Dickey CA, Koren J, Zhang YJ, Xu YF, Jinwal UK, Birnbaum MJ, Monks B, Sun M, Cheng JQ, Patterson C, Bailey RM, Dunmore J, Soresh S, Leon C, Morgan D, Petrucelli L. Akt and CHIP coregulate tau degradation through coordinated interactions. Proc Natl Acad Sci U S A. 2008 Mar 4;105(9):3622-7. PubMed.
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This is an interesting paper. Of additional relevance is the role of aluminum, usually neglected, in the obstruction of tau degradation. Walton recently demonstrated in a rat model that aluminum inhibited activity of PP2A. PP2A is the major phosphate-removing enzyme in the brain against tau and neurofilament hyperphosphorylation, and against tau accumulation and NFT formation.
Walton also demonstrated using the Walton stain in autopsied human brain that aluminum participates within the human hippocampal neurons to facilitate accumulation of NFTs and eventually kill the cells by enucleation. Control of aluminum offers inexpensive prevention of AD according to many published epidemiology studies.
References:
Walton JR. An aluminum-based rat model for Alzheimer's disease exhibits oxidative damage, inhibition of PP2A activity, hyperphosphorylated tau, and granulovacuolar degeneration. J Inorg Biochem. 2007 Sep;101(9):1275-84. PubMed.
Walton JR. Aluminum in hippocampal neurons from humans with Alzheimer's disease. Neurotoxicology. 2006 May;27(3):385-94. PubMed.
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