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

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

The immune system is the organism’s defense system 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 of those pathogenic agents (such as proteins). Any chemical substance capable of causing a response in the immune system is called an antigen.

When the immune system recognises an antigen defense 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 which has caused their production. The antigens, and along with them the pathogen agents which express them, are thus labelled so that they can be recognised by other cells in the immune system in charge of neutralization and elimination.

Moreover, the immune system grants the organism with the ability to remember antigens it has previously found; in this way it reinforces itself against further attacks from the same pathogenic agent. If in the future encounters with that pathogen, the immune system is capable of avoiding the disease we say the organism has attained immunity (natural) 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 get rid of 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 very hopeful although the complexity of the mechanisms which come into play when the immune system is activated requires numerous studies to dismiss possible side effects before these therapies can be applied to people.