI's "thinking," developed by researchers including Texas A&M University engineers, mimics the human brain and has the potential to revolutionize the AI industry.

Dr. Suin Yi, assistant professor of electrical and computer engineering at Texas A&M's College of Engineering, is on a team of researchers that developed "Super-Turing AI," which operates more like the human brain. This new AI integrates certain processes instead of separating them and then migrating huge amounts of data like current systems do.

The Energy Crisis In AI

Today's AI systems, including large language models such as OpenAI and ChatGPT, require immense computing power and are housed in expansive data centers that consume vast amounts of electricity.

"These data centers are consuming power in gigawatts, whereas our brain consumes 20 watts," Suin explained. "That's 1 billion watts compared to just 20. Data centers that are consuming this energy are not sustainable with current computing methods. So while AI's abilities are remarkable, the hardware and power generation needed to sustain it is still needed."

The substantial energy demands not only escalate operational costs but also raise environmental concerns, given the carbon footprint associated with large-scale data centers. As AI becomes more integrated, addressing its sustainability becomes increasingly critical.

Emulating The Brain

Yi and team believe the key to solving this problem lies in nature -- specifically, the human brain's neural processes.

In the brain, the functions of learning and memory are not separated, they are integrated. Learning and memory rely on connections between neurons, called "synapses," where signals are transmitted. Learning strengthens or weakens synaptic connections through a process called "synaptic plasticity," forming new circuits and altering existing ones to store and retrieve information.

By contrast, in current computing systems, training (how the AI is taught) and memory (data storage) happen in two separate places within the computer hardware. Super-Turing AI is revolutionary because it bridges this efficiency gap, so the computer doesn't have to migrate enormous amounts of data from one part of its hardware to another.

"Traditional AI models rely heavily on backpropagation -- a method used to adjust neural networks during training," Yi said. "While effective, backpropagation is not biologically plausible and is computationally intensive.

"What we did in that paper is troubleshoot the biological implausibility present in prevailing machine learning algorithms," he said. "Our team explores mechanisms like Hebbian learning and spike-timing-dependent plasticity -- processes that help neurons strengthen connections in a way that mimics how real brains learn."

Hebbian learning principles are often summarized as "cells that fire together, wire together." This approach aligns more closely with how neurons in the brain strengthen their connections based on activity patterns. By integrating such biologically inspired mechanisms, the team aims to develop AI systems that require less computational power without compromising performance.

In a test, a circuit using these components helped a drone navigate a complex environment -- without prior training -- learning and adapting on the fly. This approach was faster, more efficient and used less energy than traditional AI.

Why This Matters For The Future Of AI

This research could be a game-changer for the AI industry. Companies are racing to build larger and more powerful AI models, but their ability to scale is limited by hardware and energy constraints. In some cases, new AI applications require building entire new data centers, further increasing environmental and economic costs.

Yi emphasizes that innovation in hardware is just as crucial as advancements in AI systems themselves. "Many people say AI is just a software thing, but without computing hardware, AI cannot exist," he said.

Looking Ahead: Sustainable AI Development

Super-Turing AI represents a pivotal step toward sustainable AI development. By reimagining AI architectures to mirror the efficiency of the human brain, the industry can address both economic and environmental challenges.

Yi and his team hope that their research will lead to a new generation of AI that is both smarter and more efficient.

"Modern AI like ChatGPT is awesome, but it's too expensive. We're going to make sustainable AI," Yi said. "Super-Turing AI could reshape how AI is built and used, ensuring that as it continues to advance, it does so in a way that benefits both people and the planet."

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Making sturdy, semi-transparent wood with cheap, natural materials

 Can you imagine a smartphone with a wooden touchscreen? Or a house with wooden windows? Probably not -- unless you've heard of transparent wood. Made by modifying wood's natural structure, this material has been proposed as a sturdy, eco-friendly plastic alternative. But wood's biodegradability is often sacrificed in the process. Researchers are hoping to change that by creating transparent woods from almost entirely natural materials and making them electrically conductive.

The researchers will present their results at the spring meeting of the American Chemical Society (ACS).

"In the modern day, plastic is everywhere, including our devices that we carry around. And it's a problem when we reach the end of that device's life. It's not biodegradable," explains Bharat Baruah, a professor of chemistry at Kennesaw State University and the presenter of this research. "So, I asked, what if we can create something that's natural and biodegradable instead?"

Baruah became interested in transparent woods thanks to his outside-of-work pursuits -- namely, his woodworking hobby. But he realized that the transparent woods reported by other scientists used materials such as epoxies, a form of plastic, for strength. To find natural materials that would keep wood sturdy and stable over time, he again turned to his personal experiences.

Growing up in the state of Assam in northeastern India, Baruah encountered buildings that had been standing for centuries -- long before the modern-day version of cement was invented. Instead, ancient masons created cement by mixing sand with sticky rice and egg whites. Baruah hypothesized that those same materials might be perfect for incorporating strength and stability into his transparent woods.

