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Findings from University of Tokyo in Alzheimer Disease Reported (Differential Effects of Diet- and Genetically-induced Brain Insulin Resistance On Amyloid Pathology In a Mouse Model of Alzheimer’s Disease)

Japan Daily Report


2019 MAY 09 (NewsRx) -- By a News Reporter-Staff News Editor at Japan Daily Report -- Current study results on Neurodegenerative Diseases and Conditions - Alzheimer Disease have been published. According to news reporting out of Hongo, Japan, by NewsRx editors, research stated, “Based on epidemiological and experimental studies, type 2 diabetes mellitus (T2DM), especially insulin resistance that comprises the core mechanism of T2DM, has been recognized as a significant risk factor for Alzheimer’s disease (AD). Studies in humans and diabetic AD model mice have indicated a correlation between insulin resistance and increased amyloid deposition in the brain.”

Financial supporters for this research include Strategic Research Program for Brain Sciences (SRPBS) from Japan Agency for Medical Reserach and Development (AMED), SRPBS from the Ministry of Education, Culture, Sports, Science and Technology (MEXT), JSPS KAKENHI Grant, Japan Health Foundation.

Our news journalists obtained a quote from the research from the University of Tokyo, “Paradoxically, mice with targeted disruption of genes involved in the insulin signaling pathway showed protective effects against the AD-related pathology. These conflicting observations raise an issue as to the relationship between dysregulation of insulin signaling and AD pathophysiology. To study the causal relations and molecular mechanisms underlying insulin resistance-induced exacerbation of amyloid pathology, we investigated the chronological changes in the development of insulin resistance and amyloid pathology in two independent insulin-resistant AD mouse models, i.e., long-term high-fat diet (HFD) feeding and genetic disruption of Irs2, in combination with dietary interventions. In addition to biochemical and histopathological analyses, we examined the in vivo dynamics of brain amyloid-beta (A beta) and insulin by microdialysis technique. HFD-fed diabetic AD model mice displayed a reduced brain response to peripheral insulin stimulation and a decreased brain to plasma ratio of insulin during the hyperinsulinemic clamp. Diet-induced defective insulin action in the brain was accompanied by a decreased clearance of the extracellular A beta in vivo and an exacerbation of brain amyloid pathology. These noxious effects of the HFD both on insulin sensitivity and on A beta deposition in brains were reversibly attenuated by dietary interventions. Importantly, HFD feeding accelerated A beta deposition also in the brains of IRS-2-deficient AD mice. Our results suggested a causal and reversible association of brain A beta metabolism and amyloid pathology by diet-dependent, but not genetically-induced, insulin-resistance.”

According to the news editors, the research concluded: “These observations raise the possibility that the causal factors of insulin resistance, e.g., metabolic stress or inflammation induced by HFD feeding, but not impaired insulin signaling per se, might be directly involved in the acceleration of amyloid pathology in the brain.”

For more information on this research see: Differential Effects of Diet- and Genetically-induced Brain Insulin Resistance On Amyloid Pathology In a Mouse Model of Alzheimer’s Disease. Molecular Neurodegeneration, 2019;14():. Molecular Neurodegeneration can be contacted at: Bmc, Campus, 4 Crinan St, London N1 9XW, England. (BioMed Central -; Molecular Neurodegeneration -

Our news journalists report that additional information may be obtained by contacting T. Iwatsubol, University of Tokyo, School of Medicine, Dept. of Neuropathology, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. Additional authors for this research include T. Wakabayashi, K. Yamaguchi, K. Matsui, T. Sano, T. Hashimoto, A. Mano, K. Yamada, Y. Matsuo, T. Kubota, N. Kubota and T. Kadowaki.

The direct object identifier (DOI) for that additional information is: This DOI is a link to an online electronic document that is either free or for purchase, and can be your direct source for a journal article and its citation.

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