Detrimental effects of diet-induced obesity on [tau] pathology are independent of insulin resistance in [tau] transgenic mice.(ORIGINAL ARTICLE)

The [tau] pathology found in Alzheimer disease (AD) is crucial in cognitive decline. Midlife development of obesity, a major risk factor of insulin resistance and type 2 diabetes, increases the risk of dementia and AD later in life. The impact of obesity on AD risk has been suggested to be related t...

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Published inDiabetes (New York, N.Y.) Vol. 62; no. 5; p. 1681
Main Authors Leboucher, Antoine, Laurent, Cyril, Fernandez-Gomez, Francisco-Jose, Burnouf, Sylvie, Troquier, Laetitia, Eddarkaoui, Sabiha, Demeyer, Dominique, Caillierez, Raphaelle, Zommer, Nadege, Vallez, Emmanuelle, Bantubungi, Kadiombo, Breton, Christophe, Pigny, Pascal, Bude-Scherrer, Valerie, Staels, Bart, Hamdane, Malika, Tailleux, Anne, Buee, Luc, Blum, David
Format Journal Article
LanguageEnglish
Published New York American Diabetes Association 01.05.2013
Subjects
Alzheimer's disease
Cholesterol
Complications and side effects
Dementia
Diabetes
Diet
Glucose
Health aspects
Insulin resistance
Memory
Middle age
Obesity
Pathology
Phosphorylation
Risk factors
Software
Sucrose
Transgenic animals
Type 2 diabetes
France
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Summary:The [tau] pathology found in Alzheimer disease (AD) is crucial in cognitive decline. Midlife development of obesity, a major risk factor of insulin resistance and type 2 diabetes, increases the risk of dementia and AD later in life. The impact of obesity on AD risk has been suggested to be related to central insulin resistance, secondary to peripheral insulin resistance. The effects of diet-induced obesity (DIO) on [tau] pathology remain unknown. In this study, we evaluated effects of a high-fat diet, given at an early pathological stage, in the THY-Tau22 transgenic mouse model of progressive AD-like [tau] pathology. We found that early and progressive obesity potentiated spatial learning deficits as well as hippocampal [tau] pathology at a later stage. Surprisingly, THYTau22 mice did not exhibit peripheral insulin resistance. Further, pathological worsening occurred while hippocampal insulin signaling was upregulated. Together, our data demonstrate that DIO worsens [tau] phosphorylation and learning abilities in [tau] transgenic mice independently from peripheral/central insulin resistance.
ISSN:0012-1797
1939-327X
DOI:10.2337/db12-0866