Alzheimer’s disease could occur as a result of an infection with a very common virus

Les chercheurs de l’université de Tufts, aux États-Unis, present recent results in agreement with the hypothesis suggesting that Alzheimer’s disease could be declined by a virus.

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Près de 225,000 personnes in France declaring Alzheimer’s disease chaque année, for most after 65 years. Si cette forme de démence est fréquent, son origine est encore vivement débattue chez les spécialists. Il ya tout de même des points de consensus: les amyloid plaques et les agrégats de Tau protein dance les the neurons are involved in survenue des symptom typiques from Alzheimer’s diseaseand Iinflammation qui s’empara du brain des malades exacerbate cette toxicity.

To explain these observations, several hypotheses are proposed by scientists. Les factors genetics It seems to have played an important role in the more frequent sporadic cases of Alzheimer’s, but also the dysregulation of amyloid protein synthesis or the intervention of a microorganism – a virus la plupart du temps – could aussi avoir une implication.

Often experiences in vitro sur des neurones en culture

A team from Tufts University, aux États-Unis, presents results entering the framework of the “viral hypothesis” on the origin of Alzheimer’s disease. This ultima stipule that a dormant virus in the cerveau – le plus souvent herpes virus 1 or HSV-1 – soit « reveillé » par des factors encore mal definis, et induise les symptoms of the maladie d’Alzheimer. « The results suggest a pathway leading to Alzheimer’s disease caused by a virus infection VZV which declines an inflammation reveillant le virus HSV-1 in le cerveau », explains Dana Cairnspremière autrice de l’étude publiee dans Journal of Alzheimer’s Disease.

To corroborate this hypothesis, they infected human neural stem cells with two viruses and researched the presence of markers specific to Alzheimer’s: amyloid plaques and Tau aggregates, in gliosis (proliferation of). glial cells dans le cerveau) et la neuro-inflammation. Their results show that the virus VZV seul n’engendre step to the formation of amyloid plaques and agrégats Tau, like HSV-1, mais une neuro-inflammation and to gliosis. This suggests, selon les sciences, an indirect action of the VZV virus. In addition, it has been observed that the infection of cells, in which HSV-1 is latent, by the reactive VZV virus is the last and the cause of the typical changes of Alzheimer’s. « C’est un double coup de poing de deux viruses, which are très courants and generally inoffensifs, mais les études de laboratoire suggestent that a new exposure to VZV réveille le HSV-1 dormant, could cause problems. », stated Dana Cairns.

These experiences à elles seules are not robust enough to confirm a causal right between Alzheimer’s disease and the VZV and HSV-1 virus, even the observations vont dans ce sens. Par ailleurs, les differente hypothèses à l’étude sur l’origine de la maladie d’Alzheimer’s do not necessarily exclude others. Viral infection could be a factor to consider in Alzheimer’s disease, among others.

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