Long-term green tea catechin administration prevents spatial learning and memory impairment in senescence-accelerated mouse prone-8 mice by decreasing Aβ1-42 oligomers and upregulating synaptic plasticity–related proteins in the hippocampus
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Abstract
The senescence-accelerated mouse prone-8 (SAMP8) is characterized by early onset of
learning and memory deficits along with spontaneous overproduction of soluble beta-amyloid
peptide (Abeta) in the brain. In our study, 4 month old male SAMP8 mice were orally
administered 0.05% and 0.1% green tea catechins (GTC, w/v) in drinking water for 6
months. We found that a supplementation with 0.05% or 0.1% GTC prevented spatial learning
and memory impairments of mice in the Morris water maze. Better performance of GTC-treated
mice was associated with decreased levels of Abeta(1-42) oligomers in the hippocampus.
The activity of the protein kinase A/cAMP-response element binding protein (PKA/CREB)
pathway, one of the molecular targets of Abeta oligomers which is crucial for late
long-term potentiation and long-term memory formation, was significantly increased
after GTC administration. We also found that chronic 0.05% or 0.1% GTC consumption
prevented the reductions of three representative proteins of synaptic function and
synaptic structure, including brain-derived neurotrophic factor(BDNF), post-synaptic
density protein-95 (PSD95) and Ca(2+)/calmodulin-dependent protein kinase II (CaMKII).
These results demonstrated that long-term 0.05% or 0.1% green tea catechin administration
may prevent spatial learning and memory decline of SAMP8 mice by decreasing Abeta(1-42)
oligomers and upregulating synaptic plasticity-related proteins in the hippocampus.