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At least 307 records · Page 17Linked to original sources
PubMed2003

Phosphorylation of tau protein to sites found in Alzheimer's disease brain is catalyzed by Ca2+/calmodulin-dependent protein kinase II as demonstrated tandem mass spectrometry.

Neuronal Ca2+/calmodulin-dependent protein kinase II (CaMKII) is one of the most abundant protein kinases in the brain, and phosphorylates a broad range of substrate proteins. The phosphorylation of microtubule tau by CaMKII was investigated using tandem mass spectrometry (MS/MS). Recombinant human tau was phosphorylated at Thr212, Ser214, Ser262, and Ser356 by CaMKII. The phosphorylation of these sites is found in paired helical filament (PHF)-tau. In addition to these sites, Ser131 and Thr135 were phosphorylated by CaMKII. Phosphorylation at Ser131, Thr135, Thr212 and Ser214 by CaMKII has not been reported previously. Thr212 and Ser214 are in the consensus phosphorylation sequence of CaMKII (RXXS/T), and non-fetal-type phosphorylation sites of tau. Non-fetal-type phosphorylation may produce PHF-tau. These results suggested that CaMKII is involved in the phosphorylation of tau in Alzheimer's disease brain.

Alzheimer Disease↗
PubMed2004

Amyloid beta-peptide(1-42) contributes to the oxidative stress and neurodegeneration found in Alzheimer disease brain.

Oxidative stress is extensive in Alzheimer disease (AD) brain. Amyloid beta-peptide (1-42) has been shown to induce oxidative stress and neurotoxicity in vitro and in vivo. Genetic mutations that result in increased production of Abeta1-42 from amyloid precursor protein are associated with an early onset and accelerated pathology of AD. Consequently, Abeta1-42 has been proposed to play a central role in the pathogenesis of AD as a mediator of oxidative stress. In this review, we discuss the role of Abeta1-42 in the lipid peroxidation and protein oxidation evident in AD brain and the implications of such oxidative stress for the function of various proteins that we have identified as specifically oxidized in AD brain compared to control, using proteomics methods. Additionally, we discuss the critical role of methionine 35 in the oxidative stress and neurotoxic properties exhibited by Abeta1-42.

Alzheimer Disease↗