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------------------------------------------------------------------------ Microglial Activation By Amyloid Precursor May Be A Factor In Alzheimer's Disease ------------------------------------------------------------------------ WESTPORT, Aug 28 (Reuters) - Two scientists from Little Rock report in Nature this week new in vitro evidence that inflammatory events contribute to the development of Alzheimer's disease (AD). Furthermore, the team shows that these inflammatory events are modulated by apolipoprotein E. Briefly, Dr. Steven W. Barger of the University of Arkansas and Dr. Ashley D. Harmon at the VA in Little Rock, found that a secreted derivative of beta-amyloid precursor protein, sAPP-alpha, "...increased markers of activation in microglia and enhanced their production of neurotoxins." Incubating the protein with apolipoprotein E3 blocked the inflammatory reaction in microglia. On the other hand, apolipoprotein E4, "...a variant associated with an increased risk of Alzheimer's disease," had no effect on microglial activation by sAPP-alpha. Another product of beta-amyloid precursor protein, sAPP-beta, also activates microglia and, unlike sAPP-alpha, it lacks a neuroprotective effect. Drs. Barger and Harmon say, "Considered together with the defective neuroprotection by sAPP-beta, our results indicate that events favouring processing of beta-APP by beta-secretase might reduce the amounts of neuroprotective sAPP-alpha while retaining a detrimental activity mediated through microglia." Nature 1997;388:878-881. Westport Newsroom 203 319 2700 Copyright 1997 Reuters Limited. <http://www.reutershealth.com/news/docs/199708/19970828sca.html> ------------------------------------------------------------------------ [log in to unmask]