Fisher Center for Alzheimer’s Disease Research
The Fisher Center for Alzheimer’s Research Center at The Rockefeller University, is a world renowned research team all working under the direction of Nobel laureate Dr. Paul Greengard.
Our scientists are at the forefront of research and, based on their understanding of how the disease ravages the brain, have developed many insights into how the devastating symptoms of Alzheimer’s disease might be prevented or delayed.
We have selected recent samples of scientific studies from major publications such as Nature, Science and the Proceedings of the National Academy of Sciences (PNAS). Our lab publishes a multitude of findings per year in our quest to find the cure for Alzheimer’s disease.
Listed below you will find a synopsis of each of the studies provided, click on the link in blue, and you have the option to view a full description and to download the original version if you so desire.
Have a question about a certain type of research into Alzheimer’s disease and want to find one of our studies? Contact Betsey Odell at email@example.com
• Antidepressant Effects are Attenuated by Anti-inflammatory Drugs:
Published in the Proceedings of the National Academy of Sciences on April 25, 2011, Fisher scientists found that use of anti-inflammatory drugs such as ibuprofen, aspirin and naproxen, reduces the effectiveness of selective serotonin reuptake inhibitors (SSRIs), the most widely used class of antidepressant medications. The discovery from scientists in Nobel Prize-winner Paul Greengard's laboratory may explain why so many depressed patients taking SSRIs do not respond to antidepressant treatment and suggests that this lack of effectiveness may be preventable.
In the March 7, 2011 issue of the Journal of Federation of American Societies for Experimental Biology (FASEB), Dr. Greengard and his team of scientists succeeded in accelerating the breakdown of beta-amyloid. They discovered that a process called autophagy reduces the buildup of beta-amyloid in isolated cells and might be utilized to eliminate the buildup of beta-amyloid in the brains of Alzheimer’s patients. Autophagy is a process cells use to “clean out” the debris from their interiors, including unwanted materials such as the protein aggregates that are hallmarks of Alzheimer’s disease. The scientists discovered that a compound called SMER28 lowers the level of beta-amyloid found in nerve cells. This occurs because SMER28 stimulates autophagy, which then rids the cell of beta-amyloid.
The protein, called gamma secretase activating protein (gSAP), is expected to become a major target for anti-amyloid drugs that inhibit the brain’s ability to produce toxic beta-amyloid in Alzheimer’s disease. Fisher scientists also discovered that gSAP is a target of the anti-cancer drug, Gleevec, which they previously showed could lower beta-amyloid levels in the brain. The new study showed that Gleevec lowers beta-amyloid production by binding to gSAP and preventing it from activating an enzyme called gamma secretase, which is responsible for producing beta-amyloid. The findings are reported in the journalNature.
Understanding how the brain works is complicated by the fact that there are so many different kinds of brain cells, doing different things, which are crowded into the same regions of the brain. Previously, the only way to approach this was to look at individual cells, but that is a Herculean task. So, the scientists at our lab recently developed a new tool called TRAP (translating ribosome affinity purification) that allows them to see the nature of many cells at once, even when they lie in regions of the brain that contain a veritable jungle of different cell types. Using TRAP, they are now able to analyze the subtle differences between cells that they couldn’t detect before to see which cells are more resistant to beta-amyloid plaque, and learn what is responsible for this resistance. TRAP in Preserving Your Memory magazine.
There is no single known cause for depression. Depression is believed to result from a combination of genetic, biochemical, environment and psychological factors. Each year over 17 million American adults experienced a period of clinical depression. In Alzheimer’s patients, depression is a major problem that often results in agitation. Depression experts claim that many people with a depressive illness never seek treatment. Some have suggested that if antidepressants started working in hours or days rather than weeks or months—more people would seek treatment. Article on P11 in Preserving Your Memory magazine.
The neurofibrillary tangles characteristic of Alzheimer’s disease are composed of the protein called “tau.” In this study, Fisher scientists found a new way to inhibit production of neurofibrillary tangles. The quantity of tangles in the Alzheimer’s brain is closely correlated with the degree of cognitive decline, suggesting that tangles or the changes known to occur in the tau protein that precede tangles may contribute to cognitive loss in Alzheimer’s. • Casein Kinase 1: Casein Kinase 1 is a therapeutic target which may be the key to halting the course of Alzheimer’s disease. The findings show that chemicals that block casein kinase 1 do not interfere with an essential pathway that is often blocked by other experimental anti-amyloid compounds.
• Casein Kinase 1:
Casein Kinase 1 is a therapeutic target which may be the key to halting the course of Alzheimer’s disease. The findings show that chemicals that block casein kinase 1 do not interfere with an essential pathway that is often blocked by other experimental anti-amyloid compounds. Article on CK1 in Preserving Your Memory magazine.
• WAVE 1:
WAVE 1 is a protein and a key regulator of connections between brain cells. It controls the formation of new cell connections which influence thinking and behavior. This 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.
Fisher Alzheimer’s Disease Education and Resources Program at the New York University Langone Medical Center
“Outcome Over Seven Years of Healthy Adults With and Without Subjective Cognitive Impairment” by Dr. Barry Reisberg. This January 2010 finding, and data collection that spanned over two decades, reveals that healthy older adults with subjective memory loss are 4.5 times more likely to develop mild cognitive impairment and dementia.
Press Release - Alzheimer's & Dementia
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