After a stroke, help neurons myelinate

Stimulation of myelination of neurons helped to restore the brain after a stroke

Sofia Dolotovskaya, N+1

American scientists have managed to restore brain tissue after a stroke of white matter in mice by stimulating the myelination of damaged neurons. Article Nogo receptor blockade overcomes remyelination failure after white matter stroke and stimulates functional recovery in aged mice Sozmen et al. published in the journal Proceedings of the National Academy of Sciences.

Myelinating oligodendrocyte in rat brain (Wikimedia Commons)

Ischemic stroke is an acute violation of the cerebral blood supply as a result of thrombosis, causing the death of a section of its tissue. There are two main forms of ischemic stroke. In the first type, caused by thrombosis of the major arteries of the brain, tissue damage affects large areas of the brain, including both gray and white matter. The second type of ischemic stroke is caused by thrombosis of small arteries and affects only subcortical areas of white matter. Over time, however, the damaged areas grow. About 25 percent of stroke cases belong to this type. The probability of such a stroke increases with age and after 80 years becomes almost one hundred percent. Such a stroke is the second most common cause of dementia (acquired dementia). Despite this, there are still no ways to restore brain tissue after a stroke of white matter.

At the first stage of the experiment, the authors, using a mouse model of a white matter stroke, showed why there is no recovery of brain tissue in this disease. Stroke causes demyelination of axons (damage to their myelin sheaths). This stimulates neurogenesis: at the site of injury, the progenitor cells of oligodendrocytes (myelinating cells of neuroglia) begin to divide. In non-ischemic lesions of the white matter (for example, in multiple sclerosis), progenitor cells then differentiate into mature oligodendrocytes, which re-myelinate damaged axons, which leads to partial restoration of damaged tissue. However, with a stroke of the white matter, the progenitor cells of oligodendrocytes do not differentiate into mature oligodendrocytes, but instead turn into astrocytes, leading to tissue gliosis (proliferation of astrocytic neuroglia).

At the second stage of the experiment, the authors were able to cancel the blockade of maturation of oligodendrocyte progenitor cells. To do this, they interfered with the signaling pathway of the Nogo protein receptor (NgR1). This protein inhibits the growth of axons, and in previous studies it has been shown that during stroke, the number of ligands of the NgR1 receptor increases in brain tissue, and the number of its inhibitors decreases. It turned out that the introduction of an NgR1 antagonist into the damaged area of the white matter relieves the blockade of oligodendrocyte maturation: progenitor cells begin to mature more actively and no longer differentiate into astrocytes. This leads to myelination of damaged axons and tissue repair. In addition, in old mice with stroke, such therapy led to a noticeable recovery of motor activity – even in cases when the disease had already managed to turn into a chronic form.

Recently, scientists have demonstrated a way to restore brain tissue after a stroke by preventing inflammation: it turned out that antagonists of receptors to the inflammatory cytokine interleukin-1 contribute to partial restoration of damaged tissue in rats. Previously, scientists managed to restore functions lost after a stroke by injecting modified mesenchymal stem cells into damaged areas of the motor cortex.

Portal "Eternal youth" http://vechnayamolodost.ru  14.12.2016