Quercetin and quercetin-3-β-d-glucoside improve cognitive and memory function in Alzheimer’s disease mouse

• Published in: Applied biological chemistry Vol. 59; no. 5; pp. 721 - 728
• Main Authors: Kim, Ji Hyun, Lee, Jaemin, Lee, Sanghyun, Cho, Eun Ju
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Netherlands 01-10-2016; Springer Nature B.V; 한국응용생명화학회
• Subjects: Alzheimer's disease; Animal memory; Animal models; Applied Microbiology; Biological Techniques; Bioorganic Chemistry; Brain; Chemistry; Chemistry and Materials Science; Cognitive ability; Glucosides; In vivo methods and tests; Learning; Lipid peroxidation; Lipids; Memory; Memory tasks; Neurodegenerative diseases; Object recognition; Oral administration; Oxidative stress; Pattern recognition; Peroxidation; Quercetin; Rodents; Spatial analysis; Spatial discrimination learning; Spatial memory; 농학; Oxidative stress; glucoside; Amyloid beta; Alzheimer’s disease; Quercetin-3-β; Quercetin
• ISSN: 2468-0834; 2468-0842
• DOI: 10.1007/s13765-016-0217-0

We investigated the protective activities of quercetin (Q) and quercetin-3-β-
d
-glucoside (Q3G) under Aβ
25–35
-injected Alzheimer’s disease (AD) model mice. To induce an AD-like disease in an in vivo model, mice were injected with Aβ
25–35
via the intracerebroventricular route. Q and Q3G were administered orally for 14 days at 30 mg/kg/day. Learning and memory functions were evaluated using behavioral experiments that comprise tests like T-maze, Morris water maze, and novel object recognition. The administration of Q and Q3G improved memory and cognitive function, compared with Aβ
25–35
-injected control mice in the T-maze and object recognition test. Q and Q3G administration decreased time in order to get to the platform during the Morris water maze test. The group administered Q experienced higher protective effects from long-term spatial memory and learning ability impairments than the group administered Q3G. Furthermore, lipid peroxidation and NO formation in the brain were significantly elevated in Aβ
25–35
-injected control mice, and this was inhibited by Q and Q3G. These results demonstrated that Q and Q3G improved Aβ
25–35
-induced memory deficits and cognitive impairment and promoted protection in the brain against oxidative stress.