The foundations of our research

Alzheimer’s disease is related to an alteration in the metabolism of a protein known as beta-amyloid in the brain. Excessive production and/or reduced elimination lead to an increase of this protein in the brain, eventually reaching toxic levels for neurons, causing their death and triggering a series of degenerative mechanisms which worsen the disease.

To date, no treatment has been found which is capable of modifying the course of the illness; there are but a few drugs available which are capable of relieving some of the symptoms of the disease, and even these only work in a percentage of patients, and for a limited period of time. Research for new treatments for Alzheimer’s is a priority for scientific research in the Western world. The exploration of treatments based on immunotherapy is the line of work which currently offers the greatest hope of medium term success.

The immune system is the body’s means of defence against illnesses caused by viruses and bacteria. The efficiency of the immune system is based on the ability of its cells to recognise and react against certain chemical substances produced by those pathogenic agents (such as proteins). Any chemical substance capable of causing a response in the immune system is referred to as an antigen.

When the immune system recognises an antigen, defence barriers are activated, including the production of antibodies. Antibodies are proteins produced by particular cells in our immune system, which adhere specifically to the antigen that has caused their production. In this way, the antigens, and along with them the pathogen which express them, are labelled so that they can be recognised by other cells in the immune system responsible for their neutralization and elimination.

Moreover, the immune system grants the organism the ability to remember antigens it has previously found; in this way, it strengthens itself against further attacks from the same pathogenic agent. If, in future encounters with that pathogen, the immune system is capable of avoiding the disease, we say that the organism has attained (natural) immunity against that pathogen.

In certain circumstances, it is possible to make the immune system react against a protein belonging to the organism itself, which is in excess, such as the beta-amyloid protein in Alzheimer’s disease. The aim is to stimulate the immune system to produce antibodies to label the beta-amyloid protein, so that the same mechanisms in charge of eliminating proteins from external pathogenic agents will also act against the beta-amyloid protein. Our working hypothesis is that, by reinforcing the ability of the organism to eliminate excess beta-amyloid, it would be possible to prevent or delay the appearance of the disease and even stop it progressing in people who already have it. The preliminary results obtained from different animal models are promising, although the complexity of the mechanisms coming into play when the immune system is activated requires numerous studies to dismiss possible side effects, before these therapies can be applied to humans.