One of the current but long-developed problems in public health is a significant tendency to increase the aging population. In the Americas, forecasts show that by 2025, the number of people over the age of 65 will double and the relative increase in the problems associated with this phase of life.
Our country is in line with this trend. In the last national census (2010), Argentina had six million adults over 60 years (14% of the population). This figure sets us among the countries that have most of the population in the region.
Given that generally dementia and, in particular, Alzheimer's disease are an epidemic all over the world, researchers' greatest effort today is to identify factors that increase the risk of suffering and acting against them. so that they can be prevented.
The final diagnosis of Alzheimer's disease was confirmed during the study post mortem, although progress has been made over recent years in treatment and early detection. Finding changes in brain tissue at early stages of dementia was one of the recent development projects of Pablo Scodeller and Aman Mann at Erkki Ruoslahti Laboratory at the University of California, San Diego, USA.
Scodeller, Mendoza, who studied and received a PhD in Argentina, describes the finding of CTGF (the growth factor of connective tissues), a protein that has accumulated in the cerebral vascular wall at the beginning of Alzheimer's.
"We found that CTGF protein begins to accumulate in the cerebral vasculature even before the appearance of typical beta-amyloid plaques of Alzheimer's disease," explains Scodeller. A good way to unload this ball
Article, published in 2007 natural Communication it also describes a short amino acid or peptide chain called "DAG" having the property of adhering to CTGF. DAG can be injected into the bloodstream where it quickly retrieves its partner CTGF.
This is very important for facilitating diagnosis because DAG is able to control small iron oxide particles that are thousands of times smaller than the cell in the contaminated area. The accumulation of these particles gives rise to contrast to magnetic resonance tomography, which helps physicians and researchers locate and determine the extent of damage. For Scodeller, DAG was able to detect Alzheimer's disease much earlier than the antibodies currently approved for clinical use.
The DAG peptide can carry it with the exception of a diagnosis partner, including a therapeutic drug.
"Now you can take CTGF and do something by designing a compound that binds to an important part of this protein and thus eliminates functionality, or you can develop an antibody to prevent it," says Scodeller. "Another therapeutic option would be to prevent CTGF synthesis from two cell types produce it, brain vascular cells and astrocytes, a kind of brain cell, although the latter is harder to do than the first one, "he adds.
Another key issue in the finding is that CTGF is exposed to blood vessels, i.e. contact with blood, to access the blood of the possible therapeutic or diagnostic compound. "It's not like he has to get into the tissue or become a hard-to-reach cell to achieve the goal," Scodeller continues.
Although the study was done with mouse models with the disease, researchers found DAG bound to CTGF from tissue samples in patients with Alzheimer's disease, which is relevant to the translation's point of view. "The presence of CTGF in the early stages of the disease opens up to diagnosis and treatment," Scodeller says because CTGF occurs in the brain of Alzheimer's disease in the bloodstream long before the brain's metabolic disturbances to the disease. "
The patent was patented, Scodeller decided from Tartu University in Estonia to continue research, but the San Diego team continued to produce product development in a clinic based on this target (CTGF) because either by using peptides, small molecules or antibodies or improving the diagnosis or providing a therapeutic response.
That is why they founded a biotechnology company (AivoCode, https://aivocode.com) with a patent license. AivoCode focuses on neuroscience and is a pioneer in the development of innovative technologies and a broad range of diagnostic and therapeutic neurological diseases.
The results of this study are encouraging. Alzheimer's disease is devastating to patients and the family and must not leave anyone indifferent.
Pathology with a huge social impact
It is the third disease after social health costs after ischemic heart disease and cancer, Alzheimer's disease has become more and more commonly known as a worldwide illness. According to official data, 0.5% of the world's population now lives in exponential growth in dementia. Today, about 36 million people suffer from this disease, which is over 115 million by 2050.
In Argentina, the incidence of dementia is estimated to be 12.2% in those over 65 years of age. According to these figures, we can conclude that there are more than 600,000 people in the country with dementia, of whom about 60% have Alzheimer's disease (360 thousand lessons). If we add relatives and people interested in treating the patient, the dimension of the impact of the population is worrying.
The disease also has a great weight on the economy. According to official forecasts, it costs billions of dollars and will become a billion-dollar disease by the end of this year.
Observed abnormalities in the patient's brain
The brain microscope of a patient with Alzheimer's disease detects two types of malformations considered to be the characteristics of the disease. They are as follows:
They are "beta-amyloid" called the protein that damages and destroys neurons in the brain. Although the last cause of death of neurons is unknown, the accumulation of beta-amyloid outside the brain is the most suspect.
Neurons depend on the internal transport and support system that carries nutrients and other essential materials during their long extensions. This system requires the "Tau" protein structure and normal functioning.
Tau protein threads circulating in Alzheimer's disease form brain disorders in the brain, which is why the transport system fails and is another factor that affects the neuronal death.
The original text of this article was published on February 26, 2018 in our press release.