Journal article
S-Adenosylmethionine Rescues Cognitive Deficits in the rTg4510 Animal Model by Stabilizing Protein Phosphatase 2A and Reducing Phosphorylated Tau
LC Beauchamp, XM Liu, A Sedjahtera, M Bogeski, LJ Vella, AI Bush, PA Adlard, KJ Barnham
Journal of Alzheimer S Disease | IOS PRESS | Published : 2020
DOI: 10.3233/JAD-200756
Abstract
Background: Alterations in the methionine cycle and abnormal tau phosphorylation are implicated in many neurodegenerative diseases, including Alzheimer's disease and frontotemporal dementia. rTg4510 mice express mutant human P301L tau and are a model of tau hyperphosphorylation. The cognitive deficit seen in these animals correlates with a burden of hyperphosphorylated tau and is a model to test therapies aimed at lowering phosphorylated tau. Objective: This study aimed to increase protein phosphatase 2A activity through supplementation of S-adenosylmethionine and analyze the effect on spatial memory and tau in treated animals. Methods: 6-month-old rTg4510 mice were treated with 100 mg/kg S-..
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Awarded by State Government of Victoria
Funding Acknowledgements
The Florey Institute of Neuroscience and Mental Health acknowledges the strong support from the Victorian Government and in particular the funding from the Operational Infrastructure Support Grant. We acknowledge the assistance of A/Prof Laura Jacobson in this research, the Alzheimer's Association for a Fellowship (AARF-18-566256) to L.J.V and the Australian Research Training Scholarship for financial support of L.C.B.