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Category: neuroscience – Page 28

Scientists Discover Method To Erase Toxic Tau From Human Neurons

Researchers at the University of New Mexico have uncovered an unexpected role for OTULIN, an enzyme best known for its involvement in immune system regulation. The team found that OTULIN also plays a key role in the production of tau, a protein linked to many neurodegenerative disorders, along with brain inflammation and the biological processes associated with aging.

The findings were reported in the journal Genomic Psychiatry. In the study, scientists showed that disabling OTULIN stopped tau from being produced and cleared existing tau from neurons. This was achieved in two ways: by using a specially designed small molecule or by removing the gene responsible for producing the enzyme. The experiments were carried out in two types of cells, including cells derived from a person who had died from late-onset sporadic Alzheimer’s disease and human neuroblastoma cells that are commonly used in laboratory research.

Complement C4d Informs the Differential Diagnosis of Inflammatory Demyelinating CNS Diseases

C4d is a sensitive marker for identifying antibody-related lesion pathology, enabling differentiation of idiopathic inflammatory demyelinating diseases in tissues and distinguishing both seropositive and seronegative NMOSD from multiple sclerosis in CSF.

Background and Objectives.

Lifespan‐Extending Endogenous Metabolites

Endogenous metabolites are small molecules produced by an organism’s own metabolism. They encompass a wide range of molecules, such as amino acids, lipids, nucleotides, and sugars, which are pivotal for cellular function and organismal health (Baker and Rutter 2023). Beyond serving as biosynthetic precursors and energy substrates, many metabolites also function as dynamic modulators of signaling and gene regulatory networks by engaging in protein–metabolite interactions, allosteric regulation, and by serving as substrates for chromatin and other post-translational modifications (Boon et al. 2020 ; Hornisch and Piazza 2025). Metabolites can function as extracellular signals activating G protein-coupled receptors (GPCRs), such as free fatty acid receptors for fatty acids, GPR81 for lactate, SUCNR1 for succinate, and TGR5 for bile acids (Tonack et al. 2013). These GPCRs are expressed in gut, adipose tissue, endocrine glands, and immune cells, linking nutrient and metabolite levels to diverse physiological responses (Tonack et al. 2013). Other metabolites serve as enzyme cofactors or epigenetic regulators. For example, methyl donors like betaine provide methyl groups for DNA and histone methylation and also act as osmolytes to protect cells under stress (Lever and Slow 2010). Some metabolites even form specialized structural assemblies. For instance, guanine crystals can form structural color in feline eyes and contribute to enhanced night vision (Aizen et al. 2018).

Perturbations of endogenous metabolite levels or fluxes have been linked to genomic instability, metabolic dysfunction, and age-related diseases, motivating study of metabolites as both biomarkers and functional modulators of aging (Adav and Wang 2021 ; Tomar and Erber 2023 ; Xiao et al. 2025). Metabolomic studies reveal characteristic metabolite changes in diabetes, cardiovascular disease, and Alzheimer’s disease (AD) (Panyard et al. 2022), suggesting that metabolites not only reflect organismal state but also can actively influence aging pathways. In subsequent sections, we will examine specific endogenous metabolites implicated in longevity regulation.

Disrupting HDAC1 condensates in glioblastoma could help to overcome drug resistance

Glioblastoma (GBM) is one of the most common and aggressive primary brain tumors in adults, carrying an extremely poor prognosis and a median overall survival typically less than two years. Temozolomide (TMZ) is currently the only chemotherapeutic agent widely used in clinical practice. However, around 90% of cases experience tumor recurrence due to acquired resistance. How to overcome TMZ resistance remains a challenge.

In a study published in Nature Chemical Biology, Dr. Dong Peng’s team from the Shenzhen Institute of Advanced Technology of the Chinese Academy of Sciences and collaborators from Sun Yat-sen University have discovered that TMZ treatment induces the formation of HDAC1-CTCF condensates in GBM cells. The team identified the small-molecule compound resminostat as a therapeutic agent capable of targeting these condensates.

Through three-dimensional (3D) super-resolution imaging independently developed by Dr. Dong’s team, the researchers observed a significant reduction in chromatin accessibility in TMZ-resistant GBM cells. The team characterized their 3D genomic structural features, and revealed that the decreased chromatin accessibility in resistant cells is primarily attributed to TMZ-induced formation of HDAC1-CTCF condensates, which accumulate on chromatin and restrict local accessibility.

Q&A: What do scientists need to learn next about blocking enzymes to treat disease?

Enzymes are the molecular machines that power life; they build and break down molecules, copy DNA, digest food, and drive virtually every chemical reaction in our cells. For decades, scientists have designed drugs to slow down or block enzymes, stopping infections or the growth of cancer by jamming these tiny machines. But what if tackling some diseases requires the opposite approach?

Speeding enzymes up, it turns out, is much harder than stopping them. Tarun Kapoor is the Pels Family Professor in Rockefeller’s Selma and Lawrence Ruben Laboratory of Chemistry and Cell Biology. Recently, he has shifted the focus of this lab to tackle the tricky question of how to make enzymes work faster.

Already, his lab has developed a chemical compound to speed up an enzyme that works too slowly in people with a rare form of neurodegeneration. The same approach could open new treatment possibilities for many other diseases where other enzymes have lost function, including some cancers and neurodegenerative disorders such as Alzheimer’s.

Astonishing new study suggests Alzheimers can be fully reversed

The devastating illness deteriorates your brain’s ability to think, remember things and can even alter your behaviour.

While some studies have discovered that engaging in a pretty gross habit or reaching a daily step count can reduce the risk of developing Alzheimer’s disease (AD), for over a century, scientists have considered it an irreversible illness. This is why research has focused on preventing or slowing its progression, rather than recovery.

However, a new study challenges this long-held belief by testing whether brains already severely afflicted with advanced AD could recover.

There’s One Critical Thing You Can Do to Cut Your Risk of Dementia

Inside the body, a 24-hour rhythm, known as the circadian rhythm, quietly coordinates when we sleep, wake, eat, and recover. This internal timing system helps keep organs and hormones working in sync.

When it becomes disrupted, the effects may extend well beyond poor sleep, with growing evidence suggesting consequences for long-term brain health.

A large 2025 study of more than 2,000 people with an average age of 79 found that those with a strong circadian rhythm had an almost halved risk of developing dementia. Circadian rhythms regulate daily processes, including sleep timing, hormone release, heart rate, and body temperature.

Japanese scientists just built human brain circuits in the lab

To assess how this interaction affected development, the team compared gene expression in the cortical region of the assembloid with that of a standalone cortical organoid. The cortical tissue connected to the thalamus showed signs of greater maturity, indicating that thalamus cortex communication promotes cortical growth and development.

Thalamic Signals Drive Neural Synchrony

The scientists also examined how signals traveled through the assembloid. They found that neural activity spread from the thalamus into the cortex in wave like patterns, creating synchronized activity across cortical networks.

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