This literature review investigates the significant overlap between myelin-repair signaling pathways and pathways known to contribute to hallmark pathologies of Alzheimer’s disease(AD).We discuss previously investiga...This literature review investigates the significant overlap between myelin-repair signaling pathways and pathways known to contribute to hallmark pathologies of Alzheimer’s disease(AD).We discuss previously investigated therapeutic targets of amyloid,tau,and ApoE,as well as other potential therapeutic targets that have been empirically shown to contribute to both remyelination and progression of AD.Current evidence shows that there are multiple AD-relevant pathways which overlap significantly with remyelination and myelin repair through the encouragement of oligodendrocyte proliferation,maturation,and myelin production.There is a present need for a single,cohesive model of myelin homeostasis in AD.While determining a causative pathway is beyond the scope of this review,it may be possible to investigate the pathological overlap of myelin repair and AD through therapeutic approaches.展开更多
基金Ms.Hirschfeld received support from multiple grants during the preparation of this manuscript:T32AG071444 and F31AG074700Dr.Saykin receives support from multiple NIH grants(P30 AG010133,P30 AG072976,R01 AG019771,R01 AG057739,U19 AG024904,R01 LM013463,R01 AG068193,T32 AG071444,and U01 AG068057 and U01 AG072177)Dr.Risacher receives support from NIH grants AG061788 and K01AG049050.Dr.Nho receives support from NIH grants R01 LM012535 and R03 AG054936.
文摘This literature review investigates the significant overlap between myelin-repair signaling pathways and pathways known to contribute to hallmark pathologies of Alzheimer’s disease(AD).We discuss previously investigated therapeutic targets of amyloid,tau,and ApoE,as well as other potential therapeutic targets that have been empirically shown to contribute to both remyelination and progression of AD.Current evidence shows that there are multiple AD-relevant pathways which overlap significantly with remyelination and myelin repair through the encouragement of oligodendrocyte proliferation,maturation,and myelin production.There is a present need for a single,cohesive model of myelin homeostasis in AD.While determining a causative pathway is beyond the scope of this review,it may be possible to investigate the pathological overlap of myelin repair and AD through therapeutic approaches.
