From: deputydog23x@gmail.com   
      
   NEUROSCIENCE   
      
   Memory Loss Associated with Alzheimer's Reversed for First Time   
      
   NEUROSCIENCE NEWS   
   SEPTEMBER 30, 2014   
      
       
   Small trial from UCLA and Buck Institute succeeds using systems approach to   
   memory disorders.   
      
   Patient one had two years of progressive memory loss. She was considering   
   quitting her job, which involved analyzing data and writing reports, she got   
   disoriented driving, and mixed up the names of her pets. Patient two kept   
   forgetting once familiar    
   faces at work, forgot his gym locker combination, and had to have his   
   assistants constantly remind him of his work schedule. Patient three's memory   
   was so bad she used an iPad to record everything, then forgot her password.   
   Her children noticed she    
   commonly lost her train of thought in mid-sentence, and often asked them if   
   they had carried out the tasks that she mistakenly thought she had asked them   
   to do.   
      
   Since its first description over 100 years ago, Alzheimer's disease has been   
   without effective treatment. That may finally be about to change: in the   
   first, small study of a novel, personalized and comprehensive program to   
   reverse memory loss, nine of 10    
   participants, including the ones above, displayed subjective or objective   
   improvement in their memories beginning within 3-to-6 months after the   
   program's start. Of the six patients who had to discontinue working or were   
   struggling with their jobs at the    
   time they joined the study, all were able to return to work or continue   
   working with improved performance. Improvements have been sustained, and as of   
   this writing the longest patient follow-up is two and one-half years from   
   initial treatment. These    
   first ten included patients with memory loss associated with Alzheimer's   
   disease (AD), amnestic mild cognitive impairment (aMCI), or subjective   
   cognitive impairment (SCI; when a patient reports cognitive problems). One   
   patient, diagnosed with late stage    
   Alzheimer's, did not improve.   
      
   The study, which comes jointly from the UCLA Mary S. Easton Center for   
   Alzheimer's Disease Research and the Buck Institute for Research on Aging, is   
   the first to suggest that memory loss in patients may be reversed, and   
   improvement sustained, using a    
   complex, 36-point therapeutic program that involves comprehensive changes in   
   diet, brain stimulation, exercise, optimization of sleep, specific   
   pharmaceuticals and vitamins, and multiple additional steps that affect brain   
   chemistry.   
      
   The findings, published in the current online edition of the journal Aging,   
   "are very encouraging. However, at the current time the results are anecdotal,   
   and therefore a more extensive, controlled clinical trial is warranted," said   
   Dale Bredesen, the    
   Augustus Rose Professor of Neurology and Director of the Easton Center at   
   UCLA, a professor at the Buck Institute, and the author of the paper.   
      
   This image shows a drawing of a brain slice shrunken due to Alzheimer's   
   disease.   
   The study is the first to suggest that memory loss in patients may be   
   reversed, and improvement sustained, using a complex, 36-point therapeutic   
   program that involves comprehensive changes in diet, brain stimulation,   
   exercise, optimization of sleep,    
   specific pharmaceuticals and vitamins, and multiple additional steps that   
   affect brain chemistry. This image is for illustrative purposes only. Credit   
   NIH/NIA.   
   In the case of Alzheimer's disease, Bredesen notes, there is not one drug that   
   has been developed that stops or even slows the disease's progression, and   
   drugs have only had modest effects on symptoms. "In the past decade alone,   
   hundreds of clinical    
   trials have been conducted for Alzheimer's at an aggregate cost of over a   
   billion dollars, without success," he said.   
      
   Other chronic illnesses such as cardiovascular disease, cancer, and HIV, have   
   been improved through the use of combination therapies, he noted. Yet in the   
   case of Alzheimer's and other memory disorders, comprehensive combination   
   therapies have not been    
   explored. Yet over the past few decades, genetic and biochemical research has   
   revealed an extensive network of molecular interactions involved in AD   
   pathogenesis. "That suggested that a broader-based therapeutics approach,   
   rather than a single drug that    
   aims at a single target, may be feasible and potentially more effective for   
   the treatment of cognitive decline due to Alzheimer's," said Bredesen.   
      
   While extensive preclinical studies from numerous laboratories have identified   
   single pathogenetic targets for potential intervention, in human studies, such   
   single target therapeutic approaches have not borne out. But, said Bredesen,   
   it's possible    
   addressing multiple targets within the network underlying AD may be successful   
   even when each target is affected in a relatively modest way. "In other   
   words," he said, "the effects of the various targets may be additive, or even   
   synergistic."   
      
   The uniform failure of drug trials in Alzheimer's influenced Bredesen's   
   research to get a better understanding of the fundamental nature of the   
   disease. His laboratory has found evidence that Alzheimer's disease stems from   
   an imbalance in nerve cell    
   signaling: in the normal brain, specific signals foster nerve connections and   
   memory making, while balancing signals support memory loss, allowing   
   irrelevant information to be forgotten. But in Alzheimer's disease, the   
   balance of these opposing signals    
   is disturbed, nerve connections are suppressed, and memories are lost.   
      
   The model of multiple targets and an imbalance in signaling runs contrary to   
   the popular dogma that Alzheimer's is a disease of toxicity, caused by the   
   accumulation of sticky plaques in the brain. Bredesen believes the amyloid   
   beta peptide, the source of    
   the plaques, has a normal function in the brain - as part of a larger set of   
   molecules that promotes signals that cause nerve connections to lapse. Thus   
   the increase in the peptide that occurs in Alzheimer's disease shifts the   
   memory-making vs. memory-   
   breaking balance in favor of memory loss.   
      
   Given all this, Bredesen thought that rather than a single targeted agent, the   
   solution might be a systems type approach, the kind that is in line with the   
   approach taken with other chronic illnesses--a multiple-component system.   
      
      
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