Alterations in Glucose Metabolism Induce Hypothermia Leading to Tau Hyperphosphorylation through Differential Inhibition of Kinase and Phosphatase Activities: Implications for Alzheimer's Disease

Planel, Emmanuel; Miyasaka, Tomohiro; Lavstsen, Thomas; Chui, De Hua; Tanemura, Kentaro; Sato, Shinji; Murayama, Ohoshi; Ishiguro, Koichi; Tatebayashi, Yoshitaka; Takashima, Akihiko

doi:10.1523/jneurosci.5561-03.2004

Cited by 237 publications

(230 citation statements)

References 68 publications

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“…Further, there may be selective vulnerability of different brain regions to various pre-and postmortem factors as Bag 1 in the cerebellum was not significantly affected by 4 hr of postmortem delay. This latter finding is consistent with the view that the cerebellum is not affected by reduced metabolism and that certain cerebellar proteins (e.g., phosphatases) have an intrinsic resistance to hypothermia as well (Planel et al, 2004).…”

Section: Discussionsupporting

confidence: 91%

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Expression profile of Bag 1 in the postmortem brain

Curcio

Asheld

Chabla

et al. 2006

Journal of Chemical Neuroanatomy

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Bag 1 is a protein intimately involved in signaling pathways that regulate cell survival. Here we examined the expression profile of Bag 1 in the brain to consider issues associated with the sampling of anti-apoptotic proteins in a rat model of the human postmortem process. Following a 4 hr postmortem interval, we analyzed the hippocampus of rats maintained at 24 °C or 4 °C storage temperatures using immunocytochemical and Western blotting techniques. Remarkably, postmortem tissue (up to 4 hr) showed a significant and prominent up-regulation of Bag 1 in CA1 and CA3 subfields of the hippocampal formation. Over-expression of Bag 1, however, could only be traced down to a storage temperature of 24 °C. These data suggest that storage temperatures, but not postmortem intervals, significantly affect the expression profile and cellular stability of Bag 1 proteins.

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Section: Discussionsupporting

confidence: 91%

“…It is noteworthy that there is evidence linking aspects of low body temperature (∼29 °C) and cell dysfunction in animal models of neurodegenerative diseases (Planel et al, 2004). More specifically, abnormal tau hyperphosphorylation in the hippocampus is associated with hypothermia.…”

Section: Discussionmentioning

confidence: 99%

Expression profile of Bag 1 in the postmortem brain

Curcio

Asheld

Chabla

et al. 2006

Journal of Chemical Neuroanatomy

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“…First, it has been demonstrated that insulin activates the same signaling pathway leading to phosphorylation of Akt and GSK3 in brain as in peripheral tissues. Thus, injection of insulin increased GSK3 phosphorylation in mouse brain [131] and brain GSK3 phosphorylation was reduced by blockade of insulin signaling by knockout of the insulin receptor [132] and in mice with dietinduced insulin-resistance [133]. It is important to note that glucose levels were not changed in these latter two studies, because glucose levels were recently found to also regulate GSK3 phosphorylation.…”

Section: Diabetes and Gsk3mentioning

confidence: 89%

Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics

2006

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Deciphering what governs inflammation and its effects on tissues is vital for understanding many pathologies. The recent discovery that glycogen synthase kinase-3 (GSK3) promotes inflammation reveals a new component of its well-documented actions in several prevalent diseases which involve inflammation, including mood disorders, Alzheimer's disease, diabetes, and cancer. Involvement in such disparate conditions stems from the widespread influences of GSK3 on many cellular functions, with this review focusing on its regulation of inflammatory processes. GSK3 promotes the production of inflammatory molecules and cell migration, which together make GSK3 a powerful regulator of inflammation, while GSK3 inhibition provides protection from inflammatory conditions in animal models. The involvement of GSK3 and inflammation in these diseases are highlighted. Thus, GSK3 may contribute not only to primary pathologies in these diseases, but also to the associated inflammation, suggesting that GSK3 inhibitors may have multiple effects influencing these conditions.

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“…Since glycolysis is the main source of ATP production in brain, impairment of glycolysis may lead to shortage of ATP in brains, thus to cellular dysfunction (74,271). Moreover, decreased ATP shortage can also induce hypothermia, causing abnormal tau phosphorylation through differential inhibition of kinases and phosphatases (311).…”

Section: Identification Of Carbonylated Proteins In Brainmentioning

confidence: 99%

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

Butterfield

Perluigi

Reed

et al. 2012

Antioxidants & Redox Signaling

157

142

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Several studies demonstrated that oxidative damage is a characteristic feature of many neurodegenerative diseases. The accumulation of oxidatively modified proteins may disrupt cellular functions by affecting protein expression, protein turnover, cell signaling, and induction of apoptosis and necrosis, suggesting that protein oxidation could have both physiological and pathological significance. For nearly two decades, our laboratory focused particular attention on studying oxidative damage of proteins and how their chemical modifications induced by reactive oxygen species/reactive nitrogen species correlate with pathology, biochemical alterations, and clinical presentations of Alzheimer's disease. This comprehensive article outlines basic knowledge of oxidative modification of proteins and lipids, followed by the principles of redox proteomics analysis, which also involve recent advances of mass spectrometry technology, and its application to selected age-related neurodegenerative diseases. Redox proteomics results obtained in different diseases and animal models thereof may provide new insights into the main mechanisms involved in the pathogenesis and progression of oxidativestress-related neurodegenerative disorders. Redox proteomics can be considered a multifaceted approach that has the potential to provide insights into the molecular mechanisms of a disease, to find disease markers, as well as to identify potential targets for drug therapy. Considering the importance of a better understanding of the cause/effect of protein dysfunction in the pathogenesis and progression of neurodegenerative disorders, this article provides an overview of the intrinsic power of the redox proteomics approach together with the most significant results obtained by our laboratory and others during almost 10 years of research on neurodegenerative disorders since we initiated the field of redox proteomics. Antioxid. Redox Signal. 17, 1610-1655.

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Alterations in Glucose Metabolism Induce Hypothermia Leading to Tau Hyperphosphorylation through Differential Inhibition of Kinase and Phosphatase Activities: Implications for Alzheimer's Disease

Cited by 237 publications

References 68 publications

Expression profile of Bag 1 in the postmortem brain

Expression profile of Bag 1 in the postmortem brain

Glycogen Synthase Kinase-3 (GSK3): Inflammation, Diseases, and Therapeutics

Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications

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