期刊
AGING-US
卷 11, 期 7, 页码 1934-1964出版社
IMPACT JOURNALS LLC
DOI: 10.18632/aging.101884
关键词
Parkinson's disease; ginsenoside Rb1; memory deficits; alpha-synuclein; synaptic plasticity
资金
- National Natural Science Foundation of China [81870991, U1603281, 81704130]
- Natural Science Foundation of Fujian Province of China [2017J05139]
- Natural Science Foundation of Guangdong Province of China [2017A030310643]
- Startup Research Fund of Guangzhou Medical University [B185006002047]
Memory deficiency is a common non-motor symptom of Parkinson's disease (PD), and conventionally, alpha-synuclein is considered to be an important biomarker for both motor and cognitive characteristics attributed to PD. However, the role of physiological alpha-synuclein in cognitive impairment remains undetermined. Ginsenoside Rb1 has been shown to protect dopaminergic neurons (DA) from death and inhibit alpha-synuclein fibrillation and toxicity in vitro. Our recent study also revealed that ginsenoside Rb1 ameliorates motor deficits and prevents DA neuron death via upregulating glutamate transporter GLT-1 in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Whether Rb1 can improve memory deficiency and the underlying mechanism is still unknown. In this study, we found that Rb1 can prevent the spatial learning and memory deficits, increase long-term potentiation (LTP) and hippocampal glutamatergic transmission in the MPTP mouse model. The underlying neuroprotective mechanism of Rb1-improved synaptic plasticity involves Rb1 promoting hippocampal CA3 alpha-synuclein expression, restoring the glutamate in the CA3-schaffer collateral-CA1 pathway, and sequentially increasing postsynaptic density-95 (PSD-95) expression. Thus, we provide evidence that Rb1 modulates memory function, synaptic plasticity, and excitatory transmission via the trans-synaptic alpha-synuclein/PSD-95 pathway. Our findings suggest that Rb1 may serve as a functional drug in treating the memory deficiency in PD.
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