A new drug targets Alzheimer’s at its earliest, most silent stage — before memory loss ever begins.
Ever wondered how the different cells in our body communicate with each other to fulfill their different roles-be it cells repairing a tissue injury or immune cells moving towards an invading pathogen (microorganisms that causes disease) to engulf it? To move forward or migrate, cells must exert forces or interact with their surrounding environment. Interestingly, however, a fault in these interactions can also be the reason for spread of deadly cancer cells, such as in glioblastoma or brain tumor. While the importance of these interactions is well-understood, the machinery involved in these interactions at the molecular level remains a mystery.
Now, a team of researchers led by Professor Naoyuki Inagaki from Nara Institute of Science and Technology, Japan, along with Dr. Yonehiro Kanemura from NHO Osaka National Hospital, Japan; Dr. Tatsuo Kinashi from Kansai Medical University, Japan; and Dr. Daisuke Kawauchi from Nagoya City University, Japan, has identified the underlying mechanism involving a protein called shootin1b that promotes cell migration or movement in glioblastoma. The study was published online in Advanced Science on August 13, 2025.
“We discovered that an abnormal activity of shootin1b promotes the movement of cancer cells and spread of glioblastoma, the most common and difficult to treat brain tumor in adults,” explains Professor Inagaki.
One of the biggest quests in biology is understanding how every cell in an animal’s body carries an identical genome yet still gives rise to a kaleidoscope of different cell types and tissues. A neuron doesn’t look nor behave like a muscle cell but has the same DNA.
Researchers think it comes down to how cells allow different parts of the genome to be read. Controlling these permissions are regulatory elements, regions of the genome which switch genes on or off. A detailed overview of how they do this is largely restricted to a handful of classic model organisms like mice and fruit flies.
Attention disorders such as ADHD involve a breakdown in our ability to separate signal from noise. The brain is constantly bombarded with information, and focus depends on its ability to filter out distractions and detect what matters.
Stimulant medications improve attention by boosting activity in circuits known to govern attention, such as the prefrontal cortex. But a new study reveals a surprising alternative: reduce background activity as a way of turning down extraneous noise.
In a paper published in Nature Neuroscience, researchers show that the Homer1 gene plays a critical role in shaping attention in just that way. Mice with lower levels of two specific versions of the gene enjoyed quieter brain activity and improved ability to focus.
Stra8 links neuronal activity to inhibitory circuit protection in the adult mouse brain.
Huang et al. show that Stra8, a gene previously thought to be germline specific, is expressed in the adult mouse hippocampus in an activity-dependent manner. Stra8 protects neuronal integrity and cognition by regulating neuromodulator genes and preserving inhibitory circuit function.
A Nature analysis of a major Norwegian study challenges existing estimates of Alzheimer’s prevalence, finding that 25% of people aged 85–89 have dementia with Alzheimer’s pathology — far higher than previous 7–13% estimates — while preclinical Alzheimer’s in younger seniors (70−74) occurs at only 8% versus earlier 22% estimates. Using blood biomarker pTau217 in 11,486 participants, researchers identified that 10% of over-70s had dementia, 10% had mild cognitive impairment, and 10% had preclinical Alzheimer’s, but warn that blood tests alone are insufficient for widespread screening due to potential harm from false positives. The discrepancies highlight how previous studies may have been skewed by selection bias, while demonstrating that blood-based biomarkers require careful interpretation and comprehensive clinical assessment.
A survey of Alzheimer’s disease prevalence in Norway confirms earlier estimates and might show how education level relates to risk.
Eating more high-fat cheese and high-fat cream may be linked to a lower risk of developing dementia, according to a new study published in Neurology. This study does not prove that eating high-fat cheese and high-fat cream lowers the risk of dementia, it only shows an association.
High-fat cheeses contain more than 20% fat and include varieties such as cheddar, Brie and Gouda. High-fat creams typically contain 30–40% fat and include whipping cream, double cream and clotted cream. These are commonly labeled as “full-fat” or “regular” versions in stores.
“For decades, the debate over high-fat versus low-fat diets has shaped health advice, sometimes even categorizing cheese as an unhealthy food to limit,” said Emily Sonestedt, Ph.D., of Lund University, Sweden.