In vivo administration of inositol isomers on Alzheimer's disease pathogenesis in the TgCRND8 mouse.

摘要

Alzheimer's disease (AD) is a debilitating neurodegenerative disease and is the most common cause of dementia in the elderly. A pathological hallmark of AD is the amyloid plaque, of which the amyloid-beta (Aβ) peptide is major constituent. As Aβ is both neurotoxic and found in all senile plaques, it is an ideal target for AD therapeutics.; This thesis explores the effect of the in vivo treatment of the TgCRND8 mouse model of AD with myo-, epi-, and scyllo-inositol isomers. Behavioural studies using the Morris water maze demonstrate a role for inositol in ameliorating the cognitive impairments associated with AD. Furthermore, the inositol isomers altered Aβ deposition in the brain, as determined by immunohistochemistry and stereology. This research helps to elucidate the role of Aβ in cognition and facilitates the advancement of therapeutics not only for Alzheimer's disease, but also potentially for other amyloidogenic diseases.