Wood has three components: cellulose, hemicellulose and lignin. To make it transparent, the lignin and hemicellulose are removed, leaving behind a porous, paper-like network of cellulose. Then, a colorless material fills in those pores, also restoring some rigidity.

Joined by Ridham Raval, an undergraduate student at the university, Baruah transformed pieces of balsa wood into natural, semi-transparent woods by pulling out the lignin and hemicellulose using a vacuum chamber and chemicals, including sodium sulfite (a delignifying agent), sodium hydroxide (a version of lye) and diluted bleach. Then, the pores were refilled by soaking them in an egg white and rice extract mixture, along with a curing agent called diethylenetriamine to keep the material see-through. The researchers say that these reagents, when used in small amounts, such as in this experiment, pose little threat to the environment.

In the end, the team was left with semi-transparent slices of wood that were durable and flexible.

The team next investigated some potential applications for their engineered woods, including as a replacement for glass windows. Again, Baruah tapped into his woodworker skills and renovated a birdhouse into a tiny, one-windowed, insulated home. To test the modernized abode's energy efficiency, he put the birdhouse under a heat lamp and placed a temperature gauge inside. The temperature inside the house was between 9 to 11 degrees Fahrenheit (5 to 6 degrees Celsius) cooler when transparent wood was used than when glass was, suggesting that this new material could serve as an energy-efficient alternative to glass in windows.

To further expand the transparent wood's potential applications, the team also incorporated silver nanowires into certain samples. This addition allowed the wood to conduct electricity, which could be useful for wearable sensors or coatings for solar cells. Silver nanowires aren't biodegradable, but the team hopes to conduct further experiments using other conductive materials like graphene to maintain their fully natural transparent woods.

Though additional research is needed to boost the transparency of the woods, Baruah is happy that this initial step used natural and inexpensive materials. "I want to send a message to my undergraduate students that you can do interesting research without spending thousands of dollars," he concludes.

The research was funded by Kennesaw State University and Purafil Inc., an air filtration manufacturer.

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How cells respond to stress is more nuanced than previously believed

 The body's cells respond to stress -- toxins, mutations, starvation or other assaults -- by pausing normal functions to focus on conserving energy, repairing damaged components and boosting defenses.

If the stress is manageable, cells resume normal activity; if not, they self-destruct.

Scientists have believed for decades this response happens as a linear chain of events: sensors in the cell "sound an alarm" and modify a key protein, which then changes a second protein that slows or shuts down the cell's normal function.

But in a new study published today in the journal Nature, researchers at Case Western Reserve University have discovered a cell's response is more nuanced and compartmentalized -- not fixed or rigid, as previously thought.

The groundbreaking research suggests this adaptive response to stress -- which the researchers call "split-integrated stress response" or s-ISR -- could potentially be exploited to kill cancer cells and more effectively treat neurodegenerative diseases.

Maria Hatzoglou, professor of the Department of Genetics and Genome Sciences at the Case Western Reserve School of Medicine and the study's principal investigator, found for the first time a cell's response to stress can be fine-tuned depending its nature, intensity and duration. This flexibility provides novel insights into how cells in organisms -- from yeast to humans -- adapt to their environment.

"This study represents a new way of thinking about cellular stress," Hatzoglou said. "ISR is not a one-size-fits-all system like we used to think. Instead, it can change and adjust depending on the type, strength and length of the stress the cell is experiencing."

The study

The study used mouse models of Vanishing White Matter Disease, which causes progressive degeneration of the brain's white matter in children, leading to neurological problems like motor difficulties, seizures and cognitive decline.

Hatzoglou's research revealed that cells carrying the gene causing the disease had mutations in the key protein normally responsible for shutting down operations in the cell under stress. Somehow, the brain cells adapt and mostly function normally but are exceptionally vulnerable, self-destructing even under mild stress.

The research team, which included colleagues at Case Western Reserve, McGill University and Karolinska Institute, determined how the cells reacted explains why patients show significant decline in cognitive and motor abilities after relatively minor stressors like fever or mild head trauma.

Other late-onset neurodegenerative diseases like multiple sclerosis and amyotrophic lateral sclerosis (better known as ALS) may share a similar mechanism, the researchers said. Diseased brain cells adapt to preserve functions under normal conditions, but modest stressors accelerate decline.

Understanding this adaptation to stress could lead to new targets for cancer chemotherapy, Hatzoglou said, because cancer cells respond to stressors like chemotherapy in one of two ways: either self-destruct or mutate to preserve their function, becoming resistant to the treatment.

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Melting ice, more rain drive Southern Ocean cooling

 Global climate models predict that the ocean around Antarctica should be warming, but in reality, those waters have cooled over most of the past four decades.

The discrepancy between model results and observed cooling, Stanford University scientists have now found, comes down mainly to missing meltwater and underestimated rainfall.

"We found that the Southern Ocean cooling trend is actually a response to global warming, which accelerates ice sheet melting and local precipitation," said Earle Wilson, an assistant professor of Earth system science in the Stanford Doerr School of Sustainability and senior author of the March 27 study in Geophysical Research Letters.

