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Exclusive eBook: How AI is becoming the next military advisor

A collection of stories about how militaries are using AI models to make decisions.

This subscriber-only eBook is a package of six stories that were originally published in MIT Technology Review between April 11, 2025, and April 21, 2026, and have been updated to reflect recent developments.

by James O’Donnell

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Mini Brains Help Identify Treatment for Rare Form Parkinson’s Disease

Brain organoids created in the lab using patient cells have allowed researchers based at the Wilhelmina Children’s Hospital in Utrecht to find out more about the progression of an ultra-rare type of childhood Parkinson’s disease.

Notably, as reported at the European Society of Human Genetics meeting in Gothenburg this week, the study also identified that an affordable and readily available form of vitamin B3 could help improve symptoms in these children.

Irena Muffels, MD, PhD, a clinical genetics resident at the Wilhemina Children’s Hospital, was working at the Icahn School of Medicine at Mount Sinai, New York, when the study began. Two parents contacted the lab where she was working to ask if they could look into the condition their children had been diagnosed with, a rare form of early Parkinson’s caused by mutations in the DHDDS gene.

“They contacted Professor Eva Morava, for whom I was then working. We started creating mini-brains—tiny blobs of brain tissue grown in the lab from patients’ own cells—thus avoiding the need to take samples directly from the children’s brains,” she explained.

Muffels and colleagues observed these mini brains in the lab and found there were significant signs of deterioration after four months mirroring that seen in the brains of children with this rare condition.

In healthy cells, DHDDS helps make dolichol, a small fat-like molecule that acts as a platform for attaching sugars to proteins. When DHDDS doesn’t work properly, dolichol levels fall. As a result, cells struggle to attach sugar chains, called glycans, to proteins in the usual way.

Those glycans are important because they help proteins fold correctly, reach the right place in the cell, and function as they should. In the patient‑derived mini brains, the team could see that these sugar chains were formed incorrectly.

Low dolichol also disrupts overall lipid regulation and causes cholesterol to build up in astrocytes, the brain’s supportive cells. “This accumulation builds over time, and this is why we think the disease progresses,” said Muffels, “since the accumulation of cholesterol leads to mitochondrial dysfunction, leading in turn to reduced energy production.”

Perlara, a rare‑disease biotech public benefit corporation that runs phenotypic screens in simple ‘patient avatar’ organisms, helped Muffels and colleagues identify nicotinamide mononucleotide, a naturally occurring type of vitamin B3, in a yeast‑based assay as a potential modifier of DHDDS‑driven cellular stress.

The vitamin appeared to have positive effects on the mini brains, and when the families of patients heard about it, they began using the supplement as it is readily available without a prescription and known to be safe. Within a few weeks, the patient’s walking got better and they had more energy and less tremors.

“The word about nicotinamide mononucleotide reached more DHDDS patients, and we currently have 12 patients taking it. We recently received funding from Congenital Disorders of Glycosylation UK…  to start an international trial for nicotinamide mononucleotide supplementation in DHDDS-related disease,” said Muffels.

“Patients will take nicotinamide mononucleotide for a year and will be evaluated every three months. Although I have now left the U.S., I hope that the Wilhemina Hospital in Utrecht will be one of the official sites and that I may continue to work with these patients.”

The post Mini Brains Help Identify Treatment for Rare Form Parkinson’s Disease appeared first on Inside Precision Medicine.

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Single-Cell RNA Sequencing Reveals Gene Activity Changes in Crohn’s Disease

Researchers from the Wellcome Sanger Institute, Cambridge University Hospitals NHS Foundation Trust (CUH), and Open Targets have created a detailed cellular study of Crohn’s disease (CD), mapping how gene activity changes across more than 50 cell types in the gut. (Founded in 2014, Open Targets is a pre-competitive, public-private partnership that uses human genetics and genomics data to systematically identify and prioritize drug targets.)

Co-led by Tim Raine, MD, PhD, consultant gastroenterologist at Cambridge University Hospitals NHS Foundation Trust, the team analyzed over a million gut cells from people with Crohn’s and from healthy controls, comparing changes in the gut lining and identifying immune cells that drive inflammation. The resulting single cell RNA-sequencing (sc-RNA-seq) resource, IBDverse, characterizes each cell type and those whose activity shifts in disease, uncovering new molecular and cellular signatures of immune activity in the gut lining.

