Scientists at Pacific Northwest Research Institute (PNRI) have overturned a long-held belief in genetics: that inheriting two harmful variants of the same gene always worsens disease. Instead, the team found that in many cases, two harmful variants can actually restore normal protein function.
Their work appears in the Proceedings of the National Academy of Sciences.
Parkinson’s disease (PD) is a debilitating and progressive neurodegenerative disorder caused by the loss of dopamine-producing neurons in the substantia nigra, a brain region essential for motor control. Clinically, it is marked by tremor, rigidity, bradykinesia and postural instability, symptoms that progressively erode independence and quality of life.
PD affects millions of people worldwide, including nearly one million individuals in the United States, making it one of the fastest-growing neurological disorders. In the U.S. alone, the disease imposes a profound health care and socioeconomic burden, with annual costs reaching tens of billions of dollars due to medical care, lost productivity and long-term disability.
While environmental factors contribute to disease risk, genetic drivers are increasingly recognized, with mutations in the leucine-rich repeat kinase 2 (LRRK2) gene representing one of the most common causes of both familial and sporadic PD. Understanding how LRRK2 mutations drive disease is therefore central to developing therapies that go beyond symptoms control.
Over 70 million Americans wear digital activity trackers (DATs) to record their sleep, steps and heart rate. A new study from Scripps Research found that these devices could also provide insight into even more, including individual health risks like obstructive sleep apnea (OSA) and high blood pressure.
The findings, published in the Journal of Medical Internet Research on December 3, 2025, used DATs to identify an association between sleep variability—the night-to-night fluctuation of when an individual falls asleep and wakes—and their risk of developing sleep apnea and hypertension. This research joins a growing body of evidence that DATs could become more useful clinical tools to assess health risks in the near future.
“Data from digital activity trackers provides a unique way to detect meaningful health patterns from the devices that people already own,” says Stuti Jaiswal, senior author and assistant professor at Scripps Research, who is also a faculty hospitalist at Scripps Clinic. “Digital health studies have been gaining acceptance over the past decade, and we’re now demonstrating what these technologies can reveal about how sleep influences cardiovascular health.”
Long-term exposure to fine particulate matter like PM2.5 components in polluted air can not only cause respiratory diseases, but also increase the risk of depression in older people, especially in those living with preexisting heart, metabolic and neurological conditions.
Depression has caused more loss of healthy life worldwide than any other mental health condition. This disorder has snatched away people’s will to perform the basics of daily activities. An analysis of global health data in 2021 showed that all the years people lived with disability or reduced quality of life because of depression added up to about 56.3 million years.
A recent population-based cohort study collected data from nearly 23.7 million U.S. Medicare beneficiaries aged 65 years and older between 2000 and 2018 to examine specific components of PM2.5 exposure, both individually and in combination, and its associations with the risk of developing depression. Among those tracked, more than 5.5 million developed depression during the follow-up period. These findings are published in JAMA Network Open.
Wearable electronics could be more wearable, according to a research team at Penn State. The researchers have developed a scalable, versatile approach to designing and fabricating wireless, internet-enabled electronic systems that can better adapt to 3D surfaces, like the human body or common household items, paving the path for more precise health monitoring or household automation, such as a smart recliner that can monitor and correct poor sitting habits to improve circulation and prevent long-term problems.
The method, detailed in Science Advances, involves printing liquid metal patterns onto heat-shrinkable polymer substrates—otherwise known as the common childhood craft “Shrinky Dinks.” According to team lead Huanyu “Larry” Cheng, James L. Henderson, Jr. Memorial Associate Professor of Engineering Science and Mechanics in the College of Engineering, the potentially low-cost way to create customizable, shape-conforming electronics that can connect to the internet could make the broad applications of such devices more accessible.
“We see significant potential for this approach in biomedical uses or wearable technologies,” Cheng said, noting that the field is projected to reach $186.14 billion by 2030. “However, one significant barrier for the sector is finding a way to manufacture an easy-to-customize device that can be applied to freestanding, freeform surfaces and communicate wirelessly. Our method solves that.”
Immune cells work to fight infection and other diseases. Different subsets work together to elicit a healthy immune response; however, infections and disease can dysregulate cells and prevent effective immunity. Interestingly, cancer can use immune cells to its advantage.
Cancer employs various mechanisms to alter the immune system. Once established, tumor cells secrete proteins and molecules to generate a favorable environment. In this case, the tumor microenvironment (TME) becomes hypoxic due to a lack of oxygen with increased blood vessel growth to bring nutrients to the tumor and altered cell types that promote tumor progression. Specifically, tumor-secreted molecules polarize healthy immune cells, which allow cancer cells to proliferate and travel to distal tissues of the body.
T cells are specific immune cells responsible for identifying and targeting pathogens. Receptors on T cells recognize proteins on the surface of infected cells, which stimulate an immune response that eliminates the disease. These cells are critical for effective health and many immunotherapies aim to amplify or enhance T cell function. In the context of cancer, these T cells lose their function and, in some cases, promote tumor growth by inhibiting other immune cells. Unfortunately, treatment efficacy is limited to specific subsets of patients due to tumor type and stage of disease. Scientists are currently working to understand more about T cell biology and enhance immunotherapy.
The 2026 Timeline: AGI Arrival, Safety Concerns, Robotaxi Fleets & Hyperscaler Timelines ## The rapid advancement of AI and related technologies is expected to bring about a transformative turning point in human history by 2026, making traditional measures of economic growth, such as GDP, obsolete and requiring new metrics to track progress ## ## Questions to inspire discussion.
Measuring and Defining AGI
🤖 Q: How should we rigorously define and measure AGI capabilities? A: Use benchmarks to quantify specific capabilities rather than debating terminology, enabling clear communication about what AGI can actually do across multiple domains like marine biology, accounting, and art simultaneously.
🧠 Q: What makes AGI fundamentally different from human intelligence? A: AGI represents a complementary, orthogonal form of intelligence to human intelligence, not replicative, with potential to find cross-domain insights by combining expertise across fields humans typically can’t master simultaneously.
📊 Q: How can we measure AI self-awareness and moral status? A: Apply personhood benchmarks that quantify AI models’ self-awareness and requirements for moral treatment, with Opus 4.5 currently being state-of-the-art on these metrics for rigorous comparison across models.
AI Capabilities and Risks.