Beneficial effects of melatonin in experimental models of Alzheimer disease

被引:56
作者
Cheng, Y
Feng, Z
Zhang, QZ
Zhang, JT [1 ]
机构
[1] Chinese Acad Med Sci, Inst Mat Med, Dept Pharmacol, Beijing 100050, Peoples R China
[2] Peking Union Med Coll, Beijing 100050, Peoples R China
[3] Univ Calif San Diego, Dept Anesthesiol, La Jolla, CA 92161 USA
[4] Vet Affairs Med Ctr, La Jolla, CA 92161 USA
[5] Shandong Univ, Coll Pharm, Dept Pharmacol, Jinan 250012, Peoples R China
关键词
melatonin; Alzheimer disease; beta-amyloid protein; calcium overload; APP transgenic mice; ovariectomized rats; tau protein hyperphosphorylation;
D O I
10.1111/j.1745-7254.2006.00267.x
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
Alzheimer's disease (AD), a progressive degenerative disorder, is characterized by the presence of amyloid deposits, neurofibrillary tangles and neuron loss. Emerging evidence indicates that antioxidants could be useful either for the prevention or treatment of AD. It has been shown that melatonin is a potent antioxidant and free radical scavenger. Additionally, melatonin stimulates several antioxidative enzymes and improves mitochondrial energy metabolism. These findings led us to study amyloid precursor protein transgenic mice, ovariectomized rats, and pheochromocytoma and astroglioma cell lines, to observe whether melatonin had any effect on Alzheimer's symptoms or pathological changes. We found that melatonin had many beneficial effects in experimental models of AD, including improvement of cognitive function, anti-oxidative injury, anti-apoptosis, inhibition of beta-amyloid (A beta) deposition and A beta fiber formation. Several groups have shown that melatonin has an inhibitory effect on tau protein hyperphosphorylation. These actions may potentially slow down or stop the progression of dementia.
引用
收藏
页码:129 / 139
页数:11
相关论文
共 94 条
[61]   Melatonin - An antioxidant in edible plants [J].
Reiter, RJ ;
Tan, DX .
ALCOHOL AND WINE IN HEALTH AND DISEASE, 2002, 957 :341-344
[62]   Regulation of antioxidant enzymes:: a significant role for melatonin [J].
Rodriguez, C ;
Mayo, JC ;
Sainz, RM ;
Antolín, I ;
Herrera, F ;
Martín, V ;
Reiter, RJ .
JOURNAL OF PINEAL RESEARCH, 2004, 36 (01) :1-9
[63]   The role of mitochondrial oxidative stress in aging [J].
Sastre, J ;
Pallardó, FV ;
Viña, J .
FREE RADICAL BIOLOGY AND MEDICINE, 2003, 35 (01) :1-8
[64]   Effects of ovariectomy and calcium deficiency on learning and memory of eight-arm radial maze in middle-aged female rats [J].
Sato, T ;
Teramoto, T ;
Tanaka, K ;
Ohnishi, Y ;
Irifune, M ;
Nishikawa, T .
BEHAVIOURAL BRAIN RESEARCH, 2003, 142 (1-2) :207-216
[65]   Mechanisms of antiapoptotic effects of estrogens in nigral dopaminergic neurons [J].
Sawada, H ;
Ibi, M ;
Kihara, T ;
Urushitani, M ;
Honda, K ;
Nakanishi, M ;
Akaike, A ;
Shimohama, S .
FASEB JOURNAL, 2000, 14 (09) :1202-1214
[66]   THE EFFECT OF OVARIECTOMY AND ESTRADIOL REPLACEMENT ON BRAIN-DERIVED NEUROTROPHIC FACTOR MESSENGER-RIBONUCLEIC-ACID EXPRESSION IN CORTICAL AND HIPPOCAMPAL BRAIN-REGIONS OF FEMALE SPRAGUE-DAWLEY RATS [J].
SINGH, M ;
MEYER, EM ;
SIMPKINS, JW .
ENDOCRINOLOGY, 1995, 136 (05) :2320-2324
[67]   Bax protein expression is increased in Alzheimer's brain: Correlations with DNA damage, Bcl-2 expression, and brain pathology [J].
Su, JH ;
Deng, GM ;
Cotman, CW .
JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1997, 56 (01) :86-93
[68]   Amyloid precursor protein, presenilins, and α-synuclein:: Molecular pathogenesis and pharmacological applications in Alzheimer's disease [J].
Suh, YH ;
Checler, F .
PHARMACOLOGICAL REVIEWS, 2002, 54 (03) :469-525
[69]  
Summers WK, 2004, J ALZHEIMERS DIS, V6, P651
[70]   Astrocyte apoptosis: implications for neuroprotection [J].
Takuma, K ;
Baba, A ;
Matsuda, T .
PROGRESS IN NEUROBIOLOGY, 2004, 72 (02) :111-127