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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: Myelin in Alzheimer’s disease: culprit or bystander?

Fig. 1

(modified from [175]). The differentiated oligodendrocytes of OPCs migrate to different axons via positive chemotactism [216]. A variety of growth and trophic factors regulate the development of oligodendrocytes and their temporal and geographical attractions [17]. Many of these factors are produced by both neurons and astrocytes, regulating the proliferation, survival, or degeneration of OPCs. The neuroregulin, which activates Erb-tyrosines kinases receptors, promotes the survival and proliferation of oligodendrocytes. The activation of the Notch 1 cascade inhibits the differentiation of oligodendrocytes, and an integrin/contactin complex coordinates signals from the extracellular matrix and the axonal surface to regulate oligodendrocyte survival and myelination. This also depends closely on the electrical activity propagated in the axons. OPCs express functional adenosine receptors, activated by action potential [149, 183]. Adenosine acts as a powerful transmitter between glia and neurons to inhibit the proliferation of OPCs, stimulate their differentiation and stimulate myelin production. The LIF (leukemia inhibitory factor) is heavily involved in oligodendrocyte development kinetics and in the overall myelination process [133, 198]. Abbreviations: CNTF, ciliary neurotrophic factor; FGF, fibroblast growth factor; IGF, insulin-like growth factor; LIF, leukemia inhibitory factor; NCAM, neural cell adhesion molecule; NT-3, neurotrophin 3; OPCs, oligodendrocyte precursor cells; PDGF-A, platelet-derived growth factor-A

Oligodendrocytes are derived from the differentiation of oligodendrocyte precursor cells (OPCs) and are the main cell for remyelination.

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