A research group led by Professor Michael Glickman, dean of Technion’s Faculty of Biology, has uncovered a key mechanism in the development of Alzheimer’s. The mechanism in question identifies toxic proteins and disposes of them.
In most cases, harmful proteins are degraded inside the cell. However, the researchers found that in certain situations, the very system meant to eliminate these proteins simply transfers them outside the cell. This discovery may explain how a disease that begins randomly in individual neurons can spread to large regions of the brain.
The study, published in Proceedings of the National Academy of Sciences, was led by Prof. Glickman and postdoctoral researcher Dr. Ajay Wagh. In their article, they describe how brain cells deal with UBB+1, a defective and toxic variant of the protein ubiquitin.
Exciting to see this modern genomic approach to classification of psychiatric disorders! Hopefully this will eventually lead to potential new gene therapy targets for treatment.
Analysis of more than one million people shows that mental-health disorders fall into five clusters, each of them linked to a specific set of genetic variants.
Astrocytic lipid metabolism in brain signaling.
Glia previously thought to be support cells of brain but recent evidence suggest that the astrocytes, the most abundant glial cell type in addition to supplying neurons with lactate via glycolysis also actively engage in lipid metabolism, especially mitochondrial fatty acid β-oxidation.
Researchers in this review integrate astrocytic fatty acid ß-oxidation and ketogenesis, alongside other metabolic pathways converging on reactive oxygen species dynamics, including cholesterol metabolism and peroxisomal β-oxidation.
Thus, convergence of energy metabolism to signaling may provide new insights to central nervous system function and dysfunction. https://sciencemission.com/astrocytic-lipid-metabolism
Astrocytes, the most abundant glial cell type in the central nervous system, have traditionally been viewed from the perspective of metabolic support, particularly supplying neurons with lactate via glycolysis. This view has focused heavily on glucose metabolism as the primary mode of sustaining neuronal function. However, recent research challenges this paradigm by positioning astrocytes as dynamic metabolic hubs that actively engage in lipid metabolism, especially mitochondrial fatty acid β-oxidation. Far from serving solely as an energy source, fatty acid ß-oxidation in astrocytes orchestrates reactive oxygen species-mediated signaling pathways that modulate neuron-glia communication and cognitive outcomes.
Temporal lobe epilepsy, which results in recurring seizures and cognitive dysfunction, is associated with premature aging of brain cells.
A new study by researchers at Georgetown University Medical Center found that this form of epilepsy can be treated in mice by either genetically or pharmaceutically eradicating the aging cells, thereby improving memory and reducing seizures as well as protecting some animals from developing epilepsy.
The study appears in the journal Annals of Neurology.
Which genes are required for turning embryonic stem cells into brain cells, and what happens when this process goes wrong? In a new study published today in Nature Neuroscience, researchers led by Prof. Sagiv Shifman from The Institute of Life Sciences at The Hebrew University of Jerusalem, in collaboration with Prof. Binnaz Yalcin from INSERM, France, used genome-wide CRISPR knockout screens to identify genes that are needed for early brain development.
The study set out to answer a straightforward question: which genes are required for the proper development of brain cells?
Using CRISPR-based gene-editing methods, the researchers systematically and individually “switched off” roughly 20,000 genes to study their role in brain development. They performed the screen in embryonic stem cells while the cells changed into brain cells. By disrupting genes one by one, the team could see which genes are required for this transition to proceed normally.
