What science says about possible links

Alzheimer’s disease is a neurodegenerative pathology that affects older subjects in its most common form. Nevertheless, It is estimated that 1,200,000 people suffer from Alzheimer -type neurodegenerative diseases in France.

Discovered a century ago. However, this pathology remains very largely enigmatic and the exact mechanisms at the origin of its trigger and its poorly known evolution.

Among the hypotheses that are the subject of research. However, that of a link between Alzheimer’s and exposure to the herpes virus is reinforced by recent publications.

Brain lesions that cause a major cognitive disorder – What science says about possible

Alzheimer’s disease is characterized by a set of microscopic lesions. In addition, initially confined in certain brain regions. Nevertheless, The lesions then spread, over the evolution of the disease, in multiple areas of the brain.

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This slow. Meanwhile, stereotypical progression what science says about possible of brain damage is accompanied by graduated clinical symptoms (memory disorders, disruption of language, difficulty reasoning and planning actions, etc.). Furthermore, Patients with Alzheimer’s disease will thus develop a major neurocognitive disorder (the term dementia is sometimes used) leading to loss of autonomy. Furthermore, social isolation and the disappearance of the most complex, advanced and representative mental faculties of the human species.

The brain lesions that cause these dramatic clinical manifestations are schematically of two types:

• 1) Certain lesions are present inside neurons in the form of fibrillar tangles (we speak of “neurofibrillar degeneration”) made up of a protein. Consequently, the tau protein, which accumulates in an abnormal form. Similarly,

• 2) Other lesions are identified in the extracellular space of the cerebral tissue. In addition, in the form of plates, whose chemical nature is mainly composed of a protein (amyloid -ß or Aß peptide): amyloid plates.

Neurofibrillar degeneration and amyloid plates constitute the neuropathological signature of Alzheimer’s disease. However, other lesions are observed in patients’ brains.

To date. no preventive or curative treatment – What science says about possible

Regarding the mechanisms at the origin of the disease, a significant advance occurred at the turn of the 90s with the identification, in some patients, of genetic mutations involved in the production of the Aß peptide.

These discoveries have made it possible to sketch the hypothesis of the “amyloid waterfall” which proposes that the accumulation of aß peptide in the brain is a princeps. founder event which will cause all the other brain lesions and lead to dementia.

However. mutations responsible for an overproduction of Aß concern only a very low minority of patients (less than 1 %) and it is likely that a multitude of other causal factors are at work in the disease.

Without in -depth knowledge of the mechanisms responsible for what science says about possible Alzheimer’s disease. it is not illogical to note that today no effective or effective preventive treatment is available, despite the very substantial therapeutic research effort.

The identification of causal determinants that cause Alzheimer’s disease. factors that modulate the risk of developing this disease or that modify the trajectory is a priority and mobilizes many research teams.

Possible links between Alzheimer’s and the herpes virus – What science says about possible

Recently, a scientific article published in the prestigious review Neuron reported new data. This study analyzed two cohorts of several thousand Finnish. English subjects and shown that viral encephalitis (inflammation of the brain following a viral infection) increased by 20 to 30 times the risk of subsequently developing an Alzheimer’s disease.

These works followed other studies. in different countries, which indicated an increased risk of developing an Alzheimer’s disease after infection of the herpes virus (HSV-1), a highly neurotropic virus (that is to say capable of entering the brain). what science says about possible These same studies underlined the protective effect (a reduction in the risk of Alzheimer’s disease) of an antiviral treatment.

More recently. even more convincingly, almost experimental studies in human population have shown, in Wales, Australia and the USA, than vaccination against chickenpox-zona virus (VZV), a virus of the same family as the herpes virus (HSV-1), significantly reduced the risk of developing dementia.

A hypothesis already defended 40 years ago

The hypothesis of a role of viruses. in particular herpes viruses, in Alzheimer’s disease is not new. It was defended more than 40 years ago by a Canadian neurologist. Melvyn Ball, who suggested that the reactivations of the HSV-1 herpes virus (the famous fever button) could be accompanied by a neuroinvasion (that is to say a penetration of the virus in the brain) and a degeneration of the brain tissue Alzheimer’s.

Research works have later come to support the hypothesis. by identifying “viral signatures” what science says about possible (corresponding to the proteins or the genome of the virus) which mark the presence of herpes viruses (HSV-1) in the brains of patients with Alzheimer’s disease, especially in amyloid plates.

These observations. as well as the first epidemiological studies, can however be criticized: highlighting an association between infection and Alzheimer’s disease is not enough to establish a causal link!

We could even apply. provocatively, that it is Alzheimer’s disease that makes the organism permissive to viral infections (and not the other way around!), Explaining the presence of viral material in the brains of Alzheimer’s patients.

Alzheimer’s. HSV-1: why research bounces today

The infectious hypothesis of Alzheimer’s disease has nevertheless been reinforced, more recently, by two series of experimental results:

• 1) The discovery that the Aß peptide which precipitates at the heart of amyloid plates has antimicrobial functions and could thus participate in a physiological (immune) response in reaction to a viral infection, what science says about possible
• 2) The fact of succeeding in inducing, after infection by the herpes virus (HSV-1) in vitro (in cell cultures) or in vivo in animals, of an overproduction of aß peptides and pathological protein (the tau protein being, as reminded, the other molecular marker of Alzheimer’s disease).

The hypothesis of a scenario with several stages

Understanding the relationships between viral infections. Alzheimer’s disease has therefore progressed in recent years and new hypotheses are emerging.

Regarding HSV-1. the most studied virus, a scenario in several stages can be offered:

• 1) Herpes virus infection (HSV-1) is common in our populations and the virus is able to sleep (latency phase) for several decades in certain nervous nodes,
• 2) During aging, the body faces different stress which, combined with a drop in efficiency of the immune defenses of the elderly, will promote the release of latency from the virus and its propagation what science says about possible in the brain,
• 3) The presence of active viruses in the brain will cause a local Aß and Tau response, with low noise, in infected areas,
• 4) These Aß and Tau lesions, associated with cerebral inflammation, will initiate a vicious self -employment circle leading to the intensification and propagation of lesions in other brain regions.

This hypothetical scenario will require an important effort of research to be validated (or deconstructs, thus goes science!). Experimental work is necessary in animals. on three -dimensional tissue preparations (brain organoids) to finely study the causal relationship between infection and biological markers of Alzheimer’s disease.

Studies continue

Epidemiological studies. in human populations, also continue and seek to refine the impact of levels of infection on the appearance or worsening of biomarkers of Alzheimer’s disease.

In the end. it is a set of disciplinary fields which is summoned and which requires the communication and sharing what science says about possible of knowledge and ideas between virologists, neurologists, epidemiologists, pathologists, etc.

Confirm the role of viral agents in Alzheimer’s disease. but also in other neurodegenerative diseases (such as multiple sclerosis closely associated with Epstein-Barr virus, still a herpes virus!) Certainly open the door to new preventive (vaccination) or curative (antiviral) (antiviral) tracks.

It should nevertheless be kept in mind that Alzheimer’s disease is an extremely complex pathology. most certainly multiderminated by different elements or risk factors, genetic or environmental.

Concluding a unique cause of triggering the disease (like that of an earlier viral infection) is obviously an ineptus. It will be recalled in this regard that although a large part (70-80 %) of the human population is infected with the herpes virus (HSV-1). this infection is not a sine qua non condition to develop the disease!