Allicin can reduce neuronal death and ameliorate the spatial memory impairment in Alzheimer's disease models.
OBJECTIVE
To investigate the mechanisms and protective effects of allicin on learning and memory in a mouse model of Alzheimer's disease (AD).


METHODS
This study took place in the Institute of Medicine of Jishou University, Jishou, China, between January and September 2009. Allicin was given as preventive administration after AD was induced by amyloid beta (Aß[1-42]), and the protective effects of Allicin against learning and memory impairment were investigated. Sixty mice were randomly divided into 3 groups including the sham-operated+phosphate buffer solution (PBS) group, the Aß(1-42)+PBS group, and the Aß(1-42)+allicin group. The Aß(1-42) (1 µL = 4µg) was injected into the bilateral hippocampi. Sham-operated mice were infused with PBS. Allicin or PBS was then injected intraperitoneally for 14 days. The animals were trained, and learning and memory abilities tested using the Morris Water-Maze. The changes of Aß(1-42) and P38 mitogen-activated protein kinase (p38MAPK) were recorded to explore the mechanism of allicin's protective effects on learning and memory deficits.


RESULTS
The Aß(1-42)-infused allicin-treated group showed significantly shorter latency times than the PBS treated Aß(1-42)-infused group from the second day of learning sessions (p=0.031), accompanied with significant reduction of malondialdehyde (MDA) (p=0.035) and an increase of superoxide dismutase (SOD) activity (p=0.041). Allicin also decreased Aß and p38MAPK expressions in the cerebral cortex of AD mice model (p=0.031).


CONCLUSIONS
Preventive administration of allicin prevented learning and memory impairment, the mechanism may be due to an increase in the activity of SOD, a reduction in the levels of MDA and the expressions of Aß and p38MAPK in the brain.
Li
Xian-Hui
XH
Institute of Medicine of Jishou University, Jishou 416000, Hunan Province, China. lxhsurgeon@163.com
Li
Chun-Yan
CY
Xiang
Zhi-Gang
ZG
Zhong
Fei
F
Chen
Zheng-Ying
ZY
Lu
Jiang-Ming
JM
D000544:Alzheimer Disease / Q000139:chemically induced / Q000150:complications*; D016229:Amyloid beta-Peptides / Q000633:toxicity; D000704:Analysis of Variance; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D016923:Cell Death / Q000187:drug effects; D004195:Disease Models, Animal; D004220:Disulfides; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects; D006624:Hippocampus / Q000473:pathology*; D008297:Male; D018782:Maze Learning / Q000187:drug effects; D008569:Memory Disorders / Q000188:drug therapy / Q000209:etiology / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D009474:Neurons / Q000187:drug effects*; D010446:Peptide Fragments / Q000633:toxicity; D013441:Sulfinic Acids / Q000494:pharmacology / Q000627:therapeutic use*; D013997:Time Factors; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D016229:Amyloid beta-Peptides; D000975:Antioxidants; D004220:Disulfides; D010446:Peptide Fragments; D013441:Sulfinic Acids; C075222:amyloid beta-protein (1-42); C006452:allicin; D048051:p38 Mitogen-Activated Protein Kinases