Amyloid

For a long time now, scientists studying treatments for Alzheimer's disease have focused on telltale plaques that appear in patients' diseased brains as a target for therapy. The plaques are clumps of a small protein called beta-amyloid that build up in the space around nerve cells and interfere with normal brain function. Thus, the thinking goes, if plaques can be prevented from forming or cleared with medicine, the disease could be slowed. But earlier this month at an international conference, different tangled structures inside neurons took center stage alongside plaques.

No one wants to hear that he or she has Alzheimer's disease. But if the beta-amyloid plaques that are the disorder's key physical hallmark could be detected before memory loss and cognitive troubles were evident to all, would you want to know? And since no treatment currently works to stem the inexorable progress ofAlzheimer's, who would pay for a costly test to detect it early -- and why? Those questions are no longer hypothetical. Last week, the FDA approved an agent called Florbetapir F 18 injection (to be marketed as Amyvid)

No one wants to hear that he or she has Alzheimer's disease. But if the beta-amyloid plaques that are the disorder's key physical hallmark could be detected before memory loss and cognitive troubles were evident to all, would you want to know? And since no treatment currently works to stem the inexorable progress ofAlzheimer's, who would pay for a costly test to detect it early -- and why? Those questions are no longer hypothetical. Last week, the FDA approved an agent called Florbetapir F 18 injection (to be marketed as Amyvid)

Alzheimer's disease is progressive and incurable, but doctors say there is still value in having the disease diagnosed as early as possible. Drugs can be taken to treat some of the symptoms of the disease, they say. And just knowing that you have the disease can help with planning for the future. PET scans that show the early stages of Alzheimer's disease by detecting a protein in the brain called beta-amyloid will reach the marketplace within a year, researchers reported Monday at the annual meeting of the Society of Nuclear Medicine . While scientists work out the best way to conduct screening for the disease, consumers will need to decide if they want to have a brain scan.

Alzheimer's disease research in the last two decades has focused on the theory that beta-amyloid plaque accumulates in the brain and leads to the loss of cognitive function. However, this theory has not produced advances in treating the disease, with many clinical trials on drugs targeted at amyloid plaques failing. A new hypothesis on the cause of Alzheimer's should be considered, a leading researcher said Tuesday. Age is the most important risk factor in the disease, said Karl Herrup, chairman of the department of cell biology and neuroscience at Rutgers University.

A vaccine for Alzheimer's disease has been a long-held goal of researchers studying the devastating disease. Research presented Tuesday at the Society for Neuroscience meeting showed one potential vaccine under study appears both safe and effective in an animal model. Most Alzheimer's vaccine research aims to prevent the accumulation of amyloid-beta plaque in the brain that can interfere with memory and cognition. However, work on a vaccine was derailed when a study in 2002 showed that an investigational vaccine targeting amyloid-beta also caused an autoimmune response that led to dangerous inflammation in the brain.

Alzheimer's disease is progressive and incurable, but doctors say there is still value in having the disease diagnosed as early as possible. Drugs can be taken to treat some of the symptoms of the disease, they say. And just knowing that you have the disease can help with planning for the future. PET scans that show the early stages of Alzheimer's disease by detecting a protein in the brain called beta-amyloid will reach the marketplace within a year, researchers reported Monday at the annual meeting of the Society of Nuclear Medicine . While scientists work out the best way to conduct screening for the disease, consumers will need to decide if they want to have a brain scan.

Omega-3 fatty-acid supplements, often called fish-oil capsules, did not curb the mental decline in people with mild to moderate Alzheimer's disease, researchers said Tuesday. The study marks yet another attempt to treat the disease that has failed in clinical trials. Treatment with omega-3 supplements had generated considerable enthusiasm because, unlike the other unsuccessful experimental therapies, it was a natural therapy and would not have required development of a new prescription drug.

For the first time in 27 years, health authorities have expanded the definition of Alzheimer's disease. The change, announced last week by the National Institutes of Health and the Alzheimer's Assn., is intended to help doctors diagnose patients in the very early stages of the neurological disorder, including those who have yet to develop any outward symptoms. The new approach could ultimately help millions of older Americans spend more years with their mental faculties intact. By the time a patient becomes demented, it is "too late" for medications to be of any help, says William H. Thies, chief scientific and medical officer of the Alzheimer's Assn.

Like aspirin and the heart medicine digitalis, resveratrol is a plant extract -- one with seemingly powerful and broad effects on living organisms. It acts as a phytoestrogen, mimicking many of the hormone estrogen's effects. In the cells of rodents as well as humans, it disrupts the genetic machinery that gives rise to inflammation and to cancerous tumors. In cell cultures of brain tissue, it even cleans up the tangled amyloid deposits that are the hallmark of Alzheimer's disease.

For the first time in 27 years, health authorities have expanded the definition of Alzheimer's disease. The change, announced last week by the National Institutes of Health and the Alzheimer's Assn., is intended to help doctors diagnose patients in the very early stages of the neurological disorder, including those who have yet to develop any outward symptoms. The new approach could ultimately help millions of older Americans spend more years with their mental faculties intact. By the time a patient becomes demented, it is "too late" for medications to be of any help, says William H. Thies, chief scientific and medical officer of the Alzheimer's Assn.

Alzheimer's disease research in the last two decades has focused on the theory that beta-amyloid plaque accumulates in the brain and leads to the loss of cognitive function. However, this theory has not produced advances in treating the disease, with many clinical trials on drugs targeted at amyloid plaques failing. A new hypothesis on the cause of Alzheimer's should be considered, a leading researcher said Tuesday. Age is the most important risk factor in the disease, said Karl Herrup, chairman of the department of cell biology and neuroscience at Rutgers University.

A vaccine for Alzheimer's disease has been a long-held goal of researchers studying the devastating disease. Research presented Tuesday at the Society for Neuroscience meeting showed one potential vaccine under study appears both safe and effective in an animal model. Most Alzheimer's vaccine research aims to prevent the accumulation of amyloid-beta plaque in the brain that can interfere with memory and cognition. However, work on a vaccine was derailed when a study in 2002 showed that an investigational vaccine targeting amyloid-beta also caused an autoimmune response that led to dangerous inflammation in the brain.

Omega-3 fatty-acid supplements, often called fish-oil capsules, did not curb the mental decline in people with mild to moderate Alzheimer's disease, researchers said Tuesday. The study marks yet another attempt to treat the disease that has failed in clinical trials. Treatment with omega-3 supplements had generated considerable enthusiasm because, unlike the other unsuccessful experimental therapies, it was a natural therapy and would not have required development of a new prescription drug.

For a long time now, scientists studying treatments for Alzheimer's disease have focused on telltale plaques that appear in patients' diseased brains as a target for therapy. The plaques are clumps of a small protein called beta-amyloid that build up in the space around nerve cells and interfere with normal brain function. Thus, the thinking goes, if plaques can be prevented from forming or cleared with medicine, the disease could be slowed. But earlier this month at an international conference, different tangled structures inside neurons took center stage alongside plaques.

USC researchers have discovered that a relatively common muscle disorder may be a form of Alzheimer's disease that strikes muscle cells rather than brain cells. Both diseases are characterized by deposits of an abnormal protein, called beta-amyloid. The discovery of the protein in the muscle disease marks the first time that beta-amyloid has been found in a disease that does not involve the brain, Dr.

USC researchers have discovered that a relatively common muscle disorder may be a form of Alzheimer's disease that strikes muscle cells rather than brain cells. Both diseases are characterized by deposits of an abnormal protein, called beta-amyloid. The discovery of the protein in the muscle disease marks the first time that beta-amyloid has been found in a disease that does not involve the brain, Dr.

USC researchers have developed a new clue about the cause of Alzheimer's disease, a mystifying disease that causes mental deterioration in as many as 4 million aging Americans. The primary physical manifestation of Alzheimer's in the brain is the accumulation of clumps of a protein called amyloid. These protein deposits may interfere with normal communication between brain cells.