With more than 850 000 people in France, Alzheimer’s disease and related diseases represent the first cause of dementia in the country. Alzheimer’s disease is a neurodegenerative disease characterized by impairment of memory and other cognitive deficits/behavioral : aggression, aphasia (language disorder), agnosia (disorder of recognition of the surroundings), apraxia (clumsy gestures).

If the diagnostic probability of Alzheimer’s disease is based on different clinical criteria aided by the determination of biomarkers in the cerebrospinal fluid, or imaging MRI or metabolic, the diagnosis of certainty is based on the observation of neuropathological plaques extraneuronales formed peptide amyloid (a small protein formed normally and accumulate in a manner toxic to the outside of the neurons) and injury intraneuronales composed of abnormal Tau proteins (proteins promoting normally the cellular communication within the neuron). These lesions cause dysfunction of neuronal cells, leading to cognitive disorders.

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The first risk factor of Alzheimer’s disease is aging. However, a combination of genetic and environmental factors also plays an important role.

Caffeine and Alzeihmer

The consumption of coffee has a particular impact on this risk. Coffee is the most consumed beverage in the world after water. The cafe is also the first source of caffeine, which remains to this day, his being the best characterized. Caffeine is the psychoactive substance most widely consumed in the world. It is well established that it promotes the attentional processes, arousal, information processing, and has made a significant impact on cognitive performance in humans and animals.

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recent work also suggest an effect of caffeine on the process memory, and long-term memory in particular, independent of its effects attentional. This observation has to be linked with various epidemiological studies suggesting that the usual consumption of caffeine reduces cognitive decline during aging.

other prospective studies also focus on the inverse relationship between caffeine consumption and the risk of developing Alzheimer’s disease. The protective effects of caffeine would be optimal for doses corresponding to 3 to 4 cups per day. Interestingly, different experimental studies on animal models of Alzheimer’s disease reproducing the lesions and memory impairment associated with demonstrate a beneficial effect of caffeine at doses comparable, even if the effects on the behavioral symptoms of the disease have recently been discussed.

How it works ?

The main targets of caffeine are receptors called receptors adénosinergiques. The effects of caffeine are particularly related to its ability to block one of these receptors called receptor adénosinergique A2A.

a few years ago, our team has demonstrated that specifically block this receptor by genetic approaches and by a chemical derivative of caffeine reduces memory impairment, disorders of the neural communication and the dysfunction of the Tau protein in an animal model of Alzheimer’s disease.

In a new study, our team, in collaboration with colleagues from the university of Lisbon and Bonn, has demonstrated that blockage of the receptor adénosinergiques A2A by this same compound derived from the caffeine reduced the lesions amyloid in the cortex and memory disorders associated in an animal model replicating the amyloid plaques. This new study suggests, therefore, that the compounds derived from the caffeine receptor targeting adénosinergiques A2A act positively vis-à-vis the two brain lesions characteristic of the disease.

To a track that is therapeutic ?

The whole of these observations leads us to think that the use of molecules derived from caffeine would be a therapeutic option in patients with Alzheimer’s disease. It is very interesting to note that this type of molecule exists and has already been the subject of clinical trials in the context of Parkinson’s disease. It is therefore possible and interesting to repositioning these molecules in the therapeutic context of Alzheimer’s disease.

Before considering studies in humans, we need to make additional elements converging reinforcing the concept that it is important to block receptor A2A. These are the experimental studies that we are conducting currently. We hope to be able to define a strategy for clinical trial in three to five years to come, and to gather funding to this end.

*David Blum is the director of research, Inserm, university of Lille.

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