From: sheriffcoltrane23x@gmail.com   
      
   Neuroinflammation in Alzheimer's Is Again a Therapy Target   
   CereSpir among pharmaceutical firms preparing to test new anti-inflammatory   
   drugs   
    NOVEMBER 17, 2015	 Patricia Inacio, PhDBY PATRICIA INACIO, PHD IN NEWS.   
   Neuroinflammation in Alzheimer's Is Again a Therapy   
   TargetCereSpir among pharmaceutical firms   
   preparing to test new anti-inflammatory drugs   
   Neuroinflammation in the central nervous system is a known key event in   
   Alzheimer's pathogenesis and has long been proposed as a therapeutic target,   
   but studies conducted in the early 2000s of potential anti-inflammatory   
   treatments didn't produce the    
   hoped for outcomes.   
      
   Now a renewed interest is emerging in Alzheimer's disease (AD) treatments   
   targeting neuroinflammation, still a key marker with patients expressing high   
   levels of inflammatory mediators close to beta-amyloid peptide deposits and   
   neurofibrillary tangles,    
   both associated with neurodegeneration.   
      
   "The field languished for at least a decade, until three years ago when   
   intriguing findings about genetic risks for Alzheimer's disease clustering   
   around the innate immune system began to emerge, pointing to defects driving   
   pathology," Richard Margolin,    
   MD, of CereSpir Inc., a pharmaceutical company developing new treatments for   
   Alzheimers's, said in a press release. Today, "[t]he study of ne   
   roinflammation in AD is expanding by leaps and bounds."   
      
   Novel results presented at the recent 8th lnternational Conference on Clinical   
   Trials for Alzheimer's Disease (CTAD) focused on two key cells of the innate   
   immune system in the brain: astrocytes and microglia. Responsible for   
   producing cytokines and    
   engulfing injured or dead cells, debris, and toxins (a process known as   
   phagocytosis), microglia cells become dysfunctional as Alzheimer's disease   
   progresses, releasing tissue-destructive cytokines.   
      
   Researchers at of CereSpir, and elsewhere, are continuing to rise to the   
   challenge. As Dr. Margolin noted, "One strategy is to reduce cytokine   
   production, but our approach is to pair that with enhancement of phagocytosis,   
   because we think both are    
   important and the combination could be synergistic. Preclinical studies showed   
   beneficial effects for our drug CSP-1103 on both properties, and cytokine   
   reductions were also seen in healthy volunteers and patients with mild   
   cognitive impairment."   
      
   The team at CereSpir wants to better understand why previous anti-inflammatory   
   trials failed as it plans for a first late-stage trial of CSP-1103 in   
   Alzheimer's patients with mild cognitive impairment.   
      
   "Our trial will use an adaptive design because that approach enables a certain   
   degree of flexibility, for example, in determining the final sample size for a   
   trial. Regulatorily acceptable adaptive designs are attractive in late-stage   
   development because    
   they can potentially help accelerate the process, which is very important,   
   given the long treatment periods required at this time for disease-modifying   
   AD drugs," Dr. Margolin said.   
      
   TAGGED ASTROCYTES, CENTRAL NERVOUS SYSTEM, CSP-1103, CYTOKINES, DRUG, INNATE   
   IMMUNE SYSTEM, MICROGLIA, NEUROINFLAMMATION, PHAGOCYTOSIS.   
      
      
      
   http://alzheimersnewstoday.com/2015/11/17/neuroinflammation-alzh   
   imers-therapy-target/   
      
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