Amyloid plaques contribute to the formation of peroxynitrites but they are only part of the cause.
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The drugs aim to remove aberrant protein clumps called amyloid plaques from the brains of Alzheimer's patients.
As expected, the vaccine created antibodies that prevented beta amyloid plaques from forming.
To reiterate: Since 1994, the pathway that leads to the formation of amyloid plaques has been known (phospholipase C).
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Before the development of imaging agents, amyloid plaques could be determined only after death, by examining the brain during an autopsy.
But no imagery can save you from amyloid plaques and neurofibrillary tangles.
For the past two decades, therefore, most attention has been given to developing drugs that will remove amyloid plaques from an affected brain.
Other researchers had identified several related protein fragments, called beta-amyloids, inside the amyloid plaques, but they didn't know which proteins were the bad ones.
Other researchers had identified several related protein fragments, called beta-amyloid, inside the amyloid plaques, but they didn't know which proteins were the bad ones.
The hypothesis holds that these so-called amyloid plaques are a culprit in the disease's devastating symptoms, and that removing them or preventing growth could stymie Alzheimer's.
It was designed to attack and remove what some researchers believe is a root cause of Alzheimer's, the tell-tale amyloid plaques that build up in patients' brains.
If you don't have the genetic form, there's no way to tell if you will go on to develop the disease, even if you have accumulation of amyloid plaques.
The technology works by attaching a radioactive marker, called thioflavin, to the tangles of protein, known as amyloid plaques, that are found in the brains of patients with Alzheimer's.
They are also going to look at whether the presence or absence of amyloid plaques, a marker of Alzheimer's in the brain, predicts participants' cognitive status over the next five years.
For patients who already have some symptoms of cognitive decline, a positive scan suggests that moderate to frequent amyloid plaques are present in the brain, which is consistent with Alzheimer's disease.
In the late 1980s circumstantial evidence condemning the role of Alzheimer's amyloid plaques began to build when Harvard biologist Bruce Yankner showed, in test tubes, that the amyloid protein poisoned brain cells.
"There is a 50-60 percent decrease in the amount of amyloid plaques and indeed the amount of a-beta proteins in the brains of mice who have gotten chronic nasal treatment, " their report said.
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In the late 1980s circumstantial evidence that condemned the role of Alzheimer's amyloid plaques began to build when Bruce Yankner, a Harvard biologist, showed in test tubes that the amyloid protein poisoned brain cells.
The first hints about cellular debris came almost a century ago, when psychiatrist Alois Alzheimer studied the brains of demented patients after death and found them clogged with strange deposits he dubbed amyloid plaques.
The first hints about cellular debris came almost a century ago, when the psychiatrist Alois Alzheimer studied the brains of demented patients after their deaths and found them clogged with strange deposits that he named amyloid plaques.
People with a rare genetic form of Alzheimer's, whose specific genetic mutations guarantee that they will develop the disease, tended to show signs of amyloid plaques in PET scans and cerebrospinal fluid 10 to 20 years before the onset of symptoms.
Pharmaceutical companies have made a habit of targeting the wrong cause (acetylcholinesterase inhibitors which are basically useless since as the disease progresses acetylcholinesterase activity declines by 85 percent), one aspect of the disease (Namenda as an antagonist for NMDA receptors), or insisting on a partially flawed mechanism for the disease (amyloid plaques).
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Beta amyloid forms sticky plaques in the brains of Alzheimer's patients and many scientists suspect that slowing plaque formation could slow the disease.
Merck is now racing to devise the first drugs that gum up the enzymes and slow formation of the deadly amyloid peptide and plaques.
One large area of research is in plaques of beta amyloid which form on the brain.
Its causes have long been unknown, but increasing circumstantial evidence points to a toxic protein called amyloid peptide, which builds up into plaques and slowly chokes off brain cells.
The main anatomical symptoms of Alzheimer's are the growth in the brain of plaques of a protein called beta amyloid, and tangles inside cells of a second protein called tau.
The dominant explanation of Alzheimer's disease contends that the massive brain cell death is due to the buildup of plaques containing a protein called beta amyloid built up in the brain.
However, amyloid may be only one factor in Alzheimer's, and growing evidence shows that plaques form relatively late in the disease process, leading some scientists to think that attacking amyloid once the clumps have already formed is too late.
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