As rising temperatures melt Antarctica's ice sheet and cause more precipitation, the Southern Ocean's upper layer is growing less salty -- and thus, less dense. This creates a lid that limits the exchange of cool surface waters with warmer waters below. "The fresher you make that surface layer, the harder it is to mix warm water up," Wilson explained.

But this freshening is not fully represented in state-of-the-art climate models -- a flaw that scientists have long recognized as a major source of uncertainty in projections of future sea level rise. "The impact of glacial meltwater on ocean circulation is completely missing from most climate models," Wilson said.

Reconciling global discrepancies

The mismatch between observed and simulated sea surface temperatures around Antarctica is part of a larger challenge for scientists and governments seeking to prepare for climate impacts. Global climate models generally do not accurately simulate the cooling observed over the past 40 years in the Southern Ocean and the eastern Pacific around the equator or the intensity of the warming observed in the Indian and western Pacific Oceans. There is also a discrepancy between simulations and the observed frequency of La Niña weather conditions, defined by the eastern Pacific being colder than average.

Warming events in the Southern Ocean over roughly the past eight years have somewhat diminished the 40-year-long cooling trend. But if sea surface temperature trends around the globe continue to resemble patterns that have emerged in recent decades, rather than shifting toward the patterns predicted in simulations, it would change scientists' expectations for some near-term impacts from climate change. "Our results may help reconcile these global discrepancies," Wilson said.

Oceans globally have absorbed more than a quarter of the carbon dioxide emitted by human activities and more than 90% of the excess heat trapped in our climate system by greenhouse gases. "The Southern Ocean is one of the primary places that happens," said lead study author Zachary Kaufman, a postdoctoral scholar in Earth system science.

As a result, the Southern Ocean has an outsized influence on global sea level rise, ocean heat uptake, and carbon sequestration. Its surface temperatures affect El Niño and La Niña weather patterns, which influence rainfall as far away as carlifornia

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How did the large brain evolve?

 Two specific genes that evolve exclusively in humans jointly influence the development of the cerebrum. Researchers from the German Primate Center -- Leibniz Institute for Primate Research and the Max Planck Institute of Molecular Cell Biology and Genetics have discovered this in a recently published study. They have thus provided evidence that these genes contribute together to the evolutionary enlargement of the brain.

The results of the study show that the two genes act in a finely tuned interplay: one ensures that the progenitor cells of the brain multiply more, while the other causes these cells to transform into a different type of progenitor cell -- the cells that later form the nerve cells of the brain.

In the course of evolution, this interplay has led to the human brain being unique in its size and complexity.

The newly gained insights not only provide a deeper understanding of the evolutionary development of our brain but could also help to better comprehend how certain developmental disorders or diseases of the brain arise.

'Our findings deepen the fundamental understanding of brain development and provide new insights into the evolutionary origins of our large brain.

In the long term, they could contribute to the development of therapeutic approaches for malformations of the brain,' says Nesil Eşiyok, first author of the study.

Various methods were combined for the study: In addition to animal experiments with mice, alternative methods such as chimpanzee brain organoids were also used.

'The remarkable feature of our study is that the results from animal experiments and alternative methods complement each other well and mutually confirm their findings.

. This not only emphasizes the high significance of our results, but could also help to reduce the need for animal experiments in the future by further developing, refining and confirming alternative methods,' explains Michael Heide, the study's lead researcher.

The German Primate Center (DPZ) -- Leibniz Institute for Primate Research conducts biological and biomedical research on and with primates in the fields of infection research, neuroscience and primate biology. The DPZ also maintains five field stations in the tropics and is a reference and service center for all aspects of primate research. The DPZ is one of the 96 research and infrastructure facilities of the Leibniz Association.

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How movement affects the way the brain processes sound and sight

 A research team at the Institute for Basic Science (IBS) has uncovered a fundamental principle of how the brain prioritizes vision and hearing differently depending on whether we are still or in motion. The study, led by Dr. LEE Seung-Hee, Associate Director of the IBS Center for Synaptic Brain Dysfunctions and Associate Professor at KAIST, provides new insights into how movement alters the brain's sensory decision-making process.

In daily life, we constantly process visual (sight) and auditory (sound) information to navigate the world. For instance, when watching a movie, our brain seamlessly integrates images and sounds to create a complete experience. However, when moving -- such as when walking on a busy street -- our brain may prioritize visual information over sound.

Until now, it was unclear how the brain decides which sense to prioritize in different situations. This is particularly relevant for individuals with sensory processing disorders such as autism or schizophrenia, where the brain may struggle to integrate sensory information correctly. Understanding how the brain naturally shifts between sensory inputs could lead to better treatments for these conditions.

To investigate this phenomenon, the research team conducted behavioral experiments on mice while tracking real-time brain activity using miniature microscopes and optogenetics (a method that uses light to control neurons). The mice were trained to respond to both visual and auditory cues while running on a treadmill.

The researchers found that when the mice were stationary, their brains relied more on sound to make decisions. However, when they were moving, their brains shifted to prioritize vision.

Further analysis revealed the specific brain circuits responsible for this switch:

- The posterior parietal cortex (PPC), a key region for decision-making, played a central role in prioritizing sensory information. When the PPC was turned off, mice could no longer make decisions based on visual cues and relied more on sound instead.

