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The neuroscience of hypocrisy points to a communication breakdown in the brain

Half of the participants received actual stimulation aimed at the ventromedial prefrontal cortex. The other half received a fake version of the treatment, known as a sham stimulation. After the procedure, all participants completed the same card game and judgment exercises.

The people who received the real brain stimulation showed a wider gap between their behavior and their judgments. By disrupting the normal function of the brain region, the researchers successfully made people more hypocritical. This proved that the ventromedial prefrontal cortex directly controls moral consistency.

These results suggest that moral consistency is not an automatic trait. It is a biological process that relies on the brain’s ability to sync up different types of information. “Our findings suggest that we should treat moral consistency like a skill that can be strengthened through deliberate decision making,” says senior author Hongwen Song of the University of Science and Technology of China.

Scientists find a new therapeutic target present on up to half of all tumors

For five decades, scientists have known about a notorious cancer-causing enzyme called SRC. But they always assumed it only appeared on the inside of cells, where it sent signals that fueled tumor growth and stayed hidden from the immune system. But now researchers at UC San Francisco have discovered that the SRC enzyme also appears like a flag on the surface of bladder, colorectal, breast, pancreatic and probably many other tumor cells.

As cancer cells furiously divide, they produce a lot of garbage. In healthy cells, the trash gets broken down. But in tumors, the recycling system gets overwhelmed, and the cells expel some of their trash. This pushes the SRC onto the surface of the cell, where it is visible to potential therapies, like antibodies.

Researchers targeted SRC with antibodies that carried radioactive payloads or summoned immune cells. This killed the cancer cells, shrinking tumors in mice. The new target could apply to up to half of all tumors.

AI search robot uses 3D maps and internet knowledge to find lost items

A robot that can locate lost items on command, the latest development at the Technical University of Munich (TUM), combines knowledge from the internet with a spatial map of its surroundings to efficiently find the objects being sought. The new robot from Prof. Angela Schoellig’s TUM Learning Systems and Robotics Lab looks like a broomstick on wheels with a camera mounted at the top. It is one of the first robots that not only integrates image understanding but also applies it to a clearly defined task.

To find a pair of glasses misplaced in the kitchen, for example, the robot has to look around and build a three-dimensional image of the room. The camera initially provides two-dimensional images, but these pixels also contain depth information. This creates a spatial map of the environment that is accurate to the centimeter and is constantly updated. A laptop also provides the robot with information about which objects are visible in the image and what significance they have for humans.

“We have taught the robot to understand its surroundings,” says Prof. Schoellig. The head of the Robotics Lab at the TUM Chair of Safety, Performance and Reliability for Learning Systems aims to develop robots that can navigate any environment independently. Humanoid robots working in factories or robots in care settings in private homes require this newly developed basic understanding, which, as Schoellig explains, “is important for all robots that move in spaces that are constantly changing.” A paper introducing the technology is published in the journal IEEE Robotics and Automation Letters.

Pck1 Deficiency Drives Mitochondrial Dysfunction and Cellular Senescence in Adipocytes

Adipose tissue is one of the most vulnerable tissues during aging, and its dysfunction plays a pivotal role in age-associated physiological impairments (Ou et al. 2022). As the primary energy storage and endocrine organ, adipose tissue serves as a central hub for maintaining energy and metabolic homeostasis (Zwick et al. 2018). Age-related accumulation of the dysfunctional adipose tissue, particularly visceral fat, induces chronic inflammation and insulin resistance, leading to metabolic disorders (Reyes-Farias et al. 2021 ; Zhang, Jiang, et al. 2024). Clearance of senescent cells in white adipose tissue (WAT) has been shown to significantly mitigate aging-related metabolic dysfunction in murine models, highlighting a pivotal role of WAT in organismal aging (Palmer et al. 2019 ; de Oliveira et al. 2025).

Senescent cells undergo metabolic reprogramming, resulting in abnormal accumulation of detrimental metabolites that further reinforce inflammatory and senescence pathways (Maqdasy et al. 2022 ; Dou et al. 2023 ; Zhang, Higgins, et al. 2024). These cells are identified by a combination of molecular features, including elevated senescence-associated β-galactosidase (SA-β-gal) activity, increased expression of cyclin-dependent kinase inhibitors p21 and p16, persistent DNA damage response, and secretion of the senescence-associated secretory phenotype (SASP) (Di Micco et al. 2021). Mitochondrial dysfunction is a critical driver of cellular senescence (Gonzalez-Freire et al. 2015), marked by impaired mitochondrial quality control, heightened oxidative stress, accumulation of mitochondrial DNA damage, and disruption of cytosolic nicotinamide adenine dinucleotide (NAD+ and NADH) balance (de Mello et al. 2018 ; Das et al. 2021). Emerging studies indicate that impaired TCA cycle metabolism reduces mitochondrial membrane potential, exacerbates mitochondrial damage, and contributes to cellular senescence (Kurhaluk 2024 ; Cappel et al. 2019). However, the precise mechanisms linking mitochondrial dysfunction to the onset and progression of cellular senescence and age-related inflammation remain incompletely understood.

Phosphoenolpyruvate carboxykinase 1 (Pck1) is well recognized as a rate-limiting enzyme in hepatic and renal gluconeogenesis; however, in adipose tissue, it predominantly facilitates glyceroneogenesis, playing a pivotal role in modulating mitochondrial-cytosolic carbon flux via TCA cycle cataplerosis. Our prior research demonstrates that Pck1 modulates replicative lifespan in yeast (Yuan et al. 2020), suggesting its potential role in aging processes. In this study, we showed that Pck1 was essential for mitochondrial function and adipose tissue aging. Pck1 deficiency induced premature adipocyte senescence, exacerbated age-related metabolic abnormalities and inflammation in WAT. Mechanistically, Pck1 deficiency impaired TCA cycle catabolism, leading to fumarate accumulation, which further promoted cellular senescence. These findings identify Pck1 as a key metabolic effector that links mitochondrial metabolism in adipocytes to adipocyte aging and inflammation, with potential implications for targeting age-related diseases.

Potentiating dendritic cell immunotherapy by interrupting the Semaphorin 4D-induced immune-suppressive barrier

Garg et al. report that blocking the molecule SEMA4D strengthens immune responses against HER2-positive breast cancer. When paired with specialized dendritic cells, this approach boosts anti-tumor immune activity, reduces suppressive cells, and enables clearance of both local and distant tumors. Their findings support a promising and well-tolerated immunotherapy strategy.

Chemokines CXCL9 and CCL2 in Relation to Cerebral White Matter Disease, Cognitive Decline, and DementiaThe Northern Manhattan Study

This large cohort study showed that higher serum CXCL9 was associated with greater burden of white matter disease in the brain, independent of vascular risk factors, renal function, and genetic predisposition, supporting a role for CXCL9 in white matter pathogenesis.

Background and Objectives.

GLP-1 Receptor Agonists and Noncardiometabolic Outcomes: An Umbrella Review of Meta-Analyses

In this umbrella review of 60 meta-analyses of 1751 RCTs, GLP-1 RAs were associated increased GI adverse events (eg, nausea/vomiting); suggested protective associations with respiratory diseases and serious infections require further confirmation.

This meta-analysis evaluates the reported outcomes of glucagon-like peptide-1 (GLP-1) receptor agonists beyond glycemic control, weight management, and cardiorenal protection and assesses the credibility of the evidence.

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