Co-first author Monika Krzak, PhD, formerly at the Wellcome Sanger Institute and now based at the Institute of Metabolic Science, University of Cambridge, said, “Crohn’s disease is complex, variable and deeply personal to every individual living with it, which is why understanding it at the level of single cells is so important. By creating this unprecedented map of more than one million gut cells, we are giving researchers around the world a powerful new tool to uncover how inflammation begins, persists and may one day be stopped. This is the kind of open science that can accelerate discoveries and bring us closer to better treatments for patients.”

Raine added, “There is an urgent need for increased understanding of the biology of Crohn’s disease if we are to develop more effective and safe medications for people living with this condition. The patients who contributed to this research have helped us build insight into the different ways that gut function and immune function are disrupted in the disease, and with the insight comes immediate new avenues for drug development and targeted therapies.”

Reported in Nature Genetics (“Single-cell RNA sequencing of terminal ileal biopsies identifies signatures of Crohn’s disease pathogenesis,”) the research revealing the cell types and molecular changes involved in Crohn’s inflammation is one of two complementary studies—the other a paper recently published in Nature—built on IBDverse to investigate different aspects of the disease.

In their newly published report the team concluded, “These findings establish a comprehensive cellular and molecular framework for CD, offering insights into disease mechanisms and therapeutic opportunities.”

Inflammatory bowel disease (IBD) is an umbrella term used to describe disorders that cause chronic inflammation of the gastrointestinal tract. Over half a million people in the U.K. are estimated to be living with IBD, which includes Crohn’s disease and ulcerative colitis.

Crohn’s is a chronic condition that causes inflammation and ulcers in the digestive tract, from the mouth to the anus, often affecting the small intestine and colon. However, the authors noted, “Although inflammation is most commonly observed in the terminal ileum, CD exhibits substantial heterogeneity in disease location, severity and behavior, both between patients and within patients, over time.”

Although inflammation is most commonly observed in the terminal ileum—the final section of the small intestine—Crohn’s is found in many locations of the body and with variation in severity both between patients and within patients over time.

While therapies targeting immune cells have improved clinical outcomes for some patients, non-response to treatment remains high, with 15% of Crohn’s patients requiring surgery within five years of diagnosis. Consequently, there is an urgent need to better understand the etiology of CD in order to broaden therapeutic opportunities,” the investigators stated.

For their newly reported study the researchers took and analyzed biopsies from 111 patients with Crohn’s and a history of current or previous terminal ileitis—inflammation of the ileum—and 232 healthy volunteers. The team performed single-cell RNA sequencing to measure gene expression in individual cells. “Single-cell RNA sequencing (scRNA-seq) technologies provide a high-throughput means to dissect complex tissues at the resolution of single cells and cell types,” they noted.

By creating a comprehensive map of cellular and molecular differences in Crohn’s compared to healthy controls, the researchers established IBDverse as a result—an online data resource of over 1,185,000 cells isolated from small intestine samples. The large IBDverse dataset will serve as an open resource for future research.

Using the data, the scientists identified genes that are abnormally expressed in Crohn’s and those where expression is specific to given cell types and cellular processes.

One of the study’s most striking findings was a ‘molecular scar’ in the gut lining. Even after visible inflammation had healed, genes that help send messages to the immune system stayed switched on in the gut’s stem cells—the cells that constantly renew the lining. This suggests that an episode of inflammation leaves a lasting mark on these cells, which may shape how the gut responds to inflammation in future. In their paper the authors noted, “We uncovered epithelial changes marked by interferon-driven upregulation of major histocompatibility complex class I molecules that persisted in progenitor cells after macroscopic inflammation resolution.”

The researchers also identified a population of macrophages—immune cells that engulf and digest cellular debris—with high expression of the gene ITGA4. These cells were key drivers of inflammation through the JAK/STAT pathway, which carries signals from the cell surface to the nucleus to switch genes on and off. “ITGA4+ macrophages were identified as key inflammatory drivers, showing enriched JAK–STAT signaling and cytokine expression (interleukin-6 (IL-6), IL-12 and IL-23),” the investigators stated. Drugs that block this pathway, known as JAK inhibitors, are already used to treat IBD, which points to these macrophages as a likely target of therapies.

Co-first author Tobi Alegbe, PhD, at the Wellcome Sanger Institute and Open Targets, said “For inflammatory bowel diseases like Crohn’s and ulcerative colitis, it’s still unclear what is going wrong in the gut cells to cause inflammation. We have been able to compare gut cells of hundreds of people with and without IBD. This has given us new insight into the genes and cell types that are involved during active disease, and lays the groundwork for similar approaches to understand diseases of other major organs like eczema and asthma.”

