In an astonishing talk and tech demo, neurotechnologist Conor Russomanno shares his work building brain-computer interfaces that could enable us to control the external world with our minds. He discusses the quickly advancing possibilities of this field — including the promise of a \.
Category: neuroscience – Page 6
Johns Hopkins Scientists Identify Key Brain Protein That May Slow Alzheimer’s
Researchers at Johns Hopkins Medicine report that findings from a new study funded by the National Institutes of Health are helping to identify a promising new biological target for Alzheimer’s disease. The focus is a protein that produces a crucial gas within the brain.
Studies in genetically engineered mice show that the protein Cystathionine γ-lyase, also known as CSE, plays an essential role in forming memories, says Bindu Paul, M.S., Ph.D., an associate professor of pharmacology, psychiatry and neuroscience at the Johns Hopkins University School of Medicine who led the research. CSE is best known for generating hydrogen sulfide, the gas responsible for the smell of rotten eggs, but the new findings highlight its importance in brain function.
Mapping gene disruptions in sporadic early onset Alzheimer’s disease across key brain regions
A new study led by researchers at UTHealth Houston investigated both gene expression and regulation at single cell levels to reveal disruptions in gene function in three brain regions of patients with sporadic early onset Alzheimer’s disease.
The findings are published in Science Advances.
Only about 5% to 10% of patients with Alzheimer’s disease are younger than 65. Of those patients, 10% have mutations in the APP, PSEN1, and PSEN2 genes, which are associated with Alzheimer’s disease. The other 90% of these cases are classified as sporadic early onset Alzheimer’s, a rare and aggressive form of the disease that begins before age 65. The genetic tie in early onset Alzheimer’s is largely unidentified, representing a significant but understudied population.
One way brain ‘conductors’ find precise connection to target cells
New research reveals how a class of neurons that help coordinate communication in the brain link up with their target cells, identifying two molecules that must be present before synapses, the structures that carry signals between these partners, can form on the target neurons.
These cells are inhibitory interneurons that connect to a specific location on target excitatory neurons, regulating information processing and maintaining proper balance in brain circuits by controlling how active the excitatory neurons become. Loss of coordination between these two types of cells, which leads to circuit malfunction, is associated with such disorders as epilepsy, depression, autism and schizophrenia.
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.
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.