Melatonin Decreases Levels of S100β and NFΚB, Increases Levels of Synaptophysinina Rat Model of Alzheimer’s Disease
Stephen C. Bondy.
The effect of treatment with melatonin was investigated in a rat model of Alzheimer’s disease (AD) involving a
single intra-hippocampal injection of amyloid peptide Aβ1-42. Thirty days after this injection immunohistochemical analysis
revealed significant increases of both S-100β and NFΚB in cortex and hippocampus of treated animals. Levels of synaptophysin
were depressed following treatment and this was confirmed by Western blotting. Histopathological studies revealed
a diminution of neuronal cell number in the CA3 area of the hippocampus. Behaviorally, the rate of learning escape
from electroshock using a maze box was diminished in Aβ-treated mice. Another group of A treated also received
an oral gavage of 0.5 mg/kg melatonin on each of the 30 days between Aβ treatment and sacrifice. The effect of this repeated
melatonin exposure was to reverse Aβ-induced changes in CA3 cell number and S-100 levels. The increased cerebral
content of NF-ΚB and the behavioral changes caused by A treatment were partially reversed by melatonin. However,
melatonin administration had no effect on the reduced level of synaptophysin in Aβ-treated mice. Overall, these
findings suggest that melatonin may exert a potentially beneficial effect upon the progression of AD.
Keywords: Alzheimer’s disease, amyloid, hippocampus, learning, melatonin, NF-ΚB.
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