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• W2896241654 abstract "Alzheimer's disease (AD) is the most common late-onset neurodegenerative disorder where classic neuropathologic hallmarks of AD include accumulation of amyloid beta (Aβ) plaques, the development of neurofibrillary tangles (NFTs); however, AD is considered a multifactorial condition. The earliest deficits in pathological progression of AD seem to be caused by impaired metabolic activity - before the robust appearance of Aβ and NFTs. Therefore, efforts to detect alterations in brain metabolism could critically improve our ability to diagnose AD sooner, and identify more effective treatment targets. The current study utilized FDG-PET to measure aberrations in brain metabolic activity in AD mice and control mice. A total of 10 (n=5 per group) 3xTg-AD mice and aged-matched control background strain (C57BL/6) mice underwent FDG-PET neuroimaging. After PET scanning, brains of AD and control mice were collected at autopsy. In order to detect neuropathology in brain, congo red staining and immunohistochemistry was used for Aβ and NFTs confirmation in mice that underwent PET scanning. In order to measure the activity of mitochondrial enzymes involved in the metabolic pathways, brain mitochondria were isolated from both AD and control mice.Western blotting was used to determine protein levels of Complex I-V subunits in both AD and control samples. We found significant brain hypometabolic changes (p < 0.05) as measured by FDG-PET in cortical insular and piriform regions of AD brains compared to that of control brains. Also, we found significant reduction (p < 0.05) in the activity of mitochondrial cytochrome c oxidase as well as significant decreases (p < 0.05) in expression of mitochondrial complex (I-V) protein subunits in AD brain as compared to control brains. We found no significant differences in activity of citrate synthase or GAPDH between AD and their controls. No congophilic positive Aβ plaques were detected in any brain region in either AD or control mice; however, we detected pathological NFTs in the entorhinal cortex, parasubiculum, and sagulum regions of AD brain, but not in sensitive brain regions. Reduction in brain metabolic activity occurs prior AD pathology. Therefore, targeting metabolic mechanisms arises as a promising therapeutic target for preventing and/or treating AD." @default.
• W2896241654 created "2018-10-26" @default.
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• W2896241654 date "2018-07-01" @default.
• W2896241654 modified "2023-10-16" @default.
• W2896241654 title "P2‐424: EARLY DETECTION OF BRAIN HYPOMETABOLISM IN THE 3XTG MOUSE MODEL OF ALZHEIMER'S DISEASE" @default.
• W2896241654 doi "https://doi.org/10.1016/j.jalz.2018.06.1116" @default.
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