- The secondary motor cortex (M2) acted as a "sensory gatekeeper." When the mice were moving, M2 sent inhibitory signals to the auditory cortex, blocking auditory signals from reaching the PPC. This effectively made vision the dominant sense during motion.

- Despite this suppression, the auditory cortex continued processing sounds, meaning the brain was adjusting how it integrates sensory information rather than completely ignoring sound.

This study demonstrates that the brain does not treat all sensory inputs equally at all times -- instead, it dynamically adjusts depending on movement and environmental needs. When stationary, sound is more useful for detecting nearby events, while vision takes priority during movement because it is more reliable for navigation.

This discovery could have important implications for understanding and treating sensory processing disorders, where the brain may struggle to properly filter and prioritize sensory inputs.

Dr. LEE Seung-Hee, the study's lead researcher, emphasized the significance of the findings, stating, "Our study reveals how the brain flexibly shifts between vision and hearing based on behavior. This natural adaptability is crucial for survival, and understanding it could help us develop better treatments for individuals with sensory integration difficulties."

sources-science daily

Neurons in brain that regulate energy levels and body temperature

 Scientists at Pennington Biomedical Research Center have gained greater clarity in the brain regions and neurons that control metabolism, body temperature and energy use. Featured in the February edition of the journal Metabolism, Dr. Heike Münzberg-Gruening and a team of researchers discovered which chemicals influence the signals that control how much energy the body uses. In "Leptin Receptor Neurons in the dorsomedial hypothalamus require distinct neuronal subsets for thermogenesis and weight loss," researchers laid out the pathways, chemicals, neurons and brain regions that are activated.

In previous research, Dr. Münzberg-Gruening and her team identified that leptin receptors, or Lepr, control the metabolic effects of Leptin. These receptors are neurons in the dorsomedial hypothalamus, or DMH, which is a nucleus located in the hypothalamus at the base of the brain. In their latest study, researchers found that these Lepr neurons communicate using two different chemical signals: glutamate, which excites neurons, or GABA, which calms neurons.

The study revealed that the neurons that send signals to the brain region called the raphe pallidus -- a region that controls metabolism -- only use glutamate to send their signals. The neurons that signal to another brain region -- the arcuate nucleus, which regulate body weight, satiety and metabolism -- use only GABA. These neurons also have special receptors that allow them to respond to the new weight-loss medications known as GLP-1 receptor agonists.

"This discovery sheds light on the fundamental neuronal interplay that influences how much energy the body uses and how the body adjusts to changes in temperature levels or food availability," said Dr. Münzberg, professor in Pennington Biomedical's Central Leptin Signaling Lab. "This research expands our knowledge of the circuitry of thermoregulation and emphasizes the unique capability of leptin signaling in the DMH to promote beneficial metabolic effects. It also clarifies leptin signaling's role in the stability of body weight and energy usage. We believe these neurons manage the body's ability to adapt to a variety of environmental changes like ambient temperature or food scarcity by integrating signals like leptin and the gut hormone glucagon-like-peptide-1 or GLP-1."

In addition to identifying which neurons from the DMH affect certain regions and their functions, researchers further found that some Lepr neurons are muted by leptin, while others were activated specifically when certain indirect signals were blocked. This suggests that the DMH is part of a larger neuronal network and leptin increases the muting effect of outside connections with the DMH, but when these outside connections are blocked, leptin is able to un-mute DMH neurons. Such networks may be relevant to integrate and, if necessary, override environmental and humoral signals to allow proper adaptation of body energy balance.

This study further clarifies that Lepr neurons are a unique selection of DMH neurons that promote metabolic benefits. They might also explain the paradox that robust weight loss with GLP-1-based medications is able to override the slow metabolism usually associated with weight loss, but this paradox needs to be further tested in future studies.

"There are still so many fundamental processes in our bodies and brains that remain a mystery to us, and that's exactly what drives our researchers at Pennington Biomedical -- to explore these unknowns, make new discoveries and deepen our understanding of metabolism," said Dr. John Kirwan, Executive Director of Pennington Biomedical Research Center. "I want to congratulate Dr. Münzberg and her team on this exciting discovery. It really showcases the incredible work that is happening in our Pre-Clinical Basic Science labs, and I can't wait to see what they'll discover next."

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Anti-amyloid drug may help reduce the risk of early-onset Alzheimer's by 50%

 

• A recent study tests a new drug, gantenerumab on people with a genetically inherited form of Alzheimer’s disease.
• For people with this condition, dementia is almost inevitable.
• Gantenerumab helps eliminate one of the neurological hallmarks of Alzheimer’s, called amyloid plaques.
• For some participants, gantenerumab reduced their risk of developing the disease by more than 50%.

A new study provides a well-needed glimmer of hope for treating Alzheimer’s disease.

Focusing on a genetic form of early-onset dementia called dominantly inherited Alzheimer’s disease, scientists have identified a drug that halved some participants’ risk of developing the condition.

