From: judgebean23x@gmail.com   
      
   Cannabinoids, Like Those in Marijuana, May Protect Alzheimer’s Patients from   
   Plaque Buildup   
    JUNE 30, 2016 Charles MooreBY CHARLES MOORE IN NEWS.   
      
      
   Alzheimer’s disease has been described in medical literature for more than a   
   century, but still has no effective treatments. Now, scientists at the Salk   
   Institute in La Jolla, California, report finding evidence that    
   etrahydrocannabinol (THC), one of    
   several physiologically active chemical compounds in marijuana, can promote   
   cellular removal of amyloid beta, a toxic protein associated with   
   Alzheimer’s disease.   
      
   While these exploratory studies were conducted with neurons grown in a   
   laboratory, the researchers suggest they may offer insights into the role   
   inflammation plays in Alzheimer’s disease, and even point the way to   
   developing therapeutic agents to treat    
   this complex disorder.   
      
   In a paper published in the journal Aging and Mechanisms of Disease, the Salk   
   research team describes how they studied nerve cells altered to produce high   
   levels of amyloid beta to mimic aspects of Alzheimer’s disease. The paper,   
   “Amyloid    
   proteotoxicity initiates an inflammatory response blocked by cannabinoids“   
   (Aging and Mechanisms of Disease, 2016; 2: 16012 DOI: 10.1038/npjamd.2016.12),   
   notes that it is well-known that amyloid beta begins accumulating within nerve   
   cells of the aging    
   brain well before Alzheimer symptoms or plaques are evident, but the   
   mechanistic relationship between intracellular amyloid, aging, and   
   neurodegeneration is not well understood. (Amyloid beta is a major component   
   of the plaque deposits.)   
      
   SchubertDSalk“Although other studies have offered evidence that cannabinoids   
   might be neuroprotective against the symptoms of Alzheimer’s, we believe our   
   study is the first to demonstrate that cannabinoids affect both inflammation   
   and amyloid beta    
   accumulation in nerve cells,” Salk Professor David Schubert, the paper’s   
   senior author, said in a press release.   
      
   The Salk researchers found that high levels of amyloid beta accumulation were   
   associated with cellular inflammation and higher rates of neuron death in the   
   brain — a major component of the damage associated with Alzheimer’s   
   disease. Exposing the    
   nerve cells to THC reduced amyloid beta protein levels, and stopped the   
   inflammatory response caused by the amyloid protein, allowing the cells to   
   survive.   
      
   “Inflammation within the brain is a major component of the damage associated   
   with Alzheimer’s disease, but it has always been assumed that this response   
   was coming from immune-like cells in the brain, not the nerve cells   
   themselves,” said Antonio    
   Currais, a postdoctoral researcher in the Schubert laboratory at Salk and the   
   study’s first author. “When we were able to identify the molecular basis   
   of the inflammatory response to amyloid beta, it became clear that THC-like   
   compounds that the    
   nerve cells make themselves may be involved in protecting the cells from   
   dying.”   
      
   Receptors in brain cells act as “switches” that can be activated by   
   endocannabinoids, a class of lipid molecules manufactured by the body that   
   support intercellular signaling in the brain.  Physical activity stimulates   
   endocannabinoid production, and    
   the scientists noted that some studies have shown exercise can help to slow   
   the progression of Alzheimer’s disease. The psychoactive effects of   
   marijuana are caused by THC, which is molecularly similar in activity to human   
   endocannabinoids, and can    
   activate the same receptors in the brain.   
      
   David Schubert   
   David Schubert, professor at Salk’s Cellular Neurobiology Laboratory. (Photo   
   credit: Salk Institute)   
   In separate but relevant research, the Schubert lab has developed an   
   Alzheimer’s drug candidate called J147 that also removes amyloid beta from   
   nerve cells and reduces inflammatory response in both nerve cells and the   
   brain. When given to mice with    
   Alzheimer’s, J147 was seen to improve memory and prevent brain damage caused   
   by the disease. The researchers’ work with J147 led to the discovery that   
   endocannabinoids can also remove amyloid beta and reduce inflammation.   
   However, Schubert cautions    
   that his team’s findings were conducted in exploratory laboratory models,   
   and that the use of THC-like compounds as therapy for Alzheimer’s would   
   first need to undergo testing in clinical trials.   
      
   The study received support from the National Institutes of Health, The Burns   
   Foundation, and The Bundy Foundation.   
      
   According to the NIH, Alzheimer’s affects more than 5.4 million Americans,   
   and is the most common cause of dementia. Its incidence, according to   
   Alzheimer’s Association, is expected to triple to 16 million by 2050,   
   resulting in projected medical    
   costs of over $1 trillion per year during the next 50 years as the baby boom   
   generation moves into old age.   
      
   Sources:   
   Salk Institute   
   Aging and Mechanisms of Disease   
   PLOS One   
   National Institutes of Health   
   Alzheimer’s Association   
   TAGGED AMYLOID PLAQUES, AMYLOID-BETA, CANNABINOID, CANNABINOID RECEPTORS,   
   ENDOCANNABINOIDS, J147, TETRAHYDROCANNABINOL, THC.   
      
   Charles Moore   
   Charles Moore   
   Charles is a force to be reckoned with in the world of print and new media.   
   From an interview with him in LowEndMac: ”His articles, features, and   
   commentaries have appeared in more than 40 magazines, newspapers and websites   
   in Canada, the US, the UK,    
   and Australia. . . a columnist for The Halifax Daily News and the Saint John   
   Telegraph Journal, Atlantic Fisherman, and news editor and columnist for   
   Applelinks.com, a columnist and contributing editor for MacOpinion and   
   PBCentral, as well as writing for    
   Low End Mac.” Charles serves as the Senior Section Editor for the Science   
   and Research section of BioNews Texas and contributes science-related articles   
   on a daily basis.   
      
      
      
   https://alzheimersnewstoday.com/2016/06/30/cannabinoids-may-prot   
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    * Origin: you cannot sedate... all the things you hate (1:229/2)