A drug used for decades to treat other diseases could help slow the death of neurons associated with Alzheimer’s disease. The conclusion comes from a study carried out by researchers at the University of Colorado Anschutz, in the United States, and published last Friday (12/19) in the journal Cell Reports Medicine.
The research evaluated the effects of sargramostim, a synthetic version of the protein GM-CSF, which stimulates the immune system.
Although changes in neurons in the brain can begin early in life and intensify with aging, scientists observed that use of the drug was able to reduce blood markers linked to neuronal death in people with Alzheimer’s disease, in addition to improving one of the cognitive measures assessed.
According to Professor Huntington Potter, lead author of the study and director of the Anschutz Alzheimer’s and Cognition Center at the University of Colorado, the clinical trial showed detectable changes in blood tests and in a cognitive test in a relatively short interval.
In a statement, he explained that the results indicate the possibility of interfering with biological processes linked to disease progression, even after diagnosis.
Blood changes throughout life
To better understand the effects of the drug, the researchers also analyzed data from people of different ages. They observed that proteins released into the blood when neurons are damaged or enter a dying process gradually increase throughout life.
One of these proteins is UCH-L1, which is associated with neuronal death. Another is NfL, released when neurons are damaged. Both appear in low concentrations early in life and gradually increase with aging, reaching their highest levels around age 85. At later stages, high UCH-L1 values are linked to poorer cognitive outcomes.
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Scientists also identified an increase in GFAP, a protein linked to brain inflammation, after age 40. They drew attention to the fact that concentrations of these age-associated markers were higher in women, although the reasons for this difference are not yet known.
These results reinforce the idea that part of the cognitive decline observed throughout aging is linked to inflammatory processes and the progressive death of neurons, mechanisms also present in Alzheimer’s disease.
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Alzheimer’s disease is a degenerative disease caused by the death of brain cells and which can appear decades before the first symptoms appear.
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As it is a disease that tends to worsen over the years, early diagnosis is essential to delay its progression. Therefore, in case of symptoms of the disease, it is essential to consult a specialist.
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Although symptoms are more common in people over 70, it is not uncommon for them to appear in young people around age 30. In fact, when this “premature” manifestation occurs, the disease is known as early-onset Alzheimer’s.
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In the initial phase, a person with Alzheimer’s disease tends to have changes in their memory and begins to forget simple things, such as: where they kept their keys, what they ate for breakfast, someone’s name or even the season of the year.
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Disorientation, difficulty remembering where you live or the way home, difficulty making simple decisions, such as planning what to do or eat, for example, are also signs of the disease.
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Additionally, loss of desire to perform routine tasks, changes in behavior (making the person more nervous or aggressive), and repetitions are some of the most common symptoms.
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According to research conducted by the Alzheimer’s Drugs Discovery Foundation (ADDF), the presence of damaged proteins (Amyloid and Tau), vascular diseases, neuroinflammation, neuronal energy failure and genetics (APOE) could be linked to the onset of the disease.
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Treatment of Alzheimer’s disease involves the use of medications to reduce the symptoms of the disease, in addition to the need for physiotherapy and cognitive stimulation. The disease is incurable and care must be taken until the end of life
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Effects of sargramostim on Alzheimer’s disease
In the clinical trial, sargramostim was given to people with Alzheimer’s disease for a short time. During treatment, blood levels of UCH-L1 fell by about 40%, reaching values similar to those seen in early adulthood. However, this effect is temporary and disappears after stopping treatment.
Despite this, participants who received sargramostim showed improvement in one of the cognitive tests applied, the Mini Mental State Examination. This improvement was maintained even 45 days after the end of treatment, unlike the blood marker which returned to previous levels.
According to researchers, GM-CSF stimulates the production of immune cells in the bone marrow and brain and helps modulate inflammation. In animal models, the group had already observed a reversal of cognitive decline and a reduction in neuronal death after a few weeks of use.
Limitations and next steps
The authors emphasize that the results are still preliminary and do not allow us to say whether the drug is capable of lastingly reducing neuronal death linked to Alzheimer’s disease or normal aging. It is also unclear whether the benefits depend on continued use of the substance.
A second clinical trial, longer and with a larger number of participants with mild to moderate Alzheimer’s disease, is already underway. Until this data is analyzed and evaluated by regulatory agