The Annual Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) meeting in Copenhagen this week is celebrating its 40th edition. In recognition of this landmark, the plenary session and opening lecture were attended by Queen Margrethe of Denmark. Afterward, the hot topic session on neuroprotective therapies set the stage for the subsequent discussions on the latest trends in the management and treatment of multiple sclerosis (MS).
In repeated concussions, removing damaged mitochondria could prevent the neurodegeneration that occurs when pathology progresses in some patients. The key would be in the role of the p17 protein in restoring mitophagy, according to scientists from the Medical University of South Carolina (MUSC). “Brain injury is an extrinsic disease. It is not idiopathic. When the primary injury occurs, the secure mechanism only relies on an endogenous protection of the brain. If you have a good neuroprotective mechanism, then after the primary injury, basically you don’t see any symptomatic effect,” Onder Albayram told BioWorld.
Orsobio Inc., already in the clinic with three candidates, has completed its $60 million series A financing. The company, CEO Mani Subramanian told BioWorld, has taken its time to find the right programs, put them together and only raised capital when it saw the programs had legs. Even the series A is a measured step, as Subramanian called the financing “modest.”
Mitochondria regulate many processes that are altered in cancer cells, from metabolism to oxidative stress to apoptosis. The metabolic reprogramming in cancer cells promotes an immunosuppressive environment that drives cancer progression. However, in a recent study, researchers from the Salk Institute of Biological Sciences have identified succinate as a metabolite that accumulated due to specific disturbances in the mitochondrial electron transport chain.
Researchers have demonstrated that inhibiting mitophagy in ‘old’ hematopoietic stem cells (HSCs) completely restored their blood reconstitution capabilities, raising the prospect of addressing the age-related weakening of the immune system that stems from HSCs deteriorating over time.
Leukemic cells rely on excessive mitochondrial respiratory and energy metabolism. Therefore, targeting mitochondrial proteases has been proposed as a potential approach to improve therapeutic regimens for acute myeloid leukemia (AML). The mitochondrial caseinolytic protease P (ClpP), located in the mitochondrial matrix, maintains protein quality by mediating the proteolytic hydrolysis of damaged proteins. The chaperone ClpX regulates this hydrolysis and is overexpressed in AML, thus providing a rationale for using ClpP agonists to disrupt AML proliferation.
Researchers based at Northwestern University Feinberg School of Medicine have discovered that a lack of contact between mitochondria and lysosomes in the cells of patients with a genetic form of Parkinson’s disease likely contributed to their symptoms.
An oral drug has shown promise for treating metabolic syndrome in mouse models by selectively blocking the production of free radicals in the mitochondria, a research group has found. The study, carried out by a group led by Martin Brand, Professor Emeritus at the Buck Institute for Research on Aging, could lead to treatments that tackle the underlying causes of metabolic syndrome and multiple other conditions linked to aging.
Evidence of mitochondrial and lysosome dysfunction underlying Parkinson’s disease (PD) was discussed during several talks at the World Parkinson Congress 2023 (WPC) held in Barcelona. Edward A. Fon, from McGill University in Montreal, explained how eyes turned to mitochondria as key players in PD more than 30 years ago and how the explosion of genetics was fundamental to advance the knowledge and research in PD.
Over the past decade there has been much research into the use of induced pluripotent stem cells (iPSCs) as a cell therapy to regenerate tissue and treat heart disease. Now, one researcher has narrowed the focus down to treating heart disease not with whole cells, but with mitochondria derived from iPSCs. Gentaro Ikeda, a researcher at the Department of Medicine at Stanford University, has worked on generating extracellular vesicles (EVs) containing mitochondria from pluripotent stem cell-derived cardiomyocytes and administering these to restore the functionality of the myocardium in a porcine model of an infarct.
