3,6'-Disinapoylsucrose alleviates the amyloid precursor protein and lipopolysaccharide induced cognitive dysfunction through upregulation of the TrkB/BDNF pathway

Abstract

The aim of this study is to explore the effect and mechanism of 3,6’-disinapoylsucrose (DISS) on an Alzheimer's disease (AD) mice model induced by APPswe695 lentivirus (LV) and intraperitoneal injection of lipopolysaccharide (LPS). The results show that DISS improves cognitive ability, decreases the levels of IL-2, IL-6, IL-1β, and TNF-α, reduces the expression of NF-κB p65, and alleviates Aβ deposition and nerve cell damage. DISS can regulate tyrosine kinase B (TrkB)/brain-derived neurotrophic factor (BDNF) signaling in the hippocampus. In summary, DISS can significantly alleviate neuroinflammation, spatial learning and memory disorders in AD model mice.

Graphical Abstract

Keywords:

• Alzheimer's disease
• BDNF
• TrkB
• LPS
• neuroinflammation

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

National Natural Science Foundation of China [grant number 11975048]; Beijing Union University Open Project [grant number SWHX202103]; Beijing Union University Scientific Research Project Funding [grant number XP202007].