Crude caffeine reduces memory impairment and amyloid β(1-42) levels in an Alzheimer's mouse model

• Published in: Food chemistry Vol. 135; no. 3; pp. 2095 - 2102
• Main Authors: Chu, Yi-Fang, Chang, Wen-Han, Black, Richard M, Liu, Jia-Ren, Sompol, Pradoldej, Chen, Yumin, Wei, Huilin, Zhao, Qiuyan, Cheng, Irene H
• Format: Journal Article
• Language: English
• Published: England 01.12.2012
• Subjects: Alzheimer Disease - drug therapy; Alzheimer Disease - genetics; Alzheimer Disease - metabolism; Alzheimer Disease - psychology; Amyloid beta-Peptides - genetics; Amyloid beta-Peptides - metabolism; Animals; Caffeine - administration & dosage; Caspase 3 - genetics; Caspase 3 - metabolism; Coffea - chemistry; Disease Models, Animal; Humans; Male; Maze Learning; Memory - drug effects; Mice; Mice, Inbred C57BL; Mice, Transgenic; Plant Extracts - administration & dosage
• ISSN: 0308-8146; 1873-7072
• DOI: 10.1016/j.foodchem.2012.04.148

Alzheimer's disease (AD), a chronic neurodegenerative disorder associated with the abnormal accumulations of amyloid β (Aβ) peptide and oxidative stress in the brain, is the most common form of dementia among the elderly. Crude caffeine (CC), a major by-product of the decaffeination of coffee, has potent hydrophilic antioxidant activity and may reduce inflammatory processes. Here, we showed that CC and pure caffeine intake had beneficial effects in a mouse model of AD. Administration of CC or pure caffeine for 2months partially prevented memory impairment in AD mice, with CC having greater effects than pure caffeine. Furthermore, consumption of CC, but not pure caffeine, reduced the Aβ(1-42) levels and the number of amyloid plaques in the hippocampus. Moreover, CC and caffeine protected primary neurons from Aβ-induced cell death and suppressed Aβ-induced caspase-3 activity. Our data indicate that CC may contain prophylactic agents against the cell death and the memory impairment in AD.