Abstract
Therapeutic approach for Alzheimer's disease (AD) is still deficient. To find active compounds from herbal medicine is of interest in the alleviation of AD symptoms. This study aimed to investigate the protective effects of Tanshinone IIA (TIIA) on memory performance and synaptic plasticity in a transgenic AD model at the early phase. 25–100 mg/kg TIIA (intraperitoneal injection, i.p.) was administered to the six-month-old APP and PS1 transgenic mice for 30 consecutive days. After treatment, spatial memory, synaptic plasticity, and related mechanisms were investigated. Our result showed that memory impairment in AD mice was mitigated by 50 and 100 mg/kg TIIA treatments. Hippocampal long-term potentiation was impaired in AD model but rescued by 100 mg/kg TIIA treatment. Mechanically, TIIA treatment reduced the accumulations of beta-amyloid 1–42, C-terminal fragments (CTFs), and p-Tau in the AD model. TIIA did not affect basal BDNF but promoted depolarization-induced BDNF synthesis in the AD mice. Taken together, TIIA repairs hippocampal LTP and memory, likely, through facilitating the clearance of AD-related proteins and activating synaptic BDNF synthesis. TIIA might be a candidate drug for AD treatment.
Highlights
Alzheimer’s disease (AD) is an aging-related disease hallmarked by the decline of memory performance and other cognitive abilities
We provided data revealing the memory improving effect after Tanshinone IIA (TIIA) treatment in a transgenic AD model
The clearance of AD-related protein and activation of brain derived neurotrophic factor- (BDNF-)Tropomyosin receptor kinase B (TrkB) pathway might possibly contribute to the effect of TIIA on hippocampal LTP and memory
Summary
Alzheimer’s disease (AD) is an aging-related disease hallmarked by the decline of memory performance and other cognitive abilities. It is considered as the most severe neurodegenerative disease, affecting an estimated 25 million people globally [1]. Effective treatment is still lacking in AD due to the complexity of the disease pathology [2,3,4]. Impairment of synaptic plasticity and pyramid cell loss are thought to render the disease progression. Recent available drugs for AD treatment are mainly working through their activities in promoting cerebral-vascular blood flow [5]. Those drugs are either too expensive or unsatisfactory for symptoms alleviation
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