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With more than 850,000 people in France, Alzheimer's disease and related diseases are the leading cause of dementia in the country. Alzheimer's disease is a neurodegenerative disease characterized by impaired memory and other cognitive / behavioral deficits: aggression, aphasia (language disorder), agnosia (confusion of the recognition of the environment), apraxia (clumsy gesture)
If the probability diagnosis of Alzheimer's disease is based on different clinical criteria aided by the determination of biomarkers in the cerebrospinal fluid, or even the MRI or metabolic imaging, the diagnosis of certainty is based on the neuropathological observation of extraneuronal plaques consisting of amyloid peptides (normally formed small proteins that accumulate toxicly outside neurons) and intraneuronal lesions composed of abnormal Tau proteins (proteins normally promoting cellular communication within the neuron). These lesions lead to dysfunction of neuronal cells, leading to cognitive impairment
The first risk factor for Alzheimer's disease is aging. Nevertheless, a combination of genetic and environmental factors also plays an important role
Caffeine and Alzeihmer
Coffee consumption has a particular impact on this risk. Coffee is the most consumed drink in the world after water. Coffee is also the main source of caffeine, which remains to this day its best-characterized constituent.
Caffeine is the most consumed psychoactive substance in the world. It is well established that it promotes attentional processes, awakening, information processing and therefore has a significant impact on cognitive performance in humans and animals.
] Memo by Ines Scheiber, Julius Durand, Julien Becquer, Elena Dupressoir and Viviane Guimaraes (Goblins)
Recent work also suggests an effect of caffeine on memory processes), and long-term memory in particular, independent of its attentional effects. This observation is linked to different epidemiological studies suggesting that the usual consumption of caffeine reduces cognitive decline during aging.
Other prospective studies also emphasize the inverse relationship between caffeine consumption and the risk of developing Alzheimer's disease. The protective effects of caffeine would be optimal for doses of 3 to 4 cups a day.
Interestingly, various experimental studies on animal models of Alzheimer's disease reproducing lesions and badociated memory disorders demonstrate a beneficial effect of caffeine at comparable doses, even though the effects on behavioral symptoms of the disease have recently been discussed
What are the mechanisms of caffeine in the brain?
The targets Main caffeine are receptors called adenosinergic receptors. The effects of caffeine are particularly related to its ability to block one of these receptors called A2A adenosinergic receptor.
A few years ago, our team demonstrated that specifically blocking this receptor by genetic approaches and by a derivative caffeine chemistry reduced memory disorders, neural communication disorders and Tau protein dysfunction in an animal model of Alzheimer's disease
In a new study, our team, working with colleagues from the University of Lisbon and Bonn, has just demonstrated that the blockade of adenosinergic A2A receptors by this same compound derived from caffeine reduced amyloid lesions in the cortex and badociated memory disorders in an animal model reproducing amyloid plaques.
This new study therefore suggests that caffeine-derived compounds targeting caffeine A2A adenosinergic agents act positively towards the two brain lesions characteristic of the disease.
Towards a therapeutic track in humans?
All of these observations suggest that the use of derived molecules 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 reposition these molecules in the therapeutic context of Alzheimer's disease.
Before considering studies in humans, we must provide additional convergent elements reinforcing the concept that it is important to block the A2A receptors. These are the experimental studies that we are currently conducting. We hope to be able to develop a clinical trial strategy in the next 3 to 5 years and raise funds for this purpose.
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By David Blum, ] Director of research Inserm, University of Lille
The original version of this article was published on The Conversation
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