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.
We present the first comprehensive data set for the aluminium content of brain tissue in donors without a diagnosis of neurodegenerative disease. All donors fulfilled recently revised criteria for control brain tissues14. Approximately 80% of measured tissues have an aluminium content below 1.0 μg/g dry wt. (Table 1). There are some anomalies, 6 out of 191 tissues have an aluminium content ≥3.00 μg/g dry wt., and these are worth future investigation to identify possible neuropathology. There was no statistically significant relationship between brain aluminium content and age of donor and this observation is contrary to a previous investigation of brain aluminium in a neurologically normal population15. An explanation may be that herein only two out of twenty donors were below 66 years old. The data do support a conclusion that a high content of brain aluminium is not an inevitability of ageing.
When we compared the new control data set with data produced in an identical manner in donors dying with diagnoses of sporadic Alzheimer’s disease (sAD)16, familial Alzheimer’s disease (fAD)11, autism spectrum disorder (ASD)13 and multiple sclerosis (MS)12 all of these disease groups had significantly higher brain aluminium content. The differences were always highly significant regardless of the method of statistical analysis (Table 4). The largest disease group, designated as sAD, was actually composed of approximately equal numbers of donors previously described by a brain bank as controls and donors diagnosed with sAD. Unfortunately, information discriminating between control and sAD donors was not made available to us17. However, the observation that the aluminium content of brain tissue in this group as a whole was significantly higher than the similarly aged control group emphasised the likelihood that brain aluminium content is increased in sAD.
