"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
- Melatonin -

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Melatonin May Halt the Progression of Alzheimer’s Disease
By Darin Ingels, ND

"Healthnotes Newswire (December 20, 2001)—The hormone melatonin may block key steps in the development of harmful protein deposition in the brain that leads to Alzheimer’s disease, according to a new report in Biochemistry.1 Although the cause of Alzheimer’s disease is unknown, it appears that people with this disease produce a precursor protein (Ab peptide) in the brain that is transformed into amyloid, a larger protein mass that contributes to the symptoms associated with this condition. Previously published studies indicate that inheritance of a cell marker called apolipoprotein E4 (Apo E4) increases the risk of developing Alzheimer’s disease as it binds to the precursor protein and facilitates the production of amyloid.2 This current study indicates that melatonin, in the presence of Apo E4, inhibits amyloid formation and thereby possibly slows or halts the progression of Alzheimer’s disease."


Prevention of isoproterenol-induced tau hyperphosphorylation by melatonin in the rat.
Wang XC, Zhang J, Yu X, Han L, Zhou ZT, Zhang Y, Wang JZ.

Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology
Sheng Li Xue Bao. 2005 Feb 25;57(1):7-12.

"Hyperphosphorylated microtubule-associated protein tau is the major protein component of neurofibrillary tangles in the brain of patients with Alzheimer's disease (AD). Until now, there is no effective cure to arrest this hyperphosphorylation. The present study was designed to explore the in vivo preventive effect of melatonin on Alzheimer-like tau hyperphosphorylation. Isoproterenol, a beta-receptor agonist, was used to induce tau hyperphosphorylation, and for preventive effect of melatonin, the rats were injected intraperitoneally with melatonin for 5 d before hippocampi infusion of isoproterenol. The level of tau phosphorylation was detected by Western blot and immunohistochemistry using sites specific antibodies (PHF-1 and Tau-1), and it was normalized by non-phosphorylation dependent total tau antibody (111e). The results by Western blot showed that the immunoreaction of tau at PHF-1 epitope was enhanced, and the reaction at Tau-1 epitope was weakened significantly at 48 h after injection of isoproterenol, suggesting hyperphosphorylation of tau at Ser 396/Ser 404 (PHF-1) and Ser199/Ser 202 (Tau-1) sites. Similar results were observed by immunohistochemistry staining, in which hyperphosphorylated tau was mainly detected in mossy fibers of hippocampal CA3 region. Pre-injection of rats with melatonin intraperitoneally arrested effectively the isoproterenol-induced tau hyperphosphorylation at both Tau-1 and PHF-1 sites, implying the preventive effect of melatonin in Alzheimer-like tau hyperphosphorylation."

PMID: 15719129 [PubMed]




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Updated: July 25, 2012
Inception: July 25, 2012