The relationship between the two diseases is not so new. In fact, in 1991 the presence of HSV-1 was already discovered in the brain of Alzheimer’s patients, but the relationship has not been clear so far.
Only in 1997 did the virus come to be considered a risk factor, but only for patients who had the APOE4 gene – a gene involved in the synthesis of proteins that can be harmful to neurons.
Today, it is believed that the virus can become active in the brain, possibly several times, which will cause cumulative damage to brain tissue.
Without the virus, carriers of the APOE4 gene are twice as likely to develop Alzheimer’s. When HSV-1 is present, the chances are 12 times greater.
The professor then discovered, through cell cultures, that an infection by HSV-1 causes beta-amyloid and tau proteins to accumulate. The accumulation of these proteins is the main cause of neuronal death in Alzheimer’s and is a typical sign of the disease.
For this reason, it is now believed that the herpes virus type 1 is one of the main factors contributing to the development of Alzheimer’s and that it infiltrates the brain of elderly people as they age and lose their immunity.
In this way, the virus establishes a silent infection that is reactivated periodically by events such as stress, low immune system and inflammatory processes in the brain caused by the infection of other microorganisms.
Over time, damage to brain tissue becomes cumulative, leading to Alzheimer’s disease.
However, the mechanisms have not yet been fully discovered. The main hypothesis is that, in the carriers of the APOE4 gene, Alzheimer’s disease develops in the brain due to a greater formation of toxic products or a lesser repair of the damage caused by these products.
What are the prospects for the future?
If this relationship between the herpes virus and Alzheimer’s disease proves to be true (and the data points in that direction), it may be possible that antiviral agents could be used to treat Alzheimer’s disease.
The main antiviral drugs prevent the formation of new viruses, limiting the size of the damage that this invader can produce in the body.
The outlook is optimistic. In previous studies, it has been discovered that acyclovir , an antiviral drug indicated for the treatment of herpes, blocks viral DNA replication and reduces levels of beta-amyloid and tau in cell cultures.
With more time, investment and research, it may be possible, from there, to create a new form of treatment of the disease.
But not only that. Perhaps, through this new understanding, it is possible to prevent the occurrence of Alzheimer’s disease.
Large-scale population studies in Taiwan have shown that the use of specific anti-herpes agents has helped to prevent the incidence of Alzheimer’s in the population, which opens up the possibility of an Alzheimer’s “vaccine”.
What science already knew until now
Until the chance of the herpes virus gaining strength, the causes of most Alzheimer’s cases were largely unknown. This did not prevent some hypotheses from being made.
For example: it is known that approximately 15% of individuals with Down syndrome who live 40 years or more develop Alzheimer’s disease, and 50% to 70% of those up to 60 years or more also develop Alzheimer’s.
Down syndrome is a genetic disease, caused by the presence of a third copy (whole or not) of chromosome 21. There is still much to be learned, however, chromosome 21 is also involved in the plaques found in the brains of people with Alzheimer’s.
Within that chromosome are instructions for producing a protein called amyloid precursor protein, or PPA.
PPA appears to play a role in neuronal growth and repair and is found in cells throughout the body, being processed by it in different ways.
Most of the time, an enzyme called alpha-secretase divides PPA into two other molecules. Subsequently, another enzyme, called gamma-secretase, acts on these molecules and the cycle is completed
In less common situations, PPA suffers the action of another enzyme, called beta-secretase, which divides PPA in a slightly different way, releasing two other slightly different molecules.
Then, gamma-secretase appears again, only this time its action gives rise to one of the main factors related to Alzheimer’s disease: beta-amyloid.
The actual function of beta-amyloid is not yet fully understood. It is speculated that it may play a role in the healthy functioning of the brain, but if it is produced in large quantities, fragments can stick to each other, creating oligomers, which are nothing more than 4 or 5 beta-amyloid molecules joined together. .
Oligomers can bond to each other giving rise to much larger structures, called plates.
The effect that oligomers and plaques have on cells and brain health is toxic. In fact, oligomers can be even more toxic than plaques, as they can disrupt the normal functioning of neurons, causing them to die.
Over time, the cumulative death of neurons will bring cognitive impairments to the person, such as memory loss, communication difficulties and the known symptoms of Alzheimer’s.
Although the results are extremely positive, we still need to be cautious about our prospects.
The fact is that they have not yet found a cure for Alzheimer’s and that more research will be needed before reaching a definitive conclusion and, subsequently, a cure for the disease.
