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April 21, 2008
Researchers examine a key risk factor for Alzheimer's
By John Scott
Researchers at the Washington University School of Medicine have spent four years working to determine what effects a specific protein can have on Alzheimer's brain plaques, a key risk factor for the disease.
An estimated five million Americans suffer from Alzheimer's, a disease that destroys brain cells and causes people to develop memory and behavior problems.
John Cirrito, research instructor in neurology and lead researcher of the study, said that the study, published in the April 10 issue of the journal Neuron, has been underway for 1.5 years. The topic has been studied for four years.
The team of researchers examined amyloid beta, a protein derived from amyloid precursor protein. Buildups of amyloid beta can create plaques in the brain that lead to a variety of problems including death of brain cells, eventually contributing to Alzheimer's disease. According to Cirrito, scientists have been trying to determine what regulates the protein's production.
Cirrito said that amyloid beta affects two key areas of the brain, the cortex and the hippocampus. The cortex is responsible for cognitive functions while the hippocampus controls memory. The plaques inhibit the functions of these areas, leading to the symptoms indicative of Alzheimer's disease.
"Before [the plaques] kill the cells, [researchers] think they're making neurons fire incorrectly," Cirrito said.
The study targeted a cellular process known as endocytosis, a process in which cells absorb materials from their surroundings by pinching off a section of their membrane. Production of amyloid beta is linked to both endocytosis and communication between brain cells. In the study, stopping endocytosis decreased the level of amyloid beta by 70 percent.
According to Cirrito, the function of amyloid beta and its precursor are still unknown. Endocytosis, however, is a necessary function for nearly all cells in the body. Therefore, it is very difficult to inhibit the process without causing harm to the cells, so treatments must be specifically targeted.
Source: John Scott. Student Life (21 April 2008) [FullText]
Researchers at the Washington University School of Medicine have spent four years working to determine what effects a specific protein can have on Alzheimer's brain plaques, a key risk factor for the disease.
An estimated five million Americans suffer from Alzheimer's, a disease that destroys brain cells and causes people to develop memory and behavior problems.
John Cirrito, research instructor in neurology and lead researcher of the study, said that the study, published in the April 10 issue of the journal Neuron, has been underway for 1.5 years. The topic has been studied for four years.
The team of researchers examined amyloid beta, a protein derived from amyloid precursor protein. Buildups of amyloid beta can create plaques in the brain that lead to a variety of problems including death of brain cells, eventually contributing to Alzheimer's disease. According to Cirrito, scientists have been trying to determine what regulates the protein's production.
Cirrito said that amyloid beta affects two key areas of the brain, the cortex and the hippocampus. The cortex is responsible for cognitive functions while the hippocampus controls memory. The plaques inhibit the functions of these areas, leading to the symptoms indicative of Alzheimer's disease.
"Before [the plaques] kill the cells, [researchers] think they're making neurons fire incorrectly," Cirrito said.
The study targeted a cellular process known as endocytosis, a process in which cells absorb materials from their surroundings by pinching off a section of their membrane. Production of amyloid beta is linked to both endocytosis and communication between brain cells. In the study, stopping endocytosis decreased the level of amyloid beta by 70 percent.
According to Cirrito, the function of amyloid beta and its precursor are still unknown. Endocytosis, however, is a necessary function for nearly all cells in the body. Therefore, it is very difficult to inhibit the process without causing harm to the cells, so treatments must be specifically targeted.
Source: John Scott. Student Life (21 April 2008) [FullText]
Labels: Alzheimer's research
posted by Dr.Koudinov @ 21.4.08
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