Co-senior author Carl Anderson, PhD, at the Wellcome Sanger Institute, said “What makes this study different is that we designed replication in from the start and found that even with hundreds of patients and standardized protocols, fewer than half of the gene expression changes we detected in one cohort replicated in the other. That’s a sobering finding for the field. The biology that did replicate consistently points to the gut lining itself as a key player in Crohn’s with a molecular signature in epithelial cells that persists even after inflammation has resolved. We don’t yet know what that persistence means, but it likely influences how the gut responds to future inflammatory insults.”

The post Single-Cell RNA Sequencing Reveals Gene Activity Changes in Crohn’s Disease appeared first on GEN – Genetic Engineering and Biotechnology News.

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Fibroblast Signaling Pathways Linked to Angiogenesis Differences in NSCLC

An international collaboration led by researchers at the University of Barcelona, Spain, have identified why the two most common forms of non-small cell lung cancer (NSCLC)—lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC)—respond differently to anti-angiogenic therapies that target the blood vessels tumors need to grow. The study found that fibroblasts within the tumor microenvironment play a central role in shaping blood vessel formation, oxygen availability, and treatment response. The findings, published in the journal Cell Death & Disease, could pave the way for treatment decisions that are guided not only by tumor type but also by characteristics of the tumor microenvironment.

“The study reveals that the fibroblast-rich tumor microenvironment is not merely a spectator but a key player that shapes the tumor’s progression. Tumor-associated fibroblasts can influence the vascular network, the availability of oxygen and nutrients and, potentially, also metastatic dissemination and the immune response,” said senior author Jordi Alcaraz, PhD, a professor at the University of Barcelona’s Faculty of Medicine and Health Sciences and researcher at the Institute for Bioengineering of Catalonia.

The new study provides additional evidence that can be used to ascertain the viability of combining anti-angiogenic treatments with immunotherapy. Interest in this potential combination therapy has been growing over the past several years, to address the limited success of immunotherapy alone in treating NSCLC. Anti-angiogenic treatments are of interest since blood vessel growth has been shown to contribute to immune suppression and treatment resistance. But while anti-angiogenic drugs have shown benefits in lung adenocarcinoma, their efficacy has been limited or have produced toxicity as a treatment for squamous cell carcinoma.

“These contrasting outcomes and the limited overall therapeutic benefits attained by anti-angiogenic drugs in LUAD (adenomcarcinoma) underscore the need for a more nuanced understanding of the histotype-dependent complexity of angiogenesis regulation in NSCLC,” the researchers wrote.

For this study, the international team analyzed markers of angiogenesis and hypoxia across multiple patient cohorts. They used a combination of transcriptomic analyses in both lab and animal studies to examined how tumor-associated fibroblasts regulate blood vessel formation in the two major lung cancer subtypes.

The data showed clear differences between the two cancers. Adenocarcinoma tumors had greater angiogenesis, larger vessel lumens, higher oxygen availability, and less necrosis and hypoxia, while squamous cell carcinomas exhibited poorer blood vessel formation, increased hypoxia, and more necrotic tissue.

The investigators determined that fibroblasts from adenocarcinoma tumors produced a pro-angiogenic secretome characterized by elevated levels of vascular endothelial growth factor A (VEGF-A) and tissue inhibitor of metalloproteinases-1 (TIMP-1). “The LUAD-TAF secretome was primed for angiogenesis through SMAD3-dependent overproduction of key regulators, particularly TIMP-1 and VEGF-A,” the researchers wrote adding that “we also uncovered a novel function for TIMP-1 in promoting endothelial cell hyperbranching over basal VEGF signaling.” The findings showed that TIMP-1 amplified VEGF-driven angiogenesis and increased formation of the branching vascular networks commonly associated with tumors.

In squamous cell carcinoma, however, fibroblasts behaved differently. “By contrast,” Alcaraz said, “in squamous cell carcinoma, blood vessel formation is inefficient due to molecular changes in the associated fibroblasts resulting from higher tobacco exposure, resulting in tumors with lower oxygen levels, that is, more hypoxic.”

The findings may also help explain differences in disease progression between the two cancers. Because metastasis depends on tumor cells gaining access to blood vessels, the more developed vascular networks in adenocarcinoma likely play a role to its tendency to spread earlier than squamous cell carcinoma.

