Butyrylcholinesterase-Knockout Reduces Fibrillar β-amyloid and Conserves (18)FDG Retention in 5XFAD Mouse Model of Alzheimer's Disease.

Butyrylcholinesterase-Knockout Reduces Fibrillar β-amyloid and Conserves (18)FDG Retention in 5XFAD Mouse Model of Alzheimer's Disease. Brain Res. 2017 Jul 17;: Authors: DeBay DR, Reid GA, Macdonald IR, Mawko G, Burrell S, Martin E, Bowen CV, Darvesh S Abstract Alzheimer's disease (AD) is the most common neurodegenerative disorder causing dementia. One hallmark of the AD brain is the deposition of β-amyloid (Aβ) plaques. AD is also a state of cholinergic dysfunction and butyrylcholinesterase (BChE) associates with Aβ pathology. A transgenic mouse (5XFAD) is an aggressive amyloidosis model, producing Aβ plaques of which BChE also associates. A derived strain (5XFAD/BChE-KO), with the BChE gene knocked out, has significantly lower fibrillar Aβ than 5XFAD mice at the same age. Therefore, BChE may have a role in Aβ pathogenesis. Furthermore, in AD, diminished glucose metabolism in the brain can be detected in vivo with positron emission tomography (PET) imaging following fluoro[(18)F]deoxyglucose ((18)FDG) administration. To determine whether hypometabolism is related to BChE-induced changes in fibrillar Aβ burden, whole brain and regional uptake of (18)FDG in 5XFAD and 5XFAD/BChE-KO mice was compared to corresponding wild-type (WT5XFAD and WTBChE-KO) strains at 5 months. Diminished fibrillar Aβ burden was confirmed in 5XFAD/BChE-KO mice relative to 5XFAD. 5XFAD and 5XFAD/BChE-KO mice demonstrated reduction in whole brain (18)FD...
Source: Brain Research - Category: Neurology Authors: Tags: Brain Res Source Type: research