The beneficial effect of 3,6'-Disinapoyl sucrose on the cognitive decline via CREB/BDNF signal pathway in APP/PS1 transgenic mice.

Alzheimer's disease (AD) is a neurodegenerative disorder with insidious onset and progressive development. There is an urgent need to find drugs that prevent, slow the progression of AD. We focus our attention on 3,6'-disinapoyl sucrose (DISS), an oligosaccharide with antidepressant and antioxidant activities. In this work, APP/PS1 transgenic mice were utilized to explore the neuroprotective impact of DISS to provide new applications for prevention and therapy of AD. To assess DISS's neuroprotective impact on learning and memory deficits in APP/PS1 transgenic mice using behavioral tests (Morris water maze, Novel object recognition test, and Passive avoidance test). Morphological alterations of hippocampus neurons were observed by Nissl staining and neuronal of apoptosis were assessed by TUNEL assay. By using ELISA, the expressions of inflammatory factors were evaluated, and Western blotting was used to measure the protein expressions of neuron-related regulators in the hippocampus. DISS significantly ameliorated the cognitive disorder in APP/PS1 transgenic mice, reduced apoptosis by decreasing the ratio of Bax/Bcl-2 in hippocampal neurons, and restored the abnormal secretion of inflammatory factors (IL-2, TNF-α, IL-1β, and IL-6). Moreover, the gavage of high-dose DISS can boost the expressions of CREB/BDNF. Overall, our results indicate that DISS improves cognitive function in APP/PS1 transgenic mice by inhibiting neural apoptosis and activating the CREB/BDNF signal pathway.