These finding could influence new approaches for stratification and treatment selection of patients with NSCLC. Potential biomarkers include the SMAD3/SMAD2 ratio, TIMP-1 levels, VEGF-A expression, and hypoxia-associated fibroblast signatures. The researchers suggest that adenocarcinoma patients may benefit from therapies targeting stromal SMAD3 signaling or TIMP-1, while patients with squamous cell carcinoma may benefit more from treatments designed to counter hypoxia, acidosis, or other features of the tumor microenvironment.

Future research will focus on validating biomarkers such as TIMP-1 in larger patient populations and prospective studies, better understanding the molecular interactions that link SMAD3, VEGF-A, and TIMP-1, and developing treatments that target these pathways. As Alcaraz noted, the challenge now is to identify robust biomarkers, validate them prospectively, and demonstrate that modifying the tumor microenvironment can improve therapeutic responses.

The post Fibroblast Signaling Pathways Linked to Angiogenesis Differences in NSCLC appeared first on Inside Precision Medicine.

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Using AI to Detect Psychosis Relapse: Scoping Review

Background: Psychotic disorder represents a leading cause of disability worldwide, and relapse in psychosis is common. Artificial intelligence (AI) is increasingly recognized as a method that could aid clinical monitoring for individuals experiencing psychosis. Objective: This review aims to map the existing literature on AI-based approaches—including machine learning, deep learning, and natural language processing—used to detect relapse in individuals with psychotic disorders. Methods: A systematic search strategy was conducted on PubMed, PsycINFO, and Embase up to January 7, 2026. Observational studies, randomized controlled trials, and quasi-experimental studies that used AI methods to detect relapse in psychosis were eligible for inclusion. Screening and data extraction procedures were conducted by at least 2 reviewers working independently. Findings were extracted, charted, and described using narrative synthesis based on data extraction and consensus meetings with the research team. The scoping review was prospectively registered with the Open Science Framework. Results: Relevant studies identified (N=10) included the use of digital tools such as smartphone- and smartwatch-based monitoring, ecological momentary assessment tools, social media activity, and internet searches. Digital phenotyping via smartphones and wearables emerged as the most common method for data collection. The efficacy of AI models varied with sensitivity (or recall) ranging from 0.25 to 0.77 and specificity (or precision) ranging from 0.06 to 0.88. The reported area under the receiver operating characteristic curve for models ranged from 0.63 to 0.78. AI models were heterogeneous across studies, and most study findings were not replicated. Conclusions: This scoping review highlights both the promise and the current limitations of AI in psychosis relapse detection. Passive digital phenotyping research in the detection of psychosis relapse has progressed, and personalized approaches with individual-level modeling show promise; however, further studies need to include larger numbers of participants and should incorporate methods such as large language models. Future studies will require large collaborations aimed at delivering AI methods for use in real-world clinical practice.
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Introducing the 2026 IOCDF Award Winners of the 2026 Annual OCD Conference

The mission of the International OCD Foundation — to ensure that no one affected by OCD or related disorders suffers alone — requires the collaboration and dedication of countless individuals and professionals around the world. Each year, the IOCDF is honored to recognize a few of these contributors who have gone above and beyond to inspire hope, build community, and move us closer to a world where everyone has access to effective support and care.

These awards will be presented at the 31st Annual OCD Conference, sponsored by OCD Institute Texas, on Saturday, July 11, 2026.

2026 Career Achievement Award Winner: Sabine Wilhelm, PhD

Highlighting the significant and notable contributions of a professional in the field of OCD and related disorders.

Sabine Wilhelm, PhD, is the Donovan-Chien Family Endowed Professor at Harvard Medical School and Chief of Psychology at Mass General Brigham. She directs both the Center for OCD and Related Disorders and the Center for Digital Mental Health at Massachusetts General Hospital. Dr. Wilhelm’s work leverages AI and technology to improve mental health care globally, focusing on developing personalized, scalable digital treatments. She has authored 375 publications and nine books. She has received major awards, including the NAMI Scientific Research Award and the Peter Ranney Innovation Award from the World Medical Innovation Forum. Dr. Wilhelm is the outgoing Chair of the IOCDF Scientific & Clinical Advisory Council after serving since 2023, and she has served on numerous committees to support the Foundation’s work to advance research and resources for OCD and related disorders.

2026 Patricia Perkins Service Award Winner: Aureen Wagner, PhD

Honors any professional or IOCDF member who has stood out as a long-time (10+ years) and active contributor to the IOCDF in multiple ways. This award is named after Patricia Perkins, IOCDF co-founder, past president of the Board of Directors, and previous executive director.

