دورية أكاديمية
أعرض في EDS

Deregulation of protein phosphatase 2A and hyperphosphorylation of τ protein following onset of diabetes in NOD mice.

التفاصيل البيبلوغرافية
العنوان: Deregulation of protein phosphatase 2A and hyperphosphorylation of τ protein following onset of diabetes in NOD mice.
المؤلفون: Papon MA; Centre Hospitalier de l'Université Laval, Axe Neurosciences, Québec, Canada., El Khoury NB, Marcouiller F, Julien C, Morin F, Bretteville A, Petry FR, Gaudreau S, Amrani A, Mathews PM, Hébert SS, Planel E
المصدر: Diabetes [Diabetes] 2013 Feb; Vol. 62 (2), pp. 609-17. Date of Electronic Publication: 2012 Sep 06.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Diabetes Association Country of Publication: United States NLM ID: 0372763 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1939-327X (Electronic) Linking ISSN: 00121797 NLM ISO Abbreviation: Diabetes Subsets: MEDLINE
أسماء مطبوعة: Publication: Alexandria, VA : American Diabetes Association
Original Publication: [New York, American Diabetes Association]
مواضيع طبية MeSH: Diabetes Mellitus, Type 1/*metabolism , Protein Phosphatase 2/*metabolism , tau Proteins/*metabolism, Alzheimer Disease/metabolism ; Animals ; Brain/metabolism ; Brain Chemistry ; Disease Models, Animal ; Female ; Hypothermia ; Mice ; Mice, Inbred NOD ; Neurofibrillary Tangles/metabolism ; Phosphorylation ; Protein Isoforms/metabolism
مستخلص: The histopathological hallmarks of Alzheimer disease (AD) include intraneuronal neurofibrillary tangles composed of abnormally hyperphosphorylated τ protein. Insulin dysfunction might influence AD pathology, as population-based and cohort studies have detected higher AD incidence rates in diabetic patients. But how diabetes affects τ pathology is not fully understood. In this study, we investigated the impact of insulin dysfunction on τ phosphorylation in a genetic model of spontaneous type 1 diabetes: the nonobese diabetic (NOD) mouse. Brains of young and adult female NOD mice were examined, but young NOD mice did not display τ hyperphosphorylation. τ phosphorylation at τ-1 and pS422 epitopes was slightly increased in nondiabetic adult NOD mice. At the onset of diabetes, τ was hyperphosphorylated at the τ-1, AT8, CP13, pS262, and pS422. A subpopulation of diabetic NOD mice became hypothermic, and τ hyperphosphorylation further extended to paired helical filament-1 and TG3 epitopes. Furthermore, elevated τ phosphorylation correlated with an inhibition of protein phosphatase 2A (PP2A) activity. Our data indicate that insulin dysfunction in NOD mice leads to AD-like τ hyperphosphorylation in the brain, with molecular mechanisms likely involving a deregulation of PP2A. This model may be a useful tool to address further mechanistic association between insulin dysfunction and AD pathology.
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معلومات مُعتمدة: MOP-106423 Canada Canadian Institutes of Health Research; PCN-102993 Canada Canadian Institutes of Health Research
المشرفين على المادة: 0 (Protein Isoforms)
0 (tau Proteins)
EC 3.1.3.16 (Protein Phosphatase 2)
تواريخ الأحداث: Date Created: 20120911 Date Completed: 20130411 Latest Revision: 20220309
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3554372
DOI: 10.2337/db12-0187
PMID: 22961084
قاعدة البيانات: MEDLINE
الوصف
تدمد:1939-327X
DOI:10.2337/db12-0187