While hopeful, scientists need to continue their research in larger groups for longer lengths of time. Below, we outline what the scientists have found and explain some of the unanswered questions.

The amyloid hypothesis in Alzheimer’s

Although there are many outstanding questions about Alzheimer’s and a significant lack of effective drugs, scientists believe a protein called amyloid-beta plays an important role in the condition.

Although amyloid-beta is present in healthy brains, in people with Alzheimer’s, it clumps together to form plaques, which interfere with the normal workings of the brain. This, scientists believe, is the primary reason for significant cognitive decline.

The amyloid hypothesis inspired scientists to design monoclonal antibody therapies that target and destroy these protein buildups, including drugs like aducanumab, lecanemab, and donanemab.

Research shows that these drugs can inhibit the accumulationTrusted Source of amyloid-beta and may slow cognitive decline during early Alzheimer’s.

However, until now, scientists have not investigated whether taking monoclonal antibody therapies could prevent or delay the onset of Alzheimer’s in at-risk individuals. The latest study tackles this question and adds supporting evidence for the amyloid hypothesis.

What is DIAD?

In the latest study, the researchers focused on people with dominantly inherited Alzheimer’s disease (DIAD). These individuals have mutations in certain genes that cause the accumulation of amyloid-beta.

This genetic predisposition means that they have an almost 100% chance of developing Alzheimer’s in early- to mid-adulthood.

Because developing the condition is almost inevitable, these individuals provide a unique model for testing new ways to prevent Alzhemier’s.

Gantenerumab reduces risk in some patients

The participants in this study initially enrolled in the first-ever trial to try and prevent Alzheimer’s. This trial, which focused on anti-amyloid drugs, was set up in 2012 when the participants had either no symptoms or just mild cognitive symptoms. At this stage, they were within 15 years before to 10 years after their expected age of developing Alzheimer’s.

Coming to an end in 2020, the study showed that gantenerumab significantly reduced levels of amyloid-beta and improved some other markers associated with Alzheimer’s. Despite the positive signs, there were no measurable cognitive benefits compared with the placebo group simply because neither group had developed symptoms yet.

So, the researchers extended the study and upped the dosage to see how gantenerumab might work over a longer time.

Although gantenerumab did not make a significant difference for all groups involved in the study, for some, there were benefits.

For those who had been taking the drug for the longest time — around eight years — the effect was clear. Gantenerumab reduced the risk of developing symptoms by 50%.

Some participants are only just reaching or have only just passed their expected age of disease onset, so as the study continues, this percentage may rise if participants remain symptom-free or fall if they develop the disease.

“Everyone in this study was destined to develop Alzheimer’s disease and some of them haven’t yet,” explains senior author Randall J. Bateman, MD, from WashU Medicine in St Louis, MI in a press release.

“We don’t yet know how long they will remain symptom-free — maybe a few years or maybe decades,” he continues. “In order to give them the best opportunity to stay cognitively normal, we have continued treatment with another anti-amyloid antibody in hopes they will never develop symptoms at all.”

“What we do know is that it’s possible at least to delay the onset of the symptoms of Alzheimer’s disease and give people more years of healthy life,” Bateman concludes.

Does gantenerumab help late-onset Alzheimer’s?

DIAD appears to develop in a similar way to late-onset Alzheimer’s, but further research is required to understand whether gantenerumab might also prevent this much more common version of dementia.

“I am highly optimistic now,” Bateman says, “as this could be the first clinical evidence of what will become preventions for people at risk for Alzheimer’s disease. One day soon, we may be delaying the onset of Alzheimer’s disease for millions.”

Medical News Today contacted Chris Vercammen, MD, a board certified internal medicine physician and medical director at Remo Health who was not involved in the study.

“The study findings are promising but its important to keep in mind that we are still in the very early stages of this type of research.”
— Chris Vercammen, MD

However, because this study focused on patients who were in the pre-clinical stage, but with a high baseline risk, we need more research, Vercammen said.

“To truly understand the potential of these treatments, extensive further research is required,” he told MNT. “This includes large-scale, randomized trials, particularly in diverse populations and those with late-onset Alzheimer’s.”

Although gantenerumab has been discontinued by Roche/Genentech, other anti-amyloid drugs continue to be investigated.

One of the issues with studying diseases that take decades to develop is that studies on drugs need to be just as long. We need to wait for more data to roll in, but the results of this study provide hope for the future.

Side effects of anti-amyloid treatments

Not everyone is as upbeat about the recent results. MNT reached out to Deepak Nair, MD, a neurologist at OSF HealthCare who was not involved in the research. “Unfortunately, the study results are not quite as exciting as we would like.”

Although gantenerumab showed an impressive ability to remove amyloid protein plaques, he explained, “there was no statistically significant impact on clinical ratings of cognitive performance.”

“This is similar to other agents that have been shown to reduce the burden of amyloid plaque in patients with mild cognitive improvement or early stage Alzheimer’s disease,” Nair explained.

He also shared “serious concerns about the role of amyloid plaque in Alzheimer’s disease.” As we mentioned, the amyloid hypothesis of Alzheimer’s disease is still just that: a hypothesis.

