Dangerous Custodians: Immune Cells as Possible Nerve-Cell Killers in Alzheimer's Disease
It is estimated that approximately 18 million people currently suffer from Alzheimer's Disease worldwide, and the number is rising. This form of progressive dementia is due to a loss of nerve cells from the brain that is associated with the formation of insoluble protein aggregates, called beta-amyloid plagues and tangles. It has been thought that Alzheimer's Disease occurs when large numbers of microgilas gather in the vicinity of the beta-amyloid plagues and degrade the plague.
Recently a discovery by an international team under the leadership of LMU neuroscientist Professor Jochen Herms found that microgila may actually make a significant contribution to the loss of neurons associated to Alzheimer's Disease by congregrating near stressed nerve cells. Stressed nerve cells release a signal that attracts microgila. Microgilia are the cells that are responsible for the immune response inside the brain and they start a protective inflammatory response to tissue damage and infection. When the microgila causes an inflammatory response, the result can be the destruction of the neurons in the area where microgila congregate.
An experiment was done on genetically modified mice that develop many of the symptoms of Alzheimer's Disease in humans. The mice were also engineered to make fluorescent forms of proteins that are specific for neurons and microgila, and the imaging technique enabled researchers to monitor the fate of identifable neurons and microgila over periods of weeks and months. This approach made it possible for the first time to visualize the loss of nerve cells in the brains of living mice. Nerve loss was found to precede the activitation of microgila.
This discovery shows that chemical signalling between microgila and nerve cells plays a crucial role in mediating neuron loss during the course of the disease. One of the most important aspects of the discovery was announced when Professor Jochen Herms said, "The possible chemical that causes microgila to go to stressed nerve cells may be the chemokine fractalikine, which docks onto a receptor protein on the surface of the microgila cells."
I found this interesting because my great-grandmother was diagnosed with Alzheimer's Disease. Alzheimer's Disease is a terrible disease that doesn't have a cure and any discovery that may lead to the cure for Alzheimer's Disease is interesting to me. This discovery could lead to possibily manipulating the chemical signals and reducing the communication between microgila cells and stressed nerve cells by disrupting the synthesis of chemokine fractalikine or rendering it ineffective by not allowing chemokine fractalikine to bind to the receptor protein on the surface of the microgila cells.
This article can be found at
http://www.sciencedaily.com/releases/2010/03/100322083855.htm
Recently a discovery by an international team under the leadership of LMU neuroscientist Professor Jochen Herms found that microgila may actually make a significant contribution to the loss of neurons associated to Alzheimer's Disease by congregrating near stressed nerve cells. Stressed nerve cells release a signal that attracts microgila. Microgilia are the cells that are responsible for the immune response inside the brain and they start a protective inflammatory response to tissue damage and infection. When the microgila causes an inflammatory response, the result can be the destruction of the neurons in the area where microgila congregate.
An experiment was done on genetically modified mice that develop many of the symptoms of Alzheimer's Disease in humans. The mice were also engineered to make fluorescent forms of proteins that are specific for neurons and microgila, and the imaging technique enabled researchers to monitor the fate of identifable neurons and microgila over periods of weeks and months. This approach made it possible for the first time to visualize the loss of nerve cells in the brains of living mice. Nerve loss was found to precede the activitation of microgila.
This discovery shows that chemical signalling between microgila and nerve cells plays a crucial role in mediating neuron loss during the course of the disease. One of the most important aspects of the discovery was announced when Professor Jochen Herms said, "The possible chemical that causes microgila to go to stressed nerve cells may be the chemokine fractalikine, which docks onto a receptor protein on the surface of the microgila cells."
I found this interesting because my great-grandmother was diagnosed with Alzheimer's Disease. Alzheimer's Disease is a terrible disease that doesn't have a cure and any discovery that may lead to the cure for Alzheimer's Disease is interesting to me. This discovery could lead to possibily manipulating the chemical signals and reducing the communication between microgila cells and stressed nerve cells by disrupting the synthesis of chemokine fractalikine or rendering it ineffective by not allowing chemokine fractalikine to bind to the receptor protein on the surface of the microgila cells.
This article can be found at
http://www.sciencedaily.com/releases/2010/03/100322083855.htm
posted by K at 7:09 PM
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