One of the current but long-standing problems in the field of public health is the marked upward trend in population aging. In America, projections indicate that by 2025 the number of people over 65 will double, with a proportionate increase in problems related to this phase of life.
Our country is in tune with this trend. In the last National Census (2010), Argentina had six million adults over 60 (14% of the population). This number places us within the group of countries with the highest percentage of the elderly population in the region.
If we take into account that dementia in general, and Alzheimer's disease in particular, is a worldwide epidemic, the maximum effort of researchers today is to determine the factors that increase the risk of suffering and acting upon them. to prevent them.
The final diagnosis of Alzheimer's disease was confirmed during the post mortem, although in recent years there has been progress in treatment and early detection. Finding changes in brain tissue associated with the early stages of dementia was one of the recent advances by Pablo Scodeller and Aman Mann conducted in the laboratory of Erkki Ruoslahti of the University of California, San Diego, United States.
Scodeller, a Mendoza who studied and obtained a doctorate in Argentina, tells us about the finding of CTGF (connective tissue growth factor), a protein that is deposited in the walls of blood vessels in the brain in the early stages of Alzheimer's disease.
"We found that CTGF protein starts to accumulate in the cerebral blood vessels, even before the appearance of beta-amyloid plaques, typical of Alzheimer's disease," explains Scodeller. A good tip to unravel this ball
The article, published in Communication of Nature also describes a short chain of amino acids or peptide, called "DAG", which has the property of adhering to CTGF. The DAG can be injected into the bloodstream, where it quickly searches for its partner, the CTGF.
This is very important to facilitate the diagnosis because the DAG is able to direct small particles of iron oxide, a thousand times smaller than a cell, to the affected area. The accumulation of these particles generates contrast on magnetic resonance tomography, which helps doctors and researchers locate and define the extent of damage. For Scodeller, DAG has detected Alzheimer's disease much earlier than contrast agents currently approved for clinical use.
The DAG peptide may carry with it not only a partner for the diagnosis, but also a therapeutic drug.
"Now you can get CTGF and design some compounds that bind to an important site of that protein and so remove the functionality. Or you can develop an antibody to block it," says Scodeller. "Another therapeutic option would be to inhibit the synthesis of CTGF in the two cell types that produce it, the blood vessel cells in the brain and the astrocytes, a type of brain cell, although the latter is more difficult than the first." add
Another key point of the finding is that CTGF is exposed in the blood vessels, ie in contact with blood, so that any therapeutic or diagnostic compound that is injected through the blood will have access to it. "It is not that he has to penetrate the tissue or enter the cell, which is difficult to achieve, to reach his target," continues Scodeller.
Although the study was conducted in rat models with the disease, researchers found that DAG bound to CTGF in tissue samples from Alzheimer's patients, which is relevant from a translational point of view. "The presence of CTGF in an early stage of the disease opens the door to diagnosis and therapy," Scodeller says, since "CTGF appears in the blood vessels of the brain of Alzheimer's disease long before metabolic disorders of the brain." for the disease ".
The peptide was patented, Scodeller chose the University of Tartu in Estonia to continue his research, but the San Diego team continued working to bring a product to the clinic based on the concept of achieving that goal (CTGF) since either by using peptides, small molecules or antibodies, or to improve the diagnosis or to obtain a therapeutic response.
To this end, they founded a biotechnology company (AivoCode, https://aivocode.com), which holds the patent license. AivoCode is focused on neuroscience and is a pioneer in developing innovative technologies and a broad platform to improve the diagnosis and treatment of neurological diseases.
The conclusions of this study are encouraging. Alzheimer's disease is devastating to the patient and family, and should not leave anyone indifferent.
A pathology with enormous social impact
Located as the third disease in social health costs after ischemic heart disease and cancer, Alzheimer's disease has become an increasingly common disease on a global scale. According to official data, 0.5% of the world's population lives today with dementia, a number that will increase exponentially. About 36 million people suffer from this disease today, a number that will reach more than 115 million by 2050.
In Argentina, the prevalence of dementia in general is estimated at 12.2% in individuals over 65 years of age. According to these figures, we can infer that there are more than 600 thousand people with dementia in the country, of which approximately 60% are Alzheimer's type (360 thousand subjects). If we add relatives and people dedicated to patient care, the size of the impact on the population is worrying.
The disease also has a great weight in the economy. According to official forecasts, it is costing billions and will become a trillion dollar disease by the end of this year.
Abnormalities seen in the patient's brain
By observing under the microscope the brain tissue of an Alzheimer's patient, two types of abnormalities considered characteristic of the disease are appreciated. Are the following:
They are conglomerates of a protein called "beta-amyloid" that damages and destroys neurons in the brain. Although the ultimate cause of neuron death is not known, the accumulation of beta-amyloid on the outside of brain cells is the main suspect.
Neurons rely on an internal transport and support system that carries nutrients and other essential materials along their long stretches. This system requires the normal structure and function of a protein called "Tau".
In Alzheimer's disease, Tau protein strands are twisted forming true complications in brain cells, which is why the transport system fails and is another factor that contributes to the death of neurons.
The original text of this article was published on 11/26/2018 in our printed edition.