Pseudoginsenoside-F11 alleviates cognitive deficits and Alzheimer’s disease-type pathologies in SAMP8 mice

Nov 6, 2018Pharmacological research

Pseudoginsenoside-F11 reduces memory problems and Alzheimer's-like brain changes in aging mice

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Abstract

PF11 improved cognitive function in male 6-month-old SAMP8 mice over 3 months.

SAMP8 mice exhibited cognitive impairment, amyloid beta deposition, and tau hyperphosphorylation, characteristic of Alzheimer's disease.
Increased levels of cytoplasmic amyloid precursor protein (APP) and β-site APP cleavage enzyme 1 (BACE1) were observed in the hippocampus and cortex of SAMP8 mice.
PF11 enhanced learning and memory performance in tests assessing recognition and spatial navigation.
PF11 promoted the transport of APP from the cytoplasm to the plasma membrane while reducing BACE1 levels in the brain.
PF11 also normalized elevated levels of demethylated protein phosphatase 2A (PP2A) and reduced expression of leucine carboxyl methyltransferase 1 (LCMT-1) in SAMP8 mice.

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Alzheimer's disease (AD) is a common neurodegenerative disease which is characterized by aggregation of amyloid beta (Aβ) and hyperphosphorylated tau. We previously reported that pseudoginsenoside-F11 (PF11), an ocotillol-type saponin, improved cognitive function and reduced Aβ aggregation in APP/PS1 mice, a familial AD model. Here, we chose senescence-accelerated mouse prone 8 (SAMP8) mice, a widely used model of aging, to investigate the effect of PF11 on sporadic AD. PF11 was orally administered to male 6-month-old SAMP8 mice for 3 months. Consistent with previous studies, SAMP8 mice showed several AD-type pathologies including cognitive impairment, Aβ deposition and tau hyperphosphorylation. We found increased protein levels of cytoplasmic amyloid precursor protein (APP) and β-site APP cleavage enzyme 1 (BACE1) in the hippocampus and cortex of SAMP8 mice. The protein level of demethylated protein phosphatase 2A (PP2A) was elevated in SAMP8 animals and the protein level of leucine carboxyl methyltransferase 1 (LCMT-1) was reduced. PF11 attenuated learning and memory impairments in the novel object recognition test and Morris water maze. PF11 promoted the transport of APP from cytoplasm to plasma membrane and decreased the abnormally high expression of BACE1 in hippocampus and cortex of SAMP8 mice. The elevated protein level of demethylated PP2A and the reduced expression of LCMT-1 in hippocampus and cortex of SAMP8 were also attenuated by PF11. Together, our findings indicate that PF11 has beneficial effects on AD-like pathological changes in SAMP8 mice and may act by inhibiting amyloidogenic processing of APP and attenuating tau hyperphosphorylation.

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Pseudoginsenoside-F11 alleviates cognitive deficits and Alzheimer’s disease-type pathologies in SAMP8 mice

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