“Recent revelations about falsified data in early Alzheimer’s research have raised serious concerns about the role of amyloid plaque in Alzheimer’s disease,” he told MNT. He also raised concerns about so-called amyloid-related imaging abnormalities (ARIA).

ARIA are side effects of anti-amyloid therapies that produce abnormal brain signals on MRI scans. They include fluid accumulation or microhemorrhages. “In the various studies of anti-amyloid drugs, the rate of ARIAs has affected 20–25% of patients,” Nair told us.

According to Nair, symptoms can include:

• headache
• confusion
• nausea and vomiting
• difficulty walking
• worsening cognition

In the recent gantenerumab study, the rates of ARIA were particularly high, possibly due to the increased dosage. Two participants left the study due to these brain scan abnormalities, although they recovered fully once the drug had been stopped.

“Alzheimer’s disease, like all neurodegenerative diseases, is a highly complex process which affects the most complex organ system,” Nair concluded. “There is potential here, but we have much more to learn.”

What does this mean for the future?

“The accelerating rise in dementia cases presents a profound challenge, placing immense strain on families and demanding significant resources from state and federal governments,” Vercammen told MNT.

“In this context, studies like the one discussed are important, pushing the dialogue on dementia forward and bringing us closer to effective solutions,” he said.

Talking about next steps, Vercammen continued, “we must continue to prioritize large-scale, randomized clinical trials that encompass diverse populations at different stages of the disease in order to fully understand both the potential rewards and risks of any future treatments.”

Source - Medical News Today

In Conversation: Can 'biological race' explain disparities in health?

 Millions of people experience overt or covert racism that affects their day-to-day lives. But sometimes, the impact of such discrimination spills into healthcare, bringing life threatening consequences. So, when it comes to racial health disparities, can so-called biological differences explain these statistics, or is the misuse of science preventing us from getting to the root of the problem?

Have you ever been asked a seemingly innocuous question that later left you feeling uncomfortable? Perhaps it made you think, would any other person, especially someone of a different ethnic or racial background, be asked that same question?

For some of us, this can be the classic question of “Where are you really from?” or perhaps comments such as “You are so articulate” or “I’m not racist, I have several [insert race/ethnicity here] friends.”

These questions and behaviors are what are now coined as ‘microaggressions,’ which, by definition, are negative racial slights, biases, prejudices, and insults—whether intentional or unintentional—toward people of different races and ethnicities.

We can encounter such behaviors wherever we go and in a multitude of environments. One such instance is within healthcare settings. I, for example, was recently asked by a healthcare professional if I had experienced “female genital mutilation,” which at the time did not seem pertinent to the issue I was facing but left me feeling rather uncomfortable after I sat with it. Being of British-Turkish mix descent, I wondered if any of my other white friends would be asked the same question.

Although, in my case, it did not have any adverse effects on my treatments or care, that may not always be the case. And I know I receive rather ‘privileged’ treatment because of the way I present, compared to other minoritized groups.

Within healthcare contexts, the gravity of this discrimination becomes more apparent when patients and healthcare workers experience negative consequencesTrusted Source, which often lead to lower standards of care and a higher risk of illness.

This month, we sat down with Dr. Monique Rainford, obstetrician and gynecologist at the Yale School of Medicine, and author of the book “Pregnant While Black,” and Angela Saini, science journalist and author whose most recent work includes the book “Superior: The Return of Race Science,” to discuss what impact racism has on health and whether biological ‘race’ science can actually explain all the health disparities experienced by different racial groups.

You can listen to this month’s episode below, or on your preferred streaming platform:

Microaggressions and the COVID-19 pandemic

After I shared my own experience, Dr. Rainford explained what a microaggression is and how it may feel to the person experiencing it:

“[The] example that you shared is a microaggression, in the sense that when you were asked a certain history, and you wondered if you would have been asked otherwise [if you were from a different background]. You don’t necessarily realize it at the time [that] something is off [or] different. You don’t realize it at the time because it’s almost a shock. [A]nd then at some point, you realize and say ‘Oh, it is because I’m a person of this race or this ethnicity. And it is happening to me again, and again,'” she said.

Chiming into the conversation to share her own experience was Angela Saini.

“I can feel the frustration because I feel the same a lot. I’ll just give you an example. So, at the beginning of the pandemic, in 2020, there was so much speculation on the part of medical doctors as well and medical professionals, researchers about racial differences in who was catching the virus.”

Did COVID-19 affect races differently?

Describing it as “bizarre,” Saini pointed out how “bizarre” it was for the medical community to have thought that SARS-CoV-2, the virus that causes COVID-19, was affecting people of different races and ethnicities in varying severities.

“This would be the first time in history that a virus affected races differently if that had been the case with COVID-19,” she said.

“And yet there was this widespread assumption that this was possible with this particular one. And I couldn’t believe some of the things that I was reading, [t]hat was being published in the medical literature,” she continued.

During the early days of the pandemic, news outlets and the U.K. government were reporting that British Asians were dying at a higher rate than other ethnic and racial groups due to COVID-19. These concerns were reflected in the correspondence Saini received from medical professionals in the field.