Winner Bio: Aureen Pinto Wagner, PhD, has been involved with the International OCD Foundation since 1992 and a frequent presenter at its conferences and programs for families, clinicians, and youth. She serves on the IOCDF’s Scientific and Clinical Advisory Board and has been faculty with the Behavior Therapy Training Institute since 2001.

Dedicated to expanding access to evidence-based OCD treatment, Dr. Wagner provides clinician training, workshops, and consultation nationwide. She is the author of the professional treatment manual Treatment of OCD in Children and Adolescents: A Professional’s Kit and several award-winning books for families, including  “Up and Down the Worry Hill: A Children’s Book about Obsessive-Compulsive Disorder and its Treatment,” “What to do when your Child has Obsessive-Compulsive Disorder: Strategies and Solutions” and “Worried No More: Help and Hope for Anxious Children.”

At The Anxiety Wellness Center in Cary, North Carolina. Dr. Wagner provides in-person and telehealth treatment for children, adolescents, and adults with OCD, anxiety, and related conditions, along with parenting support for families.

2026 Hero Award Winner: Stephen Smith

Recognizes any individual that has stood out as a particularly effective advocate for OCD and related disorders or who helped raise awareness of these disorders. 

Stephen Smith is the Co-founder and Chief Executive Officer of NOCD, the world’s largest OCD-specialty treatment provider for both adults and children. After emerging from a personal struggle with undiagnosed OCD and experiencing the success of Exposure & Response Prevention (ERP) therapy first-hand, Stephen made it his mission to transform the behavioral health treatment system for people with OCD and related conditions. Under his leadership, NOCD has done that. NOCD drives OCD awareness campaigns that reach millions of people each year, cares for hundreds of thousands of people with OCD, and is contracted to serve more than 140 million commercial lives nationally.

2026 Youth Hero Award Winner: Gabriella Lee

Recognizes any youth (under 18) that has stood out as a particularly effective advocate for OCD and related disorders or who helped raise awareness of these disorders. This award is presented by UNSTUCK: an OCD kids movie.

Gabriella Chaeyoon Lee is a junior at Great Oak High School in California who is dedicated to promoting mental health awareness, particularly surrounding OCD. Inspired by her personal connection to OCD through her mother’s diagnosis, she actively works to reduce stigma and support others through her school club and independent initiatives. She is passionate about creating safe and inclusive spaces where individuals feel understood and supported. She hopes to continue her advocacy and contribute to meaningful change in mental health communities.

2026 Illumination Award Winner: Tiffany Jenkins

Honors media personalities who have represented OCD or related disorders in a respectful, accurate, and appropriate way, or who have challenged stereotypes and helped to fight stigma around mental health issues.

Tiffany Jenkins is a comedian, New York Times bestselling author, speaker, and podcast host with a combined social media following of over 9 million and more than one billion video views worldwide.

While widely recognized for her relatable and candid comedy, Tiffany is deeply committed to raising awareness around mental health and addiction. Drawing from her own lived experience in recovery, she travels across the United States speaking at high schools, correctional facilities, treatment centers, and conferences, where she delivers impactful, honest conversations that resonate with diverse audiences.

Above all, Tiffany is a devoted mother, bringing authenticity, resilience, and humor into both her work and her everyday life.

The post Introducing the 2026 IOCDF Award Winners of the 2026 Annual OCD Conference appeared first on International OCD Foundation.

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Adaptive Deep Brain Stimulation Improves Walking and Reduces Falls in Parkinson’s Disease

Researchers at the University of California, San Francisco (UCSF) have developed a new form of adaptive deep brain stimulation (aDBS) that adjusts therapy in real time as patients walk, improving gait stability and reducing falls in people with Parkinson’s disease.

Published in Nature Medicine, the study demonstrates for the first time that an implanted neurostimulator can detect brain signals associated with individual steps and modify stimulation within fractions of a second. The approach represents a significant advance in personalized neuromodulation and could help address one of the most difficult-to-treat symptoms of Parkinson’s disease.

“Difficulty walking is one of the most disabling symptoms of Parkinson’s disease and one of the hardest to treat,” said senior author Doris D. Wang, MD, PhD, associate professor of neurological surgery at UCSF. “Walking is a highly dynamic behavior that requires precise timing across both sides of the body. We developed a system that can recognize those movement patterns and respond in real time, effectively allowing the stimulation to work with the patient as they move.”

Addressing a major unmet need in Parkinson’s disease

More than 10 million people worldwide are living with Parkinson’s disease, a progressive neurodegenerative disorder characterized by tremor, rigidity, slowness of movement, and postural instability.

