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Diabetic Ketoacidosis Induces Tau Hyperphosphorylation in Rat Brain.
Basurto-Islas, Gustavo; Tung, Yunn Chyn; Dai, Chun-Ling; Iqbal, Khalid; Gong, Cheng-Xin.
Afiliação
  • Basurto-Islas G; Division of Science and Engineering, University of Guanajuato, Leon Guanajuato, Mexico.
  • Tung YC; Department of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA.
  • Dai CL; Department of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA.
  • Iqbal K; Department of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA.
  • Gong CX; Department of Neurochemistry, Inge Grundke-Iqbal Research Floor, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY, USA.
J Alzheimers Dis Rep ; 8(1): 615-626, 2024.
Article em En | MEDLINE | ID: mdl-38746631
ABSTRACT

Background:

Diabetes mellitus (DM) increases the risk for cognitive impairment and Alzheimer's disease (AD). Diabetic ketoacidosis (DKA), a serious complication of DM, may also cause brain damage and further AD, but the underlying molecular mechanisms remain unclear.

Objective:

Our objective was to understand how DKA can promote neurodegeneration in AD.

Methods:

We induced DKA in rats through intraperitoneal injection of streptozotocin, followed by starvation for 48 hours and investigated AD-related brain alterations focusing on tau phosphorylation.

Results:

We found that DKA induced hyperphosphorylation of tau protein at multiple sites associated with AD. Studies of tau kinases and phosphatases suggest that the DKA-induced hyperphosphorylation of tau was mainly mediated through activation of c-Jun N-terminal kinase and downregulation of protein phosphatase 2A. Disruption of the mTOR-AKT (the mechanistic target of rapamycin-protein kinase B) signaling pathway and increased levels of synaptic proteins were also observed in the brains of rats with DKA.

Conclusions:

These results shed some light on the mechanisms by which DKA may increase the risk for AD.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: J Alzheimers Dis Rep Ano de publicação: 2024 Tipo de documento: Article País de afiliação: México País de publicação: Holanda
Texto completo
Adicionar na Minha BVS
Imprimir
XML
PubMed Links
Buscar no Google

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: J Alzheimers Dis Rep Ano de publicação: 2024 Tipo de documento: Article País de afiliação: México País de publicação: Holanda