“I remember one dentist, Asian dentists, emailing me and saying, ‘Is it safe for me to go to work because I’ve heard that Asian people are more susceptible to this virus naturally, genetically more susceptible than other people.’ And I just said ‘The reason that British Asians are dying in larger numbers, especially that year was because we tended to work in frontline professions more than anybody else,'” she said.

Saini also pointed out that the first SARS-CoV-2 outbreaks hit London, which is “a minority white British city with a huge British Asian population.”

She said comparatively, “the statistics are not going to look the same” as the rest of the U.K. This not only propagated misinformation at the time but also affected vaccine uptake.

Racism: A maternal health problem

Dr. Rainford also shared Shalon Irving’s story, a 36-year-old Black mother, who was an epidemiologist at the Centers for Disease Control and Prevention (CDC), but died three weeks after giving birth due to complications of high blood pressure.

“Dr. Shalon Irving was a double Ph.D., and she worked at the CDC. So she was a woman, an educated woman with means who had a successful delivery by cesarean section for other reasons. But after delivery, she had some issues, and she kept returning to seek medical care for those issues related to high blood pressure, which was existing,” she said.

“She kept returning, however, it seems—based on everything I’ve read and know—that the system failed her. They kept telling her everything was okay. They kept telling her; she was alright, they kept sending her home. And the last time they sent her home, they gave her a prescription for an antihypertensive pill. And she went home collapsed, and was immediately rushed to the hospital life support. Shortly after that, she died, that was within weeks of delivery of her very first child,” she continued.

Dr. Rainford said Dr. Irving’s story was one that influenced her to discover more about the disparities that Black women face in the U.S. and write her book, in which she aimed to uncover, expose, and explain this problem.

How the stress of racism affects aging and health

When one talks of the impact of racism on health, epigenetics is an important area of study to include in the discussion. In essence, epigenetics is rooted in the idea that people’s behaviors and their environment can cause changes in the way genes are expressed.

Such changes—or in other words, the transgenerational effects of adversity—have been observed in the immune system, on mental health, and even the gut microbiome.

A recent study, for example, found that hardships experienced by mothers during their childhood or pregnancy were reflected in the composition of their children’s gut microbiomes.

Dr. Rainford said that the works of Dr. David Barker originally from the U.K. and Dr. Kent Thornburg in the U.S. are of particular importance when discussing epigenetics.

“They found that epigenetic changes [d]on’t change the genes, but they change how genes are expressed that can be passed from generation to generation. And they’ve noted that stress, including the chronic stresses of racism, can cause those epigenetic effects that affect the children of people suffering those stressors, and the grandchildren of people suffering those stressors. And those stressors could be both economic and racial discrimination,” she said.

Racial weathering

Dr. Rainford introduced the terms “weathering” and “allostatic load” to our conversation when discussing the long-term health impacts of racism. The latter can be described as “the wear and tear on the body” from the chronic stress and cumulative burden an individual faces.

“Another effect that is ‘biological’ but due to the stress of racism is something called weathering, quantifying this allostatic load,” she said, referring to Dr. Arline T. GeronimusTrusted Source‘ work.

“She found that Black women have a biological age of 10 years in excess of their chronological age because of the stresses of racism,” said Dr. Rainford.

Multiple studies have since found evidence of this type of accelerated aging. One, for example, found that Black people are approximately three years olderTrusted Source biologically than white people.

Dr. Rainford also touched on the work of Dr. Elizabeth Blackburn on telomeres, the protective tips at the end of chromosomes, which have been hailed as the “secret to longevity.”

“[Dr. Blackburn] found that chronic caregivers had shorter telomeres because of the stress of giving chronic care to someone who’s ill. And she found that non-poor Black women also had shorter telomeres compared to white women and even men,” she said.

Dr. Rainford said this can explain why chronic stressors such as racism often lead to having diseases at an earlier age than one normally would.

Can science explain racial health disparities?

When discussing racial differences in health outcomes, the renin-aldosterone-angiotensin systemTrusted Source is often one of the first things to come to mind. Dr. Hilary Guite asked our guests what their take on it was.

“We know that hypertension is higher among Black Americans and Black Britons. Preventable heart disease and stroke resulting from high blood pressure are two to three times more likely to kill a Black American than a white American. So it’s very easy for physicians then to draw correlations between some kind of biological difference and race,” said Saini.

She quoted research by Canadian epidemiologist Jay Kaufman, and American hypertension expert Richard Cooper, who found little to no genetic evidence that can account for such differences.

“[G]enetics has hugely undermined our ideas about deep-seated racial difference. And sometimes to the surprise of some geneticists who are expecting to see, for example, some kind of exceptional genetic groups in faraway places among indigenous groups, [they see] they are not particularly genetically exceptional. So, the vast majority of genetic difference is at the individual level, not at the group level,” she said.

Making a distinction between biology and genetics, Dr. Rainford further explained that the environmental conditions people grow up in are more likely to have a larger effect on health outcomes.

