Premium
Chronic administration of melatonin reduces cerebral injury biomarkers in SAMP8
Author(s) -
GutierrezCuesta Javier,
Sureda Francesc X.,
Romeu Marta,
Canudas Anna M.,
Caballero Beatriz,
CotoMontes Ana,
Camins Antoni,
Pallàs Mercè
Publication year - 2007
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2007.00433.x
Subject(s) - melatonin , senescence , neuroprotection , cyclin dependent kinase 5 , hyperphosphorylation , oxidative stress , medicine , endocrinology , cerebral cortex , apoptosis , biology , kinase , microbiology and biotechnology , protein kinase a , biochemistry , mitogen activated protein kinase kinase
Certain effects of melatonin on senescence were investigated. The experimental model used was 10‐month‐old senescence‐accelerated mouse prone 8 (SAMP8). The mice in the experiment were administered melatonin (10 mg/kg) from the age of 1 month. Results showed that chronic administration of melatonin decreased cell loss in the cerebral cortex and reduced oxidative damage in protein and lipids. There are several studies suggesting that the activation of the cdk5/p35 pathway at its cleavage to cdk5/p25 may play a role in hyperphosphorylation of tau during aging and neurodegenerative diseases. Melatonin not only reduced the cerebral aging disturbances, but also prevented tau hyperphosphorylation present in the experimental model used in this study. Melatonin reduced cdk5 expression, as well as the cleavage of p35 to p25. The other tau kinase studied, GSK3 β , showed a reduction in this activity in comparison with SAMP8 nontreated SAMP8. These data indicate that melatonin possesses neuroprotective properties against cerebral damage gated to senescence. Moreover, these data suggest that the cdk5/GSK β signaling cascade has a potential role as a target for neurodegenerative diseases related to aging.