Deep brain stimulation has become an established treatment for many motor symptoms of the disease, particularly tremor and rigidity. However, gait impairment, freezing of gait, and falls often persist despite therapy and are major contributors to disability, hospitalization, and loss of independence.

One limitation of conventional DBS is that it delivers continuous stimulation regardless of a patient’s activity. While effective for relatively stable symptoms, this approach may not adequately support complex behaviors such as walking, which require rapid and constantly changing coordination between the brain, spinal cord, and muscles.

The UCSF team hypothesized that stimulation timed to a patient’s actual movements might provide more effective support for gait control.

Turning brain signals into therapeutic feedback

To develop the system, researchers identified neural activity patterns associated with movements of the left and right legs. These movement-related signals were then incorporated directly into an implanted neurostimulator capable of adjusting therapy automatically during different phases of walking.

Unlike previous adaptive DBS approaches that typically respond to slower changes in disease-related brain activity, the new system operates on a timescale of milliseconds and responds directly to behavior itself.

“The brain contains remarkably rich information about movement,” said first author Kenneth H. Louie, PhD, a UCSF postdoctoral scholar. “We found that we could identify neural signatures linked to each step and use them to guide stimulation in real time.”

The researchers liken the device to a cardiac pacemaker. Rather than delivering constant stimulation, the neurostimulator continuously monitors neural signals and dynamically modifies therapy to match the brain’s walking rhythm.

The system performs these adjustments internally without requiring an external computer, making it suitable for real-world use outside the laboratory.

Testing the adaptive system

The study enrolled five individuals with Parkinson’s disease who had previously undergone DBS surgery as part of a UCSF investigational research program.

In addition to therapeutic DBS leads implanted deep within the brain, participants received research electrodes positioned over motor-related cortical regions. These electrodes allowed researchers to record neural activity associated with walking and identify personalized movement signatures for each participant.

Using these individualized neural biomarkers, investigators programmed the implanted device to automatically adjust stimulation during walking.

Laboratory testing demonstrated improvements in several objective measures of gait performance, including increased gait symmetry and reduced variability between steps. Both metrics are associated with more stable and efficient walking patterns.

The researchers then evaluated the system in participants’ daily lives through a blinded, multi-day crossover study comparing periods with adaptive stimulation and periods with conventional stimulation settings.

During adaptive stimulation, participants experienced fewer falls while maintaining overall control of their Parkinson’s symptoms.

No serious adverse events were reported, and participants tolerated the rapid stimulation changes without difficulty.

Although the trial was small, the findings provide early evidence that matching stimulation to behavior may offer benefits beyond those achieved with continuous DBS.

A shift toward behavior-responsive neuromodulation

The study highlights an emerging trend in neuromodulation: moving from static therapies toward systems that continuously sense and respond to changing neural states.

Most adaptive DBS technologies under development focus on biomarkers that fluctuate over minutes or hours. The UCSF approach instead targets neural signals associated with immediate actions, enabling stimulation to respond almost instantaneously.

“This study is about more than walking,” said Wang. “It demonstrates that brain stimulation can adapt to what a person is doing in real time. That opens the door to future therapies that respond dynamically to movement, speech, mood, cognition, and other brain functions.”

The concept could ultimately extend beyond Parkinson’s disease to other neurological and psychiatric disorders in which symptoms vary throughout the day.

Toward intelligent brain implants

Researchers envision future implanted devices that function as closed-loop systems, continuously monitoring neural activity and delivering therapy only when needed.

Such systems could potentially improve treatment efficacy while reducing side effects and conserving device battery life. By tailoring stimulation to specific behaviors or symptoms, clinicians may be able to provide more precise and individualized care.

The work also represents an important technological milestone because the adaptive algorithms were embedded directly within the implanted device rather than relying on external processing hardware.

“This is an important step toward a new generation of brain therapies,” Wang said. “Instead of delivering the same stimulation all day long, future devices may continuously listen to the brain and immediately respond to a patient’s needs. Just as pacemakers transformed the treatment of heart disease, intelligent neurostimulators may transform how we treat disorders of the brain.”

While larger clinical studies will be needed to confirm the benefits of the approach, the results provide an early demonstration that real-time, behavior-responsive neuromodulation may offer a new way to address some of Parkinson’s disease’s most challenging symptoms.

The post Adaptive Deep Brain Stimulation Improves Walking and Reduces Falls in Parkinson’s Disease appeared first on Inside Precision Medicine.