From: judgebean23x@gmail.com   
      
   The New York Times   
   Health   
      
   Could Alzheimer’s Stem From Infections? It Makes Sense, Experts Say   
      
      
   Salmonella bacteria, represented by the red spots, entrapped in a cage of   
   proteins called beta amyloid, represented in green.   
   ROBERT MOIR AND RUDOLPH TANZI / MASSACHUSSETS GENERAL HOSPITAL AND HARVARD   
   MEDICAL SCHOOL   
   By GINA KOLATA   
   MAY 25, 2016   
   Could it be that Alzheimer’s disease stems from the toxic remnants of the   
   brain’s attempt to fight off infection?   
      
   Provocative new research by a team of investigators at Harvard leads to this   
   startling hypothesis, which could explain the origins of plaque, the   
   mysterious hard little balls that pockmark the brains of people with   
   Alzheimer’s.   
      
   It is still early days, but Alzheimer’s experts not associated with the work   
   are captivated by the idea that infections, including ones that are too mild   
   to elicit symptoms, may produce a fierce reaction that leaves debris in the   
   brain, causing    
   Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard   
   group’s data, published Wednesday in the journal Science Translational   
   Medicine, supports it. If it holds up, the hypothesis has major implications   
   for preventing and treating    
   this degenerative brain disease.   
      
   The Harvard researchers report a scenario seemingly out of science fiction. A   
   virus, fungus or bacterium gets into the brain, passing through a membrane —   
   the blood-brain barrier — that becomes leaky as people age. The brain’s   
   defense system rushes    
   in to stop the invader by making a sticky cage out of proteins, called beta   
   amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage   
   and dies. What is left behind is the cage — a plaque that is the hallmark of   
   Alzheimer’s.   
      
   So far, the group has confirmed this hypothesis in neurons growing in petri   
   dishes as well as in yeast, roundworms, fruit flies and mice. There is much   
   more work to be done to determine if a similar sequence happens in humans, but   
   plans — and funding †  
   ” are in place to start those studies, involving a multicenter project that   
   will examine human brains.   
      
      
   â€œIt’s interesting and provocative,â€� said Dr. Michael W. Weiner, a   
   radiology professor at the University of California, San Francisco, and a   
   principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a   
   large national effort to    
   track the progression of the disease and look for biomarkers like blood   
   proteins and brain imaging to signal the disease’s presence.   
      
   Dr. David Holtzman, a professor and the chairman of neurology at the   
   Washington University School of Medicine in St. Louis, was also intrigued.   
   â€œIt is obviously outside the box,â€� he said. “It really is an innovative   
   and novel study.â€�   
      
   The work began when Robert D. Moir, of Harvard Medical School and   
   Massachusetts General Hospital, had an idea about the function of amyloid   
   proteins, normal brain proteins whose role had long been a mystery.   
      
   The proteins were traditionally thought to be garbage that accumulates in the   
   brain with age. But Dr. Moir noticed that they looked a lot like proteins of   
   the innate immune system, a primitive system that is the body’s first line   
   of defense against    
   infections.   
      
   Elsewhere in the body, such proteins trap microbes — viruses, fungi, yeast   
   and bacteria. Then white blood cells come by and clear up the mess. Perhaps   
   amyloid was part of this system, Dr. Moir thought.   
      
   He began collaborating with Rudolph E. Tanzi, also at Harvard Medical School   
   and Massachusetts General Hospital, in a study funded by the National   
   Institutes of Health and the Cure Alzheimer’s Fund. The idea was to see if   
   amyloid trapped microbes in    
   living animals and if mice without amyloid proteins were quickly ravaged by   
   infections that amyloid could have stopped.   
      
   The answers, they reported, were yes and yes.   
      
   In one study, the group injected Salmonella bacteria into the brains of young   
   mice that did not have plaques.   
      
   â€œOvernight, the bacteria seeded plaques,â€� Dr. Tanzi said. “The   
   hippocampus was full of plaques, and each plaque had a single bacterium at its   
   center.â€�   
      
   In contrast, mice that did not make beta amyloid succumbed more quickly to the   
   bacterial infection, and did not make plaques.   
      
      
   For years, researchers had been fixated on the idea of plaques as a sort of   
   trash that gathered in the brain. Few had asked if there might be some other   
   explanation.   
      
   As Dr. Samuel E. Gandy, a professor of neurology and psychiatry at the Icahn   
   School of Medicine at Mount Sinai Hospital in New York, explained, there was a   
   long and persuasive body of research laying out the Alzheimer’s pathway:   
   Plaques form and set    
   off the formation of tangled threadlike tau proteins. Then, as tangles of tau   
   kill nerve cells, the brain becomes inflamed, resulting in the killing of many   
   more nerve cells.   
      
   There were a few puzzling clues that something else might be going on, but   
   they did not make much sense.   
      
      
      
   For example, Dr. Weiner said, some investigators reported that people who had   
   developed Alzheimer’s had higher levels of antibodies to herpes, an   
   indicator of a previous infection, than people who did not have the disease.   
      
   â€œThe suggestion that herpes was causative seemed a bit far-fetched,â€� he   
   said.   
      
   The new paper, Dr. Gandy and Dr. Weiner said, provides a plausible explanation.   
      
   Dr. Berislav Zlokovic, the director of the Zilkha Neurogenetic Institute at   
   the University of Southern California, said his studies of the blood-brain   
   barrier also fit well with the new hypothesis. When he discovered that the   
   barrier started to break    
   down with aging, he noticed that the leakiest part was the membrane that   
   protects the hippocampus, the site of learning and memory. That is also where   
   Alzheimer’s plaques form.   
      
   Dr. Tanzi and Dr. Moir’s hypothesis, he said, “is very hypothetical at   
   this point, but it does make sense.â€�   
      
   Of course, there must be more to Alzheimer’s than the brain’s innate   
   immune system. What about people who have a mutated gene that guarantees they   
   will develop the disease at an early age?   
      
   For them, Dr. Tanzi says, the problem is that they vastly overproduce beta   
   amyloid. There is so much that it clumps on its own, without the presence of   
   microbes.   
      
      
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