Melatonin Prolongs Life In Animal Model Of Huntingtons Disease

Melatonin prolongs life in animal model of Huntington's disease

Melatonin prolongs life in animal model of Huntington's disease

Friday, October 14, 2011. An article published on October 11, 2011 in the Journal of Neuroscience reveals the discovery of researchers at the University of Pittsburgh School of Medicine and Harvard Medical School of a protective effect for melatonin against disease progression and premature death in a mouse model of Huntington's disease, an inherited disorder that results in involuntary movement, decreased intellectual function and other effects stemming from the loss of neurons in the brain due to a mutant protein. Melatonin is a hormone involved in sleep and immune function which has been found to be reduced in other neurodegenerative disorders, such as Alzheimer's and Parkinson's diseases.

"In earlier work, we screened more than 1,000 FDA-approved drugs to see which ones could block the release of a small protein called cytochrome c from the mitochondria to interrupt a key step in a chain reaction known as apoptosis, or programmed cell death," explained senior investigator Robert M. Friedlander, MD, who is the chair of the Department of Neurological Surgery and UPMC Endowed Professor of neurosurgery and neurobiology. "Melatonin, which we know to be a potent antioxidant, was one of the agents that could do this in the test tube, but we needed to determine if it would also be neuroprotective in a transgenic animal model of Huntington's disease."

In the current research, Dr Friedlander's team injected mice bred to develop Huntington's disease with melatonin or a placebo. Animals that received the hormone experienced a 19 percent delay in the onset of disease, a reduction in disease progression and an 18 percent longer life span compared with the placebo group. When the animals' brain tissue was studied, type 1 melatonin (MT1) receptors were found on the cells' mitochondria. The researchers observed that the receptors were depleted—a finding that was also detected in brain tissue derived from humans afflicted with the disease.

"Extra melatonin might help fill all the available MT1 receptors, allowing the hormone to counter the programmed cell death cascade and thus protect neurons," Dr Friedlander commented. "This suggests that melatonin or similar agents that influence the MT1 receptor have potential as a Huntington's disease treatment, which we've never had before."

"Perhaps the best approach will be to develop a cocktail of drugs that target different molecular pathways that are responsible for creating Huntington's disease," he added. "We plan to see if combining different agents leads to a greater impact on disease progression and mortality."

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Zinc aids in regulating brain cell communication

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A report published online on September 21, 2011 in the journal Neuron reveals an important role for the mineral zinc in the regulation of brain cell communication. The finding is the first instance of proof that an element, as opposed to a chemical compound, is used by the nervous system as a neurotransmitter.

In research conducted over half a century ago, high concentrations of zinc were found in nerve cell compartments known as vesicles that package neurotransmitters—the chemicals that facilitate the transmission of impulses between neurons. Neurons in the brain's hippocampus, which is the center of learning and memory, were discovered to have the highest levels of zinc. However, it remained unknown whether the zinc that was found in the cells' vesicles actually played a role in nerve cell communication.

For the current investigation, researchers at Duke University and the Massachusetts Institute of Technology utilized a novel zinc chelator to help bind and remove zinc from hippocampal brain samples derived from mice. "We discovered that zinc is essential to control the efficiency of communication between two critical populations of nerve cells in the hippocampus," senior author James McNamara, MD, of Duke University reported. "This addresses a longstanding controversy in the field."

Although having adequate zinc is essential for nerve cell communication, excessive enhancement of this communication has been observed in animals with epilepsy. "Carefully controlling zinc's regulation of communication between these nerve cells is critical to both formation of memories and perhaps to occurrence of epileptic seizures," Dr McNamara stated.

He noted that zinc supplements are widely available and are often used to treat depression and other brain disorders, however, it isn't known whether supplementing with the mineral changes the brain's zinc content or modifies the communication between its nerve cells.

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