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source: Multiple Sclerosis News Today
In a recent publication in Nature, titled “Drug-based modulation of endogenous stem cells promotes functional remyelination in vivo” a team of researchers from Case Western University and Northwestern University screened a library of small molecules to assess their ability to drive the conversion of oligodendrocyte precursor cells (OPCs) into oligodendrocytes. Initially, these experiments were performed solely in cultured OPCs, revealing seven potential drugs that could enhance the production of oligodendrocytes.
Multiple sclerosis (MS) is characterized by both demyelination (damage to the myelin sheath) and a failure to remyelinate (repair the damaged myelin). Whereas both of these processes provide attractive therapeutic targets, currently available therapies all work by targeting the immune system to stop the autoimmune response and prevent further demyelination. More recently, a lot of research focus has shifted to attempt to find treatments that work by promoting repair of the damaged myelin, thus providing recovery from symptoms.
Remyelination is performed by a type of cell known as an oligodendrocyte. Oligodendrocytes mature from OPCs, which are a type of stem cell found in the central nervous system (CNS). While these OPCs can be found in large numbers in people with MS, they fail to convert into oligodendrocytes and so cannot help to repair the damaged myelin. Therefore, finding a way to promote this process is of particular interest for the development of novel therapeutic options for the treatment of MS.
In this study, the researchers tested the potential of the newly identified drugs to enhance the production of oligodendrocytes in a mouse model of MS. In the model used, a toxin (lysolethicin) is used to create demyelination to mimic that seen in MS. Two of the drugs identified, miconazole and clobetasol, were able to promote the repair of damaged myelin in these mice. Indeed, animals that exhibited severe symptoms showed remarkable recovery after the drugs were administered at the peak of the disease process. While both drugs promote remyelination, clobetasol also functions to suppress the immune system.
These results provide evidence to test miconazole and clobetasol as potentially new therapeutic agents to promote the repair of damaged myelin in people with MS.
Read more at Multiple Sclerosis News Today
Source: Epilepsy Today
Most anti-epileptic drugs (AEDs) are believed to suppress seizures by affecting neuron activity in the brain. This new study – conducted by Tsuyoshi Inoue at Okayama University, Japan – takes a new approach.
Instead of targeting the neurons directly, this new approach affects astrocytes – the cells that support neurons and provide them with energy when they need it.
Recent studies suggest that metabolism may be important in some cases of epilepsy. By metabolism, we mean the chemical reactions that take place in the body to convert or use energy.
The ketogenic diet is a low-carbohydrate high-fat diet that affects the metabolic balance of the brain. In people whose seizures do not respond to medication, the ketogenic diet can be an effective treatment.
Rather than relying on glucose for energy, brain cells instead begin to use chemicals called ketones. Although scientists are still researching why, this switch to metabolising ketones has been found to reduce seizures.
Dr Inoue and his team found that a drug called stiripentol can mimic the effects of the ketogenic diet. It can reduce the activity of an enzyme called lactate dehydrogenase (LDH). In turn, this cuts off the fuel supply from astrocytes to neurons, preventing them from misfiring and triggering seizures. Full study findings appear in the medical journal Science.
Read more at Epilepsy Today
A team at Duke University, showed immune cells which start attacking nutrients in the brain may be a trigger for the disease.
They say their findings could open up new avenues of research for a field that has not developed a single drug to slow the progression of the disease.
Experts said the findings offered new hope of a treatment.
The researchers indentified microglia - normally the first line of defence against infection in the brain - as major players in the development of dementia.
They found some microglia changed to become exceptionally adept at breaking down a component of protein, an amino acid called arginine, in the early stages of the disease.
As arginine levels plummeted, the immune cells appeared to dampen the immune system in the brain.
In mouse experiments, a chemical was used to block the enzymes that break down arginine.
They showed fewer of the characteristics of dementia such as damaged proteins collecting in the brain and the animals performed better in memory tests.
One of the researchers, Dr Matthew Kan, said: "All of this suggests to us that if you can block this local process of amino acid deprivation, then you can protect the mouse, at least from Alzheimer's disease.
"We see this study opening the doors to thinking about Alzheimer's in a completely different way, to break the stalemate of ideas in Alzheimer's disease."
However, the findings do not suggest that arginine supplements could combat dementia as the boosted levels would still be broken down.
Dr James Pickett, from the Alzheimer's Society said the study was "offering hope that these findings could lead to new treatments for dementia".
He added: "This study in animals joins some of the dots in our incomplete understanding of the processes that cause Alzheimer's disease, in particular around the role played by the immune system."
Dr Laura Phipps, from Alzheimer's Research UK, said the study was "interesting" and shed "more light on the mechanisms of immune system involvement in Alzheimer's".
But she cautioned clinical trials in people were still needed and that "the findings do not suggest that supplementation of the amino acid could mirror the benefits seen in these mice".