From: hound23x@gmail.com   
      
   Unraveling the complex puzzle of Alzheimer's disease   
      
      
       
   Feb 16, 2015 by Bridget O'brian   
      
   Lost on Campus: Julianne Moore in the film Still Alice. Photo by JoJo   
   Whilden/Killer Films.   
   In the movie Still Alice, Julianne Moore plays a Columbia linguistics   
   professor who is diagnosed with early-onset Alzheimer's, an extremely rare   
   version of the disease. Moore's performance, for which she has already won   
   several awards and been nominated    
   for an Oscar, depicts her character's swift decline from a quick-witted   
   academic to a shadow of herself.   
   It is fitting that Moore's character teaches here, where research and   
   treatment of neurological and age-related diseases are such a priority. From   
   the Mortimer B. Zuckerman Mind Brain Behavior Institute, where Eric   
   Kandel--whose research in memory    
   brought him a Nobel Prize in 2000--is the co-director, to the Taub Institute   
   for Research on Alzheimer's and the Aging Brain, Columbia research is making   
   groundbreaking strides.   
   Scott Small, director of Columbia's Alzheimer's Disease Research Center,   
   describes the disorder. The Boris and Rose Katz Professor of Neurology   
   discusses what is known, and what's yet to be discovered, about Alzheimer's.   
      
   Can you describe the forms of the disease?   
      
   Alzheimer's comes in two very different types. One type is controlled by a   
   single gene, and if you get that gene from your parent, you develop an   
   extremely rare and aggressive form called early-onset Alzheimer's, which   
   manifests in patients who are in    
   their 30s and 40s. Less than 1 percent of all cases of patients with   
   Alzheimer's have that early onset form. The most prevalent form of the   
   disease, though, is late-onset Alzheimer's. The interaction of multiple genes   
   with each other and the environment    
   plays an important part of the risk in this form of Alzheimer's. As a result,   
   it is typically considered a complex form of the disease.   
      
   What does the current research tell us about Alzheimer's disease?   
      
   Alzheimer's is a disorder that percolates for decades before someone dies. So   
   how can we tell, when we examine a brain during autopsy, whether the changes   
   we see are caused by Alzheimer's or were consequences of having the disease?   
   This is where genetics    
   can be extremely informative. In looking at postmortem brains, we have found   
   some molecules, and Richard Mayeux [the Gertrude H. Sergievsky Professor of   
   Neurology, Psychiatry and Epidemiology] has found genes, in the same family of   
   proteins. Together    
   that makes a compelling case that there is a molecular pathway that is one   
   driving cause of Alzheimer's disease. We are working on deciphering that.   
      
   Why are genes simply causative in one version and more complex in the other?   
      
   The late onset type of the disease does in fact have a strong genetic factor.   
   But there are complicated and nuanced ways in which genes can influence the   
   risk of developing a disease, and those are called risk factors. Of all the   
   genes that can influence    
   someone's risk for getting late-onset Alzheimer's, a gene called APOE4 is by   
   far the strongest. If you have two copies of this gene, you have a 20 to 40   
   percent increased risk of developing Alzheimer's. Now that is a significant   
   risk factor, but it's not    
   the only thing at play. There are people with the APOE4 gene who don't develop   
   Alzheimer's, and people without it who do. Perhaps you have the gene but you   
   might also have other protective genes or have a healthy lifestyle. Risk   
   factor genes interact    
   with the environment or even an individual's behavior.   
      
   What is the focus of your Alzheimer's research?   
      
   We investigate the hippocampus of the brain to try to recognize the   
   distinction between normal aging and diseases that affect the brain. By   
   focusing on this one part of the brain, we can get a handle on trying to   
   separate the two, understand them,    
   diagnose them and, ultimately, to intervene. Many of my patients are people in   
   their 50s, 60s and 70s who've noticed a change in their memory and are worried   
   about whether this is an ominous sign, the beginning of Alzheimer's. And while   
   the disease does    
   begin with subtle changes in memory, what we are now learning using imaging   
   tools and genetics is that in fact it could be just normal aging.   
      
   You had a recent paper in Nature Neuroscience that suggested that a chemical   
   in a cocoa bean derivative could reverse memory-related aging. Why is that an   
   important finding?   
      
   It's been shown by us, and by others, that one small part of the brain--the   
   dentate gyrus--might be involved in normal aging. Not Alzheimer's, but just   
   the normal wear and tear of the aging process that causes memory loss. We also   
   knew of studies that    
   suggested that consuming cocoa flavanols increased function in that area of   
   the brain and reversed age-related memory decline. Our study, which was   
   conducted on people in their 50s and 60s, showed an improvement in this area.   
   The important question is    
   whether that reversal is meaningful, and that's something we're exploring in a   
   future study. From a clinical perspective our goal is to be able to   
   distinguish the earliest stages of Alzheimer's from aging, to allay concern   
   and ultimately to have    
   interventions that might ameliorate age-related memory issues or   
   -optimistically-- halt Alzheimer's entirely.   
      
      
      
   http://m.medicalxpress.com/news/2015-02-unraveling-complex-puzzl   
   -alzheimer-disease.html   
      
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