Remain healthy and young to delay the onset of Alzheimer's disease
( to maintain youth, you have to protect the proteome )
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Andrew Dillin of The Salk Institute for Biological Studies, said: "There's something about being youthful that protects us from Alzheimer's disease. People say that if you live long enough, you get Alzheimer's. But if that were true, mice that live longer should get the disease at the same rate. That's not what we found."
The study observed that mice carrying human genes, which initiate Alzheimer's, were protected by turning down a pathway that is well known for its effects on aging. The cognitive, inflammatory and neural effects of Alzheimer's were reduced by the so-called insulin/IGF signaling pathway. However, they were still riddled with amyloid plaques, packed into larger clusters than they would otherwise have been.
Dillin explained: "We expected to see less plaque in the protected mice. Instead we saw the same number of plaques, but there was a qualitative difference in how they looked. They were condensed so that they took up less area in the brain."
He further briefed that the pathway is known to negatively control two transcription factors (FOXO and HSF-1). Those transcription factors in turn control other genes encoding molecular chaperones, whose job it is to protect all of a cell''s proteins. He said: "To maintain youth, you have to protect the proteome, not just the genome."
Dillin pointed out that those who are genetically predisposed to develop early onset Alzheimer's carry the gene their whole lives, but don''t develop the disease until they reach their 50s. Seemingly, youth-extending drugs aimed at increasing the activity of the FOXO and HSF-1 transcription factors may be useful for staving off Alzheimer's disease since the IGF pathway plays so many varied roles in the body. ...http://www.hindustantimes.com
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Taking steps to remain healthy and young may help delay the onset of Alzheimer's disease, according to a new study. The researchers conducted a study on mice to reach the conclusion.
Andrew Dillin of The Salk Institute for Biological Studies, said: "There's something about being youthful that protects us from Alzheimer's disease. People say that if you live long enough, you get Alzheimer's. But if that were true, mice that live longer should get the disease at the same rate. That's not what we found."
The study observed that mice carrying human genes, which initiate Alzheimer's, were protected by turning down a pathway that is well known for its effects on aging. The cognitive, inflammatory and neural effects of Alzheimer's were reduced by the so-called insulin/IGF signaling pathway. However, they were still riddled with amyloid plaques, packed into larger clusters than they would otherwise have been.
Dillin explained: "We expected to see less plaque in the protected mice. Instead we saw the same number of plaques, but there was a qualitative difference in how they looked. They were condensed so that they took up less area in the brain."
He further briefed that the pathway is known to negatively control two transcription factors (FOXO and HSF-1). Those transcription factors in turn control other genes encoding molecular chaperones, whose job it is to protect all of a cell''s proteins. He said: "To maintain youth, you have to protect the proteome, not just the genome."
Dillin pointed out that those who are genetically predisposed to develop early onset Alzheimer's carry the gene their whole lives, but don''t develop the disease until they reach their 50s. Seemingly, youth-extending drugs aimed at increasing the activity of the FOXO and HSF-1 transcription factors may be useful for staving off Alzheimer's disease since the IGF pathway plays so many varied roles in the body. ...http://www.hindustantimes.com
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