|This blog originated as a press release from the Johns Hopkins Kimmel Cancer Center. Thanks to them for allowing us to repost it here.|
It may be possible to identify the presence of an aggressive brain tumor in children by studying their cerebrospinal fluid, according to new research led by Johns Hopkins Kimmel Cancer Center investigators.
Comparing cerebrospinal fluid samples from 40 patients with medulloblastoma — the most common malignant brain tumor in children, accounting for 10% to 15% of pediatric central nervous system tumors — and from 11 healthy children without the disease, investigators identified 110 genes, 10 types of RNA–the machinery that translates proteins–called circular RNAs, 14 lipids and several metabolites that were expressed differently between the two groups. While these details were not specific enough to distinguish among the four subtypes of medulloblastoma, they could be used to identify the presence of cancer versus normal fluid. A description of the work was published in the journal Acta Neuropathologica Communications.
Extracellular vesicles (EVs) are small membrane-bound particles that are loaded with various proteins, RNA, DNA, and lipids, and secreted by cells. Interest in these vesicles has grown in recent years with mounting evidence that EVs act as intercellular communication systems, transferring their selected cargo to other cells to confer specific effects on target cell biology. However, the processes that direct specific RNAs and proteins into these specialized vesicles remain largely unknown. In the April 25th, 2022 edition of Developmental Cell, Alissa Weaver, M.D., Ph.D. and her research team at the Vanderbilt Center for Extracellular Vesicle Research have uncovered subcellular hubs of EV formation that selectively assemble RNA-containing EVs. These hubs are located at membrane contact sites (MCS) where the endoplasmic reticulum (ER) interacts with EV biogenesis membranes, including late endosomal multivesicular bodies (MVBs) (ER-MVB MCS). Shedding much needed mechanistic light, the group further pinpointed the ER MCS membrane tether protein VAP-A and its binding partner ceramide transfer protein (CERT) as key drivers in this process.
|This blog originated as a press release from the Swiss National Centre of Competence in Research SYNAPSY. Thanks to them for allowing us to repost it here.|
A research team from Synapsy has shown that the severity of the clinical symptoms of schizophrenia is strongly linked to blood biomarkers related to the deregulation of neuronal mitochondria.
Psychotic symptoms are a characteristic clinical manifestation of schizophrenia. They go hand-in-hand with an increase in oxidative stress, which results in damage to a particular type of neurons called parvalbumin neurons. This deterioration leads to dysfunction in the activity of the prefrontal cortex, a region of the brain that is involved in cognition. A study conducted at the Centre for Psychiatric Neuroscience of the Lausanne University (UNIL) and the Lausanne University Hospital (CHUV), and supported by the National Centre of Competences in Research Synapsy (Synapsy), has shown, in an animal model, that the cellular mechanism for recycling mitochondria is deficient in parvalbumin neurons. The study – published in the journal Molecular Psychiatry – investigated the underlying biochemical mechanisms, pinpointing two key molecules, miR-137 and COX6A2, that can be detected in blood. When used as biomarkers in patients diagnosed with psychosis, they unveil two distinct clinical sub-groups with different severity of symptoms, cognitive deficits, and functioning in everyday life. This discovery represents a major breakthrough for stratifying individuals suffering from schizophrenia, whose heterogeneity of symptoms currently restricts diagnosis and treatment.