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Demyelination takes Place Prior to Neuronal Damage following Intracerebroventricular Injection of Amyloid Beta Oligomer

Author(s): Mao Zhang, Jie Zhang, Weiwei Zhang, Zhongxiang Yao

Amyloid-beta (Aβ) peptide, commonly associated with Alzheimer’s disease (AD), is known as a threat to neurons. However, the effect of Aβ peptide on myelin and oligodendrocytes (OLs) hasn’t been exclusively discussed. In this study, a low concentration of amyloid-beta oligomer (AβO) was intracerebroventricularly injected to mice at the 2nd week. Body weight and motor coordination of mice were monitored during 8 weeks. Thioflavin-S (Th-S) staining, cresyl violet staining and immunostaining were supplied to assess Aβ deposits, neuronal damage, myelin disruption and activation of inflammatory glias following AβO injection. To identify the underlying cause of AβO-induced demyelination, AβO was administrated to oligodendrocyte precursor cells (OPCs) in vitro. In addition, OPCs can differentiate into myelinating cells---OLs. It showed that AβO not only suppressed the increase of body weight, but also resulted in the dysfunction of motor coordination in mice. Besides, neuronal damage was found in hippocampus, corpus callosum (CC) and cortex at the 8th week, but not at the 3rd week. Especially, neurofilament loss in the CC was developed until the 8th week, while demyelination was developed as early as the 3rd week. About other glias, AβO simply increased the amounts of astrocytes and microglias at the 8th week, but had no effect on them at the 3rd week. In vitro, AβO induced the decrease of oligodendrocyte amount and restriction of myelin basic protein (MBP)+ membrane areas. This study proves that demyelination develops earlier than neuronal damage under AβO attack. Furthermore, it is supposed that the early detriment of AβO in myelin may further endanger neurons, and AβO-induced injury of OLs may facilitate this process. Relatively, the improvement of AβO-induced myelin damage at the early stage and the promotion of OLs may alleviate neuronal impairment, especially in AD.

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