Topic: myelin sheath

Type 2 spastic paraplegia (SPG2) is a rare genetic disorder caused by null mutations in the gene encoding for the proteolipid protein 1, essential for myelin sheath formation around nerve fibers in the central nervous system (CNS). SPG2 manifests as progressive stiffness and weakness in the legs, accompanied by white matter abnormalities and axonal degeneration in the CNS. These myelin abnormalities impair neural communication, impacting motor function, cognition and may contribute to neuropsychological conditions like anxiety. Leriglitazone, a brain-penetrant PPARγ full agonist, has shown

Oligodendrocytes, the myelinating glial cells of the central nervous system (CNS), surround axons with their membrane extensions, forming the myelin sheath. Loss of oligodendrocytes and/or myelin (demyelination) occurs in traumatic brain injury or pathologies such as multiple sclerosis. Since, there is no specific treatment for demyelination; we are interested in enhancing myelin endogenous repair. We focus our work on A Disintegrin and Metalloprotease (ADAM) 10, the major CNS α-secretase, which generates the neuroprotective soluble fragment sAPPα via cleavage of the Amyloid Precursor Protein

Tissue plasminogen activator (tPA) is a protease expressed in CNS by various cells and it is mainly known for its thrombolytic function in the treatment of stroke. While its contribution to myelination within the central nervous system is known, its involvement in peripheral remyelination processes remains to be explored. Indeed, in physiological conditions, Schwann cells, responsible for myelination, express low levels of tPA, however its expression increases following injuries to peripheral nerves. Therefore, our study focused on elucidating involvement of tPA in peripheral nervous system re