“If you are in a low-income community, and you do not have access to fresh food, you will eat what you can get, and what you can get is unhealthy for you. Also, what they found in studies is that air pollution in areas where predominantly Black people and people of color live is worse than air pollution in areas where predominantly white people live. [I]t’s a multiple of factors that ultimately have a biological effect, but nothing to do with genetic[s],” she said.

Is race a biological variable?

Using color to understand human differences and “dividing up the world by color—black, white, yellow, red, brown” was “outlandish,” said Saini.

“[Racial categories were] largely informed by the politics of the time, the transatlantic slave trade, colonialism, the patterns of economic political power at that time, which were divided along continental lines. And so this became conflated in the public imagination and in the medical imagination as some kind of meaningful way of understanding human variation,” Saini explained.

She reiterated that the classification of race has varied between countries and over time, which is testament that it is not a biological variable.

“So, for example, I moved to the U.S. two years ago. If I had moved in 1971 instead of 2021, I would be officially categorized as white. I’m now categorized as Asian. But in the U.S., people of Indian heritage were categorized as white in 1971. So we have to understand that these categories are not fixed. They’re not static; they’re always moving. And the reason for that is because the social conception of what race is, the social meaning of it is always changing,” she explained.

“Because race, I cannot stress enough, is not a biological variable. It was invented a few 100 years ago because of society and politics. If you understand the history of it, there’s no way that you can start to treat it as a biological variable because it just doesn’t make sense. It’s like talking about class as a biological variable.”
— Angela Saini

 What can we do to lessen the impact of racism on future health?

Dr. Guite recounted her own experience of being in medical school and how the teaching shaped her views and behaviors as an epidemiologist.

“[I was not] taught that different races were inferior [per se], but they were different. And as a doctor, you [might] need to know that so you’ve got a heightened awareness and a heightened trigger for action,” she said.

She went on to reference a studyTrusted Source in the U.K. that found a disparity in the link between BMI and diabetes risk for specific populations.

“For example, Dr. Tom Barber was one of our guests on a recent podcast and said he’d conducted a study showing that South Asian populations had the same risk of diabetes at a BMI of 24 compared to a white population of 30. So as a doctor, you need to have that heightened awareness to say, ‘Okay, I think I should check your HbA1c. So, in a sense, that, to me, doesn’t sound inferior. That sounds like something [like] a call to action. What am I missing here?” she asked.

Dr. Rainford said it was implicit racism.

“So, for example, you didn’t think you were taught any racist policies, but it was implicit. It’s implicit in everything that you learn,” she said.

“When you said we weren’t taught the races were inferior, we were taught that they were different — to be taught that races are different is the problem here. That is not true,” added Saini.

Is diversity the solution?

Representation for minoritized groups, although helpful, isn’t enough on its own. Looking at racism within the National Health System (NHS) in the U.K. gives a wider perspective.

“The BMJ and other journals have done some really good work lately, surveys that have looked at the experience of racism of not just patients, but staff within the NHS. The NHS in the U.K. has a disproportionately high number of ethnic minorities working within it. So we know that representation itself hasn’t made a difference there,” Saini said.

“[The way we are taught] that’s part of the problem with the medical profession. We have diversity in medicine, pretty good [in terms of] gender and ethnic diversity. And yet we still have problems with racism because of the way that we are trained, the way that we understand race, as a society hasn’t moved on.”
— Angela Saini

More support, better education

Dr. Rainford, meanwhile, drew attention to the lack of social, financial, and educational support for disadvantaged people due to structural racist policies.

“[I]t’s important that we even list the categories of race, not because of the genetic difference, but we do need to [recognize] that people who self-identify as Black are treated differently, disadvantaged, and may need more social and health support, because what racism has done to get them where they are now,” she said.

To enact greater change and see these attitudes shift, it all comes down to re-learning and re-teaching.

“[I] believe that the social sciences and humanities need to be integrated into the way that we teach race. So every year I’ve been part of a panel at Harvard Medical School for incoming undergraduates, in which myself and historians come together and explain the genesis of the idea of race to students, break down what it means to use race in medicine, and how to think about it more accurately, to remember that when you’re using it, you are talking about something that is heavily socially and politically defined,” said Saini.

Dr. Rainford was cautiously optimistic about the new generation.

“I am very hopeful for the medical students coming up because they know way more than we did; they are exposed, they are taught. However, training only works if people are concerned about learning. [I]f someone is motivated and open and recognizes that they may have limitations in their beliefs, then I believe there’s a great deal of hope,” she said.

Apart from changing the education system, on an individual level, we can also check our own biases. Dr. Rainford suggested Harvard’s Implicit Association Test to help people see their blind spots or uncover implicit racial biases.

Keeping the conversation going and engaging in such discussions, no matter how uncomfortable it may seem at first, is also crucial.

“[H]aving conversations like this is important because even a few people will listen and hopefully their eyes will be opened. And hopefully, they will think differently, even about things that were taught their whole lives. And to be clear, as a Black person, you are not exempt from holding racist attitudes against other Black people.”
— Dr. Monique Rainford

 Source - Medical News Today