From epidemiology to pathophysiology: what about caffeine in Alzheimer's disease?

Author:

Flaten Vanessa12,Laurent Cyril12,Coelho Joana E.3,Sandau Ursula4,Batalha Vânia L.3,Burnouf Sylvie125,Hamdane Malika123,Humez Sandrine12,Boison Detlev4,Lopes Luísa V.3,Buée Luc126,Blum David126

Affiliation:

1. Inserm U837, F-59045 Lille, France

2. Université Lille-Nord de France, UDSL, Jean-Pierre Aubert Research Centre, Institut de Médecine Prédictive et de Recherche Thérapeutique, F-59045 Lille, France

3. Instituto de Medicina Molecular, Faculdade de Medicina Universidade de Lisboa, Lisbon, Portugal

4. Legacy Research Institute, Portland, OR 97232, U.S.A.

5. Max Planck Institute for Biology of Ageing, Joseph-Stelzmann-Strasse 9B, D-50931 Köln, Germany

6. CHRU, F-59037 Lille, France

Abstract

AD (Alzheimer's disease) is the most prevalent form of dementia in the aged population. Definitive diagnosis of AD is based on the presence of senile plaques and neurofibrillary tangles that are identified in post-mortem brain specimens. A third pathological component is inflammation. AD results from multiple genetic and environmental risk factors. Among other factors, epidemiological studies report beneficial effects of caffeine, a non-selective antagonist of adenosine receptors. In the present review, we discuss the impact of caffeine and the adenosinergic system in AD pathology as well as consequences in terms of pathology and therapeutics.

Publisher

Portland Press Ltd.

Subject

Biochemistry

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