Liquiritigenin attenuates the learning and memory deficits in an amyloid protein precursor transgenic mouse model and the underlying mechanisms.

Abstract

The present paper is to examine whether liquiritigenin is able to attenuate the Alzheimer's-like learning and memory deficits in a transgenic (Tg) mouse model that over-expresses amyloid protein precursor (APP), and explores the underlying mechanisms. Consistent with our previous observations, we found that treatment with liquiritigenin improved the behavioral performance of Tg mice and it attenuated the protein expression of oligomeric form of amyloid β-peptide (Aβ). Furthermore, treatment with liquiritigenin inhibited astrocytosis in the hippocampus, and it may through its inhibitory activities on Notch-2, an important molecular regulating neural proliferation and differentiation. These findings provide evidence for beneficial activity of liquiritigenin in a mouse model of Alzheimer's disease and support the continued investigation of Notch signaling pathway as a target for treatment of Alzheimer's disease.

• Authors: Rui Ting Liu, Jin Tian Tang, Li Bo Zou, Jie Ying Fu, Qiu Jun Lu
• Journal: European journal of pharmacology (Eur J Pharmacol) Vol. 669 Issue 1-3 Pg. 76-83 (Nov 01 2011) ISSN: 1879-0712 [Electronic] Netherlands
• PMID: 21872584 (Publication Type: Journal Article)
• Copyright: Copyright © 2011. Published by Elsevier B.V.

Chemical References

• Amyloid beta-Peptides
• Amyloid beta-Protein Precursor
• Flavanones
• Glial Fibrillary Acidic Protein
• Nerve Tissue Proteins
• Nootropic Agents
• Notch2 protein, mouse
• Receptor, Notch2
• glial fibrillary astrocytic protein, mouse
• liquiritigenin

Topics

• Alzheimer Disease (drug therapy, metabolism, pathology)
• Amyloid beta-Peptides (metabolism)
• Amyloid beta-Protein Precursor (genetics, metabolism)
• Animals
• Astrocytes (drug effects, metabolism, pathology)
• Avoidance Learning (drug effects)
• CA1 Region, Hippocampal (drug effects, metabolism, pathology)
• Disease Models, Animal
• Female
• Flavanones (pharmacology)
• Glial Fibrillary Acidic Protein
• Gliosis (drug therapy, metabolism, pathology)
• Learning (drug effects)
• Male
• Maze Learning (drug effects)
• Memory Disorders (drug therapy, metabolism, pathology)
• Mice
• Mice, Inbred C57BL
• Mice, Transgenic
• Nerve Tissue Proteins (metabolism)
• Nootropic Agents (pharmacology)
• Receptor, Notch2 (metabolism)