EFTA02389384

From: Sent: Monday, April 10, 2017 6:46 PM To: Jeffrey Epstein Subject: wow This article has disappeared from the literature..having a real=y hard time locating Alzheimers Dis. <https://www-ncbi-nlm-nih- gov.offcampus.lib.was=ington.edu/pubmed/?term=Aluminum+and+Alzheimer%27s+disease%3A+after+a+ce=turrof+c ontroversy%2C+is+there+a+plausible+link%3Fff> 2011;23(4):567-98. doi: 10.3233/JAD=2010-101494. Al=minum and Alzheimer's disease:=C24,after a century of controversyq=pan>, is there a plausible link? Tomljenovic L <https://www-ncbi-nlm-nih- gov.off=ampus.lib.washington.edu/pubmed/?term=Tomljenovic%20L%5BAuthor%5D&ca=thor=true&cauthor_uid=2115 7018> 1. chttps://www-ncbi-nlm-nih- gov.offcampus.lib.washi=gton.edu/pubmed/?term=Aluminum+and+Alzheimera7s+disease%3A+after+a+cent=ry+of-Pc ontroversy%2C+is+there+a+plausible+link%3FSI> 1 Neural Dynamics Research Group, Department o= Ophthalmology and Visual Sciences, University of British Columbia, Vancou=er, BC, Canada /a> <mailto Abstract The=brain is a highly compartmentalized organ exceptionally susceptible to acc=mulation of metabolic errors. Alzheimer's disease=/span> (AD) is the most prevalent neurodegenerative disease of the elderly and is characterized by regional specificity of ne=ral aberrations associated with higher cognitive functions. Aluminum=/span> (Al) is the most abundant neurotoxic metal on earth, widely bi=available to humans and repeatedly shown to accumulate in AD- susceptible n=uronal foci. In spite of this, the role of Al in AD has been heavily dispu=ed based on the following claims: 1) bioavailable Al cannot enter the brai= in sufficient amounts to cause damage, 2) excess Al is efficiently excret=d from the body, and 3) Al accumulation in neurons is a consequence rather=than a cause of neuronal loss. Research, however, reveals that: 1) very sm=ll amounts of Al are needed to produce neurotoxicity and this criterion is=satisfied through dietary Al intake, 2) Al sequesters different transport =echanisms to actively traverse brain barriers, 3) incremental acquisition =f small amounts of Al over a lifetime favors its selective accumulation in=brain tissues, and 4) since 1911, experimental evidence has repeatedly dem=nstrated that chronic Al intoxication reproduces neuropathological hallmar=s of AD. Misconceptions about Al bioavailability may have misled scientist= regarding the significance of Al in the pathogenesis of AD. The hypothesi= that Al significantly contributes to AD is built upon very solid experime=tal evidence and should not be dismissed. Immediate steps should be taken =o lessen human exposure to Al, which may be the single most aggravating an= avoidable factor related to AD. P=lD: EFTA_R1_01413597 EFTA02389384 21157018 DOI: 10.3233/JAD-2010-101494 <https://doi-or=.offcampus.lib.washington.edu/10.3233/JAD-2010-101494> 2 EFTA_R1_01413598 EFTA02389385