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Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation
by
Laughton, Katrina
, Filiz, Gulay
, Donnelly, Paul S
, Volitakis, Irene
, Perez, Keyla A
, Bush, Ashley I
, Masters, Colin L
, Cherny, Robert A
, Lal, Varsha
, Nurjono, Milawaty
, Barnham, Kevin J
, Adlard, Paul A
, Caragounis, Aphrodite
, White, Anthony R
, Crouch, Peter J
, Cortes, Mikhalina
, Li, Qiao-Xin
, Du, Tai
, Cappai, Roberto
, Hung, Lin Wai
in
Alzheimers disease
/ Amyloids
/ Bioavailability
/ Long term potentiation
/ Medical treatment
/ Metal ions
/ Oligomers
/ Phosphorylation
/ Physical Sciences
/ Transgenic animals
/ Trimers
2009
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Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation
by
Laughton, Katrina
, Filiz, Gulay
, Donnelly, Paul S
, Volitakis, Irene
, Perez, Keyla A
, Bush, Ashley I
, Masters, Colin L
, Cherny, Robert A
, Lal, Varsha
, Nurjono, Milawaty
, Barnham, Kevin J
, Adlard, Paul A
, Caragounis, Aphrodite
, White, Anthony R
, Crouch, Peter J
, Cortes, Mikhalina
, Li, Qiao-Xin
, Du, Tai
, Cappai, Roberto
, Hung, Lin Wai
in
Alzheimers disease
/ Amyloids
/ Bioavailability
/ Long term potentiation
/ Medical treatment
/ Metal ions
/ Oligomers
/ Phosphorylation
/ Physical Sciences
/ Transgenic animals
/ Trimers
2009
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While trying to remove the title from your shelf something went wrong :( Kindly try again later!
Do you wish to request the book?
Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation
by
Laughton, Katrina
, Filiz, Gulay
, Donnelly, Paul S
, Volitakis, Irene
, Perez, Keyla A
, Bush, Ashley I
, Masters, Colin L
, Cherny, Robert A
, Lal, Varsha
, Nurjono, Milawaty
, Barnham, Kevin J
, Adlard, Paul A
, Caragounis, Aphrodite
, White, Anthony R
, Crouch, Peter J
, Cortes, Mikhalina
, Li, Qiao-Xin
, Du, Tai
, Cappai, Roberto
, Hung, Lin Wai
in
Alzheimers disease
/ Amyloids
/ Bioavailability
/ Long term potentiation
/ Medical treatment
/ Metal ions
/ Oligomers
/ Phosphorylation
/ Physical Sciences
/ Transgenic animals
/ Trimers
2009
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Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation
Journal Article
Increasing Cu bioavailability inhibits Aβ oligomers and tau phosphorylation
2009
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Overview
Cognitive decline in Alzheimer's disease (AD) involves pathological accumulation of synaptotoxic amyloid-β (Aβ) oligomers and hyperphosphorylated tau. Because recent evidence indicates that glycogen synthase kinase 3β (GSK3β) activity regulates these neurotoxic pathways, we developed an AD therapeutic strategy to target GSK3β. The strategy involves the use of copper-bis(thiosemicarbazonoto) complexes to increase intracellular copper bioavailability and inhibit GSK3β through activation of an Akt signaling pathway. Our lead compound CuII(gtsm) significantly inhibited GSK3β in the brains of APP/PS1 transgenic AD model mice. CuII(gtsm) also decreased the abundance of Aβ trimers and phosphorylated tau, and restored performance of AD mice in the Y-maze test to levels expected for cognitively normal animals. Improvement in the Y-maze correlated directly with decreased Aβ trimer levels. This study demonstrates that increasing intracellular copper bioavailability can restore cognitive function by inhibiting the accumulation of neurotoxic Aβ trimers and phosphorylated tau.
Publisher
National Academy of Sciences,National Acad Sciences
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