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Neurobiol Aging. 2014 Sep;35(9):2079-90. doi: 10.1016/j.neurobiolaging.2014.03.027. Epub 2014 Mar 29.

Beneficial effects of caffeine in a transgenic model of Alzheimer's disease-like tau pathology.

Author information

1
Université Lille-Nord de France, UDSL, Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, IMPRT, Lille France.
2
PharmaCenter Bonn, Pharmaceutical Institute, University of Bonn, Bonn, Germany.
3
Université Lille-Nord de France, UDSL, Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, IMPRT, Lille France; CHRU-Lille, Lille France.
4
Université Lille-Nord de France, UDSL, Lille, France; Inserm U837, Jean-Pierre Aubert Research Centre, IMPRT, Lille France; CHRU-Lille, Lille France. Electronic address: david.blum@inserm.fr.

Abstract

Tau pathology found in Alzheimer's disease (AD) is crucial in cognitive decline. Epidemiologic evidences support that habitual caffeine intake prevents memory decline during aging and reduces the risk to develop Alzheimer's disease. So far, experimental studies addressed the impact of caffeine in models mimicking the amyloid pathology of AD. However, in vivo effects of caffeine in a model of AD-like tauopathy remain unknown. Here, we evaluated effects of chronic caffeine intake (0.3 g/L through drinking water), given at an early pathologic stage, in the THY-Tau22 transgenic mouse model of progressive AD-like tau pathology. We found that chronic caffeine intake prevents from the development of spatial memory deficits in tau mice. Improved memory was associated with reduced hippocampal tau phosphorylation and proteolytic fragments. Moreover, caffeine treatment mitigated several proinflammatory and oxidative stress markers found upregulated in the hippocampus of THY-Tau22 animals. Together, our data support that moderate caffeine intake is beneficial in a model of AD-like tau pathology, paving the way for future clinical evaluation in AD patients.

KEYWORDS:

Alzheimer's disease; Caffeine; Caffeine metabolites; THY-Tau22; Tau; Transgenic

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