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A new study, published in the journal Nature, brings hope against Alzheimer's disease. The key to coping with the disease may be in a drug already used in HIV patients. The results showed that the HIV and Alzheimer's viruses use similar mechanisms to manifest themselves in the body. This could open an unprecedented opportunity to develop a new treatment strategy. At present, there is no treatment for Alzheimer's disease. The treatment consists of prescribing drugs that only relieve symptoms. In Brazil, four drugs are available both in pharmacies and in the public health network: rivastigmine, donepezil, galantamine and memantine.
The research has highlighted another interesting fact: HIV-infected older adults who use antiretrovirals tend not to develop Alzheimer's disease. The explanation lies in the fact that the therapy inhibits the enzyme reverse transcriptase – produced by the human body – which also appears in the process of development of Alzheimer's. The researchers therefore believe that, in patients with neurodegenerative disease, the blockage of the enzyme could theoretically become a new way to prevent the disease from progressing. If the effectiveness of antiretroviral drugs for Alzheimer's disease is proven, patients could rely on another drug that can improve the quality of life.
How does Alzheimer's disease manifest itself?
Although much research has been done, scientists still know little about Alzheimer's disease. Among the important information revealed, there is a tendency to the onset of the disease: the formation of amyloid plaques in the brain – they are considered the main cause of blockage and destruction of neurons. When this happens, cognitive decline occurs, characterized by memory loss and difficulty in reasoning – well-known features of Alzheimer's disease.
The formation of these plaques is related to the amyloid precursor protein (APP), but scientists still can not explain their exact role in this process. Despite this, the team found that mutations in the PPA gene, responsible for coding this protein, could increase the risk of early onset of Alzheimer's disease. The data indicates that the condition can be triggered by more than 50 different mutations. these changes in DNA account for about 10% of all first cases of the disease.
In 2012, researchers at the University of Iceland had discovered that specific mutations in the PPA gene were also able to reduce up to 40% the likelihood of amyloid plaque formation. However, it is still not possible to specify which changes increase or decrease the risks.
What does Alzheimer's and HIV have in common?
According to researchers, the PPA gene generates new genetic variations within neurons through a process called genetic recombination. for this to happen, it is necessary to use reverse transcriptase, the same enzyme used by the HIV virus to enter human cells and infect the individual. This action is a normal process of the brain. However, when something goes wrong in genetic recombination, this mistake can trigger Alzheimer's disease.
To reach this conclusion, the team used samples of diseased cells and healthy brain samples. The analysis showed that 100% of the samples with neurodegenerative disease had a high number of genetic variations other than APP compared to healthy varieties.
"If we imagine DNA as a language that every cell uses to" talk ", we find that in neurons, a single word can produce thousands of new words that have not been recognized before. to a secret code embedded in our normal language and decoded by genetic recombination.This code is used in healthy brains, but it also appears to be affected by Alzheimer's disease, "said Jerold Chun, lead author of research, at Medical News Today.
Alternative treatment
The researchers believe that reverse transcriptase blocking of the enzyme could be a way to prevent genetic recombination that can cause Alzheimer's disease. Therefore, since antiretroviral therapies used to treat HIV are able to inhibit the enzyme, this would indicate that anti-HIV drugs may have good results in the treatment of this degenerative disease. In addition, Chun thinks that the study could be important for high-risk populations, as in the case of people with rare genetic forms.
New look at Alzheimer's
In addition to suggesting a new form of treatment, the research also helps to explain why many treatments to prevent the accumulation of beta amyloid protein – present in amyloid plaque – may have failed. For the team, mutations produced by the PPA gene can produce a number of changes in toxins and proteins related to the disease. Therefore, an approach that looks for unique forms of the enzymes involved can not succeed.
While highlighting a problem of concern to researchers around the world, Chun admits that much remains to be discovered. He said that he intended to evaluate genetic recombination in different parts of the brain and determine the involvement of other people recombined in Alzheimer's disease and other neurodegenerative diseases.
With so much to study, the development of the new treatment may be slow. The good news is that researchers want to find as many possible solutions to improve the lives of patients with Alzheimer's disease.
Alzheimer
Alzheimer's disease is a neurodegenerative disease that causes a decrease in cognitive function because brain cells degrade and die, leading to a steady decline in mental function. The main symptoms of the disease are: memory difficulties (especially recent events), vague speech during conversations, delays in routine activities, forgetting known people and places, deteriorating social skills and emotional unpredictability .
According to the World Health Organization (WHO), this disease accounts for 60 to 70% of dementia cases – a group of brain disorders resulting in loss of intellectual and social skills. An estimated 47 million people worldwide have dementia and 10 million new cases are registered each year. In Brazil, Alzheimer's disease is among the top 10 causes of death and affects 1.2 million people.
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