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Co-author Marc Tessier-Lavigne, who is executive vice president of research drug discovery at the company said in a web interview: "In the field of Alzheimer's disease, it is well known that a bad actor in the brain is a protein called APP, and what we found is a new twist on our understanding of what APP does. APP is a large protein that sits in the cell membrane. It's been argued that Abeta is toxic and contributes to the degeneration that occurs in the disease", said Tessier-Lavigne, who explained that for many years research on Alzheimer's had focused on a section of the protein called Abeta.
But what he and his team found almost by mistake was that a different part of APP, which they call N-APP, may also be involved. N-APP can trigger neuron death and degeneration, "we've figured out how it is that it triggers that degeneration. We believe that this could be involved in either the initiating or helping the progression of Alzheimer's disease", said Tessier-Lavigne, and that is the subject of the paper they have published.
In their background information the authors explain that scientists have already discovered there are natural mechanisms through which unwanted axons and neurons are pruned and killed to help "sculpt neuronal connections during development", but exactly how they do this is still somewhat of a mystery.
In this study the researchers discovered that beta-amyloid precursor protein (APP) and death receptor 6 (DR6, also known as TNFRSF21) trigger a widespread self destruction program that relies on caspases (sometimes called "executioner proteins" because of the role they play in apoptosis or programmed cell death). DR6 is a receptor expressed by developing neurons and is used in normal cell death and pruning of axons (the fibre that carries the eletrical signal from the neuron). The researchers were working on something else and came across DR6 and they wondered what triggered it. That is what started them down this route. What they discovered was that while caspase 3 is involved in cell death of the neuron body, it is caspase 6 that is required for axon degeneration and this is triggered when a relatively unknown part of APP (N-APP, a cleaved amino-terminal fragment of APP) binds to DR6. ...http://www.medicalnewstoday.com
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Researchers from a leading US biotech company have discovered a new route through which Alzheimer's disease may either trigger or maintain the destruction of brain cells: the mechanism that it hijacks is normally used to prune unwanted brain cells in early development and involves a hitherto unsuspected part of a known culprit, APP, the precursor of the amyloid plaques found in the brains of people with Alzheimer's disease.
Co-author Marc Tessier-Lavigne, who is executive vice president of research drug discovery at the company said in a web interview: "In the field of Alzheimer's disease, it is well known that a bad actor in the brain is a protein called APP, and what we found is a new twist on our understanding of what APP does. APP is a large protein that sits in the cell membrane. It's been argued that Abeta is toxic and contributes to the degeneration that occurs in the disease", said Tessier-Lavigne, who explained that for many years research on Alzheimer's had focused on a section of the protein called Abeta.
But what he and his team found almost by mistake was that a different part of APP, which they call N-APP, may also be involved. N-APP can trigger neuron death and degeneration, "we've figured out how it is that it triggers that degeneration. We believe that this could be involved in either the initiating or helping the progression of Alzheimer's disease", said Tessier-Lavigne, and that is the subject of the paper they have published.
In their background information the authors explain that scientists have already discovered there are natural mechanisms through which unwanted axons and neurons are pruned and killed to help "sculpt neuronal connections during development", but exactly how they do this is still somewhat of a mystery.
In this study the researchers discovered that beta-amyloid precursor protein (APP) and death receptor 6 (DR6, also known as TNFRSF21) trigger a widespread self destruction program that relies on caspases (sometimes called "executioner proteins" because of the role they play in apoptosis or programmed cell death). DR6 is a receptor expressed by developing neurons and is used in normal cell death and pruning of axons (the fibre that carries the eletrical signal from the neuron). The researchers were working on something else and came across DR6 and they wondered what triggered it. That is what started them down this route. What they discovered was that while caspase 3 is involved in cell death of the neuron body, it is caspase 6 that is required for axon degeneration and this is triggered when a relatively unknown part of APP (N-APP, a cleaved amino-terminal fragment of APP) binds to DR6. ...http://www.medicalnewstoday.com
Cinnamon may improve blood sugar levels
Consumption of three grams of cinnamon a day may improve people’s control of blood glucose levels, Scandinavian scientists have reported. ...http://www.nutraingredients.com
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21 февраля 2009 Новость дня Віктар КОРБУТ, Алег ГАРУНОВІЧ, Народная газета З 2000 года адзначаецца Міжнародны дзень роднай мовы. Читать дальше |
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