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  Our Latest Scientist Approved Alzheimer's News
  
  Eight Resolutions for a Brain-Healthy New Year
  A few simple measures may help keep the brain young for years to come.
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• Gene May Keep the Mind Sharp into Old Age
  Men and women who inherit a certain gene lived to a ripe old age with memory intact.
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  Cognitive Training Boosts Daily Living Skills in Healthy Seniors Older Adults
  Sessions aimed at memory, reasoning, and speed boosted ability to perform day-to-day tasks.
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  Experimental Brain Scan Technique Detects Early Alzheimer's
  A chemical called FDDNP allows doctors to peer inside the brain.
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  Protein "Fingerprint" May One Day Lead to an Alzheimer's Test
  Scientists have uncovered markers that may identify people living with Alzheimer's.
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  Ways to Say "Thank You" to a Longtime Caregiver
  For an illness like Alzheimer's, years of caregiving service may call for extra compensation.
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  Alzheimer's Stories
  
  James Smith Alzheimer's Story
  I'm 46 Years Old - I Can't Have Alzheimers%u2026
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  Shirl Garnett | Audio Alzheimer's Story
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  Cat | Audio Story
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  Sams | Audio Story
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  Barbara's | Audio Story
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  Audio Story | Terry Griggs
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  Audio Story | Mary Lockart
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  Audio Story | Irma
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  Story of Jeanne L. Lee
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  Audio Alzheimer's Story | Mary McKinlay
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  The Story Of John
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  10 warning signs of Alzheimer's:
  
  1. Memory loss. Forgetting recently learned information is one of the most common early signs of dementia. A person begins to forget more often and is unable to recall the information later.
  
  What's normal? Forgetting names or appointments occasionally.
  
  2. Difficulty performing familiar tasks. People with dementia often find it hard to plan or complete everyday tasks. Individuals may lose track of the steps involved in preparing a meal, placing a telephone call or playing a game.
  
  What's normal? Occasionally forgetting why you came into a room or what you planned to say.
  
  3. Problems with language. People with Alzheimer's disease often forget simple words or substitute unusual words, making their speech or writing hard to understand. They may be unable to find the toothbrush, for example, and instead ask for "that thing for my mouth."
  
  What's normal? Sometimes having trouble finding the right word.
  
  4. Disorientation to time and place. People with Alzheimer's disease can become lost in their own neighborhood, forget where they are and how they got there, and not know how to get back home.
  
  What's normal? Forgetting the day of the week or where you were going.
  
  5. Poor or decreased judgment. Those with Alzheimer's may dress inappropriately, wearing several layers on a warm day or little clothing in the cold. They may show poor judgment, like giving away large sums of money to telemarketers.
  
  What's normal? Making a questionable or debatable decision from time to time.
  
  6. Problems with abstract thinking. Someone with Alzheimer's disease may have unusual difficulty performing complex mental tasks, like forgetting what numbers are for and how they should be used.
  
  What's normal? Finding it challenging to balance a checkbook.
  
  7. Misplacing things. A person with Alzheimer's disease may put things in unusual places: an iron in the freezer or a wristwatch in the sugar bowl.
  
  What's normal? Misplacing keys or a wallet temporarily.
  
  8. Changes in mood or behavior. Someone with Alzheimer's disease may show rapid mood swings - from calm to tears to anger - for no apparent reason.
  
  What's normal? Occasionally feeling sad or moody.
  
  9. Changes in personality. The personalities of people with dementia can change dramatically. They may become extremely confused, suspicious, fearful or dependent on a family member.
  
  What's normal? People's personalities do change somewhat with age.
  
  10. Loss of initiative. A person with Alzheimer's disease may become very passive, sitting in front of the TV for hours, sleeping more than usual or not wanting to do usual activities.
  
  What's normal? Sometimes feeling weary of work or social obligations
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  Scientific Studies
  
  The Fisher Center laboratory is the world's leader in understanding the signaling pathways within brain cells that regulate brain functions. Our scientists have had several major findings this year. One in particular was published in Nature on August 17, 2006. It concerned our research on a protein called "WAVE 1," which our scientists found controls the formation of new cell connections that affect thinking and behavior. . One of the most serious changes in brain structure in Alzheimer's disease is the loss of connections among brain cells. This breakthrough made by Fisher scientists concerns the mechanism of how brain cell connections are initially formed. That knowledge will one day allow doctors to administer drugs that may either prevent the loss of brain cell connections in Alzheimer's or stimulate the growth of new connections to restore memory and lost function.
  
  Another breakthrough, published in Science on Jan 6, 2006, was our discovery of a blueprint for a new way to treat depression and agitation. The focus of this new possibility is a protein called p11. In Alzheimer's patients, depression is a major problem that often results in agitation. Depression in normal people is also a risk factor making it more likely that a person will eventually develop Alzheimer's. P11 is a protein found in the brain of humans and other mammals. Our study found that p11 controls the brain's response to the neurotransmitter, serotonin, and can cure a depression-like state in mice. This discovery has been hailed as the most important event in depression research in the last 25 years because it is expected to provide a new way to treat depression.
  
  One of our major goals is to develop drugs that effectively lower beta-amyloid levels in the brain, and by doing so, alleviate the mayor symptoms of Alzheimer's disease. In Alzheimer's the progressive loss of cognitive function is accompanied by pathologic (disease associated) changes in the brain. One of these is the formation of plaques sometimes described as tiny "Brillo pads" in the space between nerve cells. Unlike plaques in blood vessels, which are composed of the fatty substance cholesterol, the brain plaques in Alzheimer's are comprised of a sticky protein called beta-amyloid. As amyloid build-up it injures and kills brain cells and brings on the terrible symptoms of the disease.
  
  In earlier studies, Fisher scientists determined that they could produce a compound that lowered beta-amyloid levels by as much as 90%, but the compound had serious toxic side effects. Our scientists continued to study this important phenomenon and have now discovered a substance that dramatically lowers beta-amyloid in several animal models of Alzheimer's. At this point we have a crucial obstacle to overcome: finding a way to deliver this drug to the brain without it being stopped by the blood-brain-barrier. We are now working to overcome this hurdle. Success in this area could result in the first truly effective anti-Alzheimer's drug, one capable of stopping the progression of the disease and alleviating symptoms, and we are at the threshold.
  
  Breakthrough Cancer Drug Offers New Hope For Alzheimer's
  
  NEW YORK CITY (September 29, 2003) The laboratories of the Fisher Center for Research on Alzheimer's Disease at The Rockefeller University in New York City report that a novel cancer drug hailed in recent years for its ability to halt a deadly form of leukemia and stomach cancer may offer new hope for those afflicted with the mind-robbing ravages of Alzheimer's disease. The new study carried out by researchers at the Fisher Center has been published in the September 29th issue of the Proceeding of the National Academy of Sciences.
  
  The drug, called Gleevec, was shown to lower production of a toxic substance called beta-amyloid that is thought to underlie the development of Alzheimer's disease. Beta-amyloid builds up in the brains of those with the disease, forming sticky patches called plaque and killing off healthy cells. In recent years, scientists and pharmaceutical companies have been searching avidly for medicines that will stem the production of this poison in the hopes of offering new ways to treat, prevent and potentially even reverse the brain ailment. Paul Greengard, Ph.D., 2000 Nobel Laureate in Physiology or Medicine and Director of the Fisher Center for Alzheimer's Research at The Rockefeller University, along with other members of his laboratory at the Fisher Center, previously have unraveled the roles of various cellular factors that affect beta-amyloid production. They were also the first to show that estrogen and testosterone have beta-amyloid lowering effects on cells.
  
  "We are very excited by this discovery, because it provides a novel approach to the development of new therapies for Alzheimer's disease," says Dr. Greengard, one of the study's authors. "It reveals a previously unknown mechanism by which the toxic substance beta-amyloid is controlled, and opens up a new area of research for developing drugs for the treatment of Alzheimer's."
  
  Scientists at the Fisher Center and other research institutes had previously shown that the brain toxin beta-amyloid is produced when a large protein called APP, or amyloid precursor protein, is chopped into smaller pieces by scissor-like proteins called beta-secretase and gamma-secretase . Drug researchers have been searching for compounds that inhibit these secretases, because blocking their activity would halt production of beta-amyloid.
  
  "One of the reasons Gleevec differs from other gamma-secretase inhibitors is that it probably does not inhibit gamma-secretase directly," says William Netzer, Ph.D., lead author of the current study. "Rather, it seems to affect another protein or proteins that regulate gamma-secretase."
  
  As a result of these findings, researchers are one step closer to finding a much-needed cure for Alzheimer's disease.

• Beating Back Beta Amyloid

  
  

  The Fisher Center Foundation funds scientists who continue to be at the forefront of research into the understanding of beta amyloid, a protein thought to be at the root of Alzheimer's disease. Beta amyloid forms dense protein deposits called plaques. Sometimes compared to tiny scouring pads, these beta amyloid plaques accumulate in the spaces between brain cells, choking them off and causing them to die. Fisher Center scientists were among the first to define the specific steps by which beta amyloid is produced, and their discovery that pharmacological substances can interrupt this process set off a worldwide race to develop drugs to inhibit beta amyloid buildup. The Foundation's beta amyloid research is now focused on a protein called amyloid precursor protein (APP). When broken down in a certain way, APP results in the formation of beta amyloid plaque. When scientists unravel the process by which APP breaks down, they may be able to develop ways to slow the accumulation of plaque in the brain and reduce its toxic effects on nerve cells, moving much closer to a cure for Alzheimer's disease. In fact, Fisher Center Foundation scientists are making significant progress in developing therapies aimed at reducing the production of toxic beta-amyloid, and achievement that will ultimately prevent, slow or even cure the disease.

  
  

  Fisher scientists have recently discovered how beta-amyloid damages communication between brain cells. With this understanding of the molecular events involved, it is likely that therapies will be devised that protect the brain even when beta-amyloid production goes awry.

  
   Read More About Beating Back Beta Amyloid
  

  Improving The Quality Of Life For Alzheimer's Patients

  
  

  Most Alzheimer's disease patients show some signs of agitation and as Alzheimer's disease progresses through its later stages, as many as 75% of patients begin to exhibit aggressive or agitative behaviors, which are often treated with potent antipsychotic drugs. While useful, these drugs may cause incapacitating side effects such as uncontrollable tremors and heavy sedation. Building on two decades of research, Fisher Center Foundation scientists are exploring the mechanisms by which these antipsychotic drugs work in an effort to develop new and safer "anti-agitation" therapies that will improve the quality of life for patients while easing the burden on caregivers.

  
  

  Reversing Nerve Cell Damage

  
  

  The devastating loss of memory that is the hallmark of Alzheimer's disease is caused by the death of nerve cells "strangled" by beta amyloid. In what would have seemed like science fiction a decade ago, the Foundation's scientists are making progress in reversing this damage by actually inducing nerve cells to grow new connections with other cells, thus improving communication between remaining healthy cells. This work builds on Fisher Foundation scientists' recent discovery that a protein called "WAVE1" regulates the growth of structures called spines that ultimately connect nerve cells, the Foundation's scientists are exploring ways to compensate for the death of nerve cells in Alzheimer's. These techniques might some day not only reverse symptoms such as memory loss in Alzheimer's patients, but might also treat other nervous system disorders such as Parkinson's and Huntington's disease, strokes, head trauma and spinal cord injuries.

  
  

  
   Read More About Reversing Nerve Cell Damage
  

  
  

  Using Hormones To Slow The Progression Of Disease

  
  

  In 1998, our Foundation scientists were among the first to research the effects of hormones on Alzheimer's disease. We are also supporting research into the effects of the hormone, insulin on beta amyloid and on cognitive and memory functions of the brain. Clinical studies have found a number of links between insulin resistance, diabetes and Alzheimer's disease, so the Foundation's scientists are attempting to unravel these links and develop therapeutic strategies that will help in the treatment of Alzheimer's.

  
  

  Curing Early-Onset Alzheimer's

  
  

  While being diagnosed with Alzheimer's can be overwhelming at any age, it is particularly devastating when the disease strikes early in one's life. Early-onset Alzheimer's can present itself in people as young as 30 and it is often hereditary, affecting generation after generation. It is known that certain genetic mutations alter a set of proteins in the brain called "presenilins" and these alterations in turn lead to increased production of a toxic form of beta amyloid. Research funded by the Foundation recently determined the particular roles of three presenilin-associated proteins, nicastrin, PEN2 and APH1, which are likely involved in critical steps in the onset of Alzheimer's. Foundation scientists are also continuing to research the two presenilin proteins, PS1 and PS2, which are closely linked to early-onset Alzheimer's. Understanding the exact roles of PS1, PS2, PEN2, APH1 and nicastrin proteins in the development of Alzheimer's is a crucial step in developing therapies and drugs to slow or reverse the progression of the disease.

  
  

  The Science Of Caring

  
  

  While searching for the cause and developing a cure for Alzheimer's disease, the Foundation is also funding projects to support the many family members and friends who are on the front lines of caring for the more than 5 million Alzheimer's patients in the US and beyond. Despite the massive burden of coping with a long list of patients' behavioral problems, such as aggressiveness and anxieties, little information is available for caregivers about effective treatments and interventions.

  
  

  The Foundation funds research at the Fisher Alzheimer's Disease Education and Resources Program at New York University School of Medicine under the direction of Dr. Barry Reisberg. This research has led to the development of a new science of management for Alzheimer's and other dementias. Our next challenge is to raise funds to implement a caregiver training program based on this research and management principles. This program allows Alzheimer's patients to regain basic skills of daily living and reduces the patient's dependence on a caregiver, thus improving the quality of life for all involved.

  
  

  In addition to numerous research projects, the Foundation also funds the Alzheimer's Information Program, which provides timely, accurate and reliable information to the general public through a number of tools.

  
  

  The Foundation underwrote the production and distribution of a documentary entitled "Alzheimer's: Is Their Hope?" that provides an overview of the disease and introduces viewers to patients, caregivers and researchers battling Alzheimer's. Since it first aired in November 2002, the program has been shown on more than 60 public television stations in hundreds of communities across the US.

  
  

  In November 2002, the Foundation launched the website www.alzinfo.org, which has been recognized by doctors, caregivers, professional organizations, and the general public as the premier resource on Alzheimer's disease. Users are able to access a vast array of information through a single, easy to navigate source.

  
  

  
   Read More About The Science Of Caring
  

  
  
  Our Scientists
  

  Dr. Paul Greengard

  
  Director of the Fisher Center for Alzheimer's Disease Research at The Rockefeller University
  
  
  Dr. Paul Greengard earned the 200 Nobel Prize in Physiology or Medicine for his pioneering work in delineating how neurons communicate with one another in the brain. During a half-century of research, he has arguably contributed more than any other single scientists to our understanding of the complex signaling process that occur within each of the 100 billion or more nerve cells in the human brain. Dr. Greengard's discoveries helped establish phosphorylation as the major mechanism by which every cell in the body regulates bodily functions.
  

  Dr. Barry Reisberg

  
  Professor of Psychiatry at New York University School of Medicine Clinical Director of the Aging and Dementia Research Center of the NYU School of Medicine
  
  
  Dr. Reisberg has directed research over the past quarter century which has significantly advanced the current understanding and treatment of Alzheimer's disease. He was the first to describe many of the most important symptoms of Alzheimer's disease. He was the first to describe many of the most important symptoms of Alzheimer's and the characteristic clinical course of the disease with the Global Deterioration Scale in 1982 and the Functional Assessment Staging measure in 1984.
  

  Dr. William J. Netzer

  
  Research Associate at the Fisher Center for Alzheimer's Research Foundation, and Scientific Liaison to the Fisher Foundation
  
  
  Dr. Netzer's research led to the recent discovery that Gleevec, a successful anti-cancer drug, lowers beta-amyloid production, suggesting that Gleevec or compounds similar to it might be useful in treating Alzheimer's disease.
  

  Dr. Michael Kaplitt

  
  Assistant Professor of Neurological Surgery; Director, Center for Stereotactic & Functional Neurosurgery; and Director, Laboratory of Molecular Neurosurgery Weill Medical College of Cornell University
  
  
  Dr. Kaplitt is a Tara and Victor Menezes Clinical Scholar in Neurological Surgery. He specializes in Parkinson's disease, Tremors and Movement Disorders. Dr. Kaplitt has completed the first phase 1 human clinical protocol of gene therapy for Parkinson's disease; expansion of this study is currently in preparation.

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