|
UWM brain research supports drug development from jellyfish protein
October 30, 2006Testing of aequorin yields promising results
With the research support from the University of Wisconsin-Milwaukee, a Wisconsin biotech company has found that a compound from a protein found in jellyfish is neuro-protective and may be effective in treating neurodegenerative diseases.
Testing of aequorin has yielded promising results, said Mark Y. Underwood of Quincy Bioscience located in Madison. Researcher James Moyer, Jr., an assistant professor at UW-Milwaukee, subjected brain cells to the "lab" equivalent of a stroke, and more than half treated with aequorin survived without residual toxicity.
Why does it work? Diseases like Alzheimer's are associated with a loss of "calcium-binding" proteins that protect nerve cells, said Moyer. Calcium is necessary for communication between neurons in the brain, and learning and memory are not possible without it. But too much of it leads to neuron death, interfering with memory and contributing to neurodegenerative diseases.
"There are ways in which cells control the influx of calcium, such as sequestering it by binding it with certain proteins," said Moyer. "If it weren't for these proteins, the high level of calcium would overwhelm the neuron and trigger a cascade of events ultimately leading to cell death."
Calcium-binding proteins decline with age, however, limiting the brain's ability to control or handle the amount of calcium "allowed in."
Aequorin, the jellyfish protein, appears to be a viable substitute.
Moyer, like Underwood, is interested in the "calcium hypothesis of aging and dementia," which is just one of many theories that attempts to explain what is going on in neuron degeneration.
He became interested in aequorin as an undergraduate at UW-Milwaukee, after reading an article that linked the stings of jellyfish with the symptoms of multiple sclerosis, a disease of the central nervous system that his mother has.
Aequorin was discovered in the 1960s and has been used in research for a long time as an indicator of calcium. But the protein has never been tried as a treatment to control calcium levels. Underwood believes his company is at about the 12-year mark in the typical 15-year cycle for a new drug to be developed.
Moyer's research centers on brain changes that occur as a result of aging. Specifically, he is interested in the part of the brain called the hippocampus, which is responsible for forming new memories. These capabilities not only deteriorate in neurodegenerative disorders such as Alzheimer's disease, but they also become impaired simply by aging.
Aging increases the number of "doors" that allow calcium ions to enter the cells, he said.
Moyer, who came to UW-Milwaukee from a post-doctoral position at Yale University, performs Pavlovian trace conditioning experiments to evaluate aging-related learning and memory deficits. These tasks first teach rodents to associate one stimulus with another and then test their memory of the association. During training, the stimuli are separated by a brief period of time, which requires the animal to maintain a memory of the first stimulus. The "stimulus free" period makes the task more difficult, especially for older animals.
Moyer's work also has implications outside of disease. He is able to show that at middle age, when the animal's learning ability or memory is not yet impaired, it already shows a drop in the number of neurons that contain an important calcium-binding protein.
"That cellular changes precede memory deficits indicates there is a window of opportunity for intervention before it's too late," he says. "Once the cells are lost, there is little chance of regaining normal brain function."
University of Wisconsin - Milwaukee
Why does it work? Diseases like Alzheimer's are associated with a loss of "calcium-binding" proteins that protect nerve cells, said Moyer. Calcium is necessary for communication between neurons in the brain, and learning and memory are not possible without it. But too much of it leads to neuron death, interfering with memory and contributing to neurodegenerative diseases.
"There are ways in which cells control the influx of calcium, such as sequestering it by binding it with certain proteins," said Moyer. "If it weren't for these proteins, the high level of calcium would overwhelm the neuron and trigger a cascade of events ultimately leading to cell death."
Calcium-binding proteins decline with age, however, limiting the brain's ability to control or handle the amount of calcium "allowed in."
Aequorin, the jellyfish protein, appears to be a viable substitute.
Moyer, like Underwood, is interested in the "calcium hypothesis of aging and dementia," which is just one of many theories that attempts to explain what is going on in neuron degeneration.
He became interested in aequorin as an undergraduate at UW-Milwaukee, after reading an article that linked the stings of jellyfish with the symptoms of multiple sclerosis, a disease of the central nervous system that his mother has.
Aequorin was discovered in the 1960s and has been used in research for a long time as an indicator of calcium. But the protein has never been tried as a treatment to control calcium levels. Underwood believes his company is at about the 12-year mark in the typical 15-year cycle for a new drug to be developed.
Moyer's research centers on brain changes that occur as a result of aging. Specifically, he is interested in the part of the brain called the hippocampus, which is responsible for forming new memories. These capabilities not only deteriorate in neurodegenerative disorders such as Alzheimer's disease, but they also become impaired simply by aging.
Aging increases the number of "doors" that allow calcium ions to enter the cells, he said.
Moyer, who came to UW-Milwaukee from a post-doctoral position at Yale University, performs Pavlovian trace conditioning experiments to evaluate aging-related learning and memory deficits. These tasks first teach rodents to associate one stimulus with another and then test their memory of the association. During training, the stimuli are separated by a brief period of time, which requires the animal to maintain a memory of the first stimulus. The "stimulus free" period makes the task more difficult, especially for older animals.
Moyer's work also has implications outside of disease. He is able to show that at middle age, when the animal's learning ability or memory is not yet impaired, it already shows a drop in the number of neurons that contain an important calcium-binding protein.
"That cellular changes precede memory deficits indicates there is a window of opportunity for intervention before it's too late," he says. "Once the cells are lost, there is little chance of regaining normal brain function."
University of Wisconsin - Milwaukee
Neurodegenerative Disease News and Current Neurodegenerative Disease Events RSSCan tomatoes carry the cure for Alzheimer's?
The humble tomato could be a suitable carrier for an oral vaccine against Alzheimer's disease, according to HyunSoon Kim from the Korea Research Institute of Bioscience and Biotechnology (KRIBB) in Korea and colleagues from Digital Biotech Inc. and the Department of Biological Science at Wonkwang University. Although their research1, just published online in Springer's journal Biotechnology Letters, is still in the early stages, it is a promising first step towards finding an edible vaccine against the neurodegenerative disease.
Scientists find how neural activity spurs blood flow in the brain
New research from Harvard University neuroscientists has pinpointed exactly how neural activity boosts blood flow to the brain. The finding has important implications for our understanding of common brain imaging techniques such as fMRI, which uses blood flow in the brain as a proxy for neural activity.
Molecular imaging sheds new light on progression of Alzheimer's disease
In the past, physicians were able only to follow the progression of Alzheimer's disease (AD) through careful clinical histories, noting the often subtle changes associated with cognitive decline over a number of years.
RNA Toxicity Contributes to Neurodegenerative Disease, University of Pennsylvania Scientists Say
Expanding on prior research performed at the University of Pennsylvania, Penn biologists have determined that faulty RNA, the blueprint that creates mutated, toxic proteins, contributes to a family of neurodegenerative disorders in humans.
Vaccine triggers immune response, prevents Alzheimer's
A vaccine created by University of Rochester Medical Center scientists prevents the development of Alzheimer's disease-like pathology in mice without causing inflammation or significant side effects.
Researchers find first conclusive evidence of Alzheimer's-like brain tangles in nonhuman primates
Researchers at the Yerkes National Primate Research Center, Emory University, have discovered the first conclusive evidence of Alzheimer's-like neurofibrillary brain tangles in an aged nonhuman primate.
Gene therapy slows progression of fatal neurodegenerative disease in children
Gene therapy to replace the faulty CLN2 gene, which causes a neurodegenerative disease that is fatal by age 8-12 years, was able to slow significantly the rate of neurologic decline in treated children.
Seeing Alzheimer's amyloids
In an important step toward demystifying the role protein clumps play in the development of neurodegenerative disease, researchers have created a stunning three-dimensional picture of an Alzheimer's peptide aggregate using electron microscopy.
Researchers uncover mechanism of action of antibiotic able to reduce neuronal cell death in brain
Virginia Commonwealth University researchers have discovered how an antibiotic works to modulate the activity of a neurotransmitter that regulates brain functions, which eventually could lead to therapies to treat Alzheimer's disease, Huntington's disease, epilepsy, stroke, dementia and malignant gliomas.
Ground-breaking new insight into the development of Alzheimer's disease
According to estimates there are 85,000 Alzheimer patients in our country and approximately 20,000 new cases every year. This spectacular increase is due to the increasing ageing population. Unfortunately it is still unclear precisely which ageing process forms the basis of this spectacular rise in the occurrence of the disease.
More Neurodegenerative Disease News Articles
| © 2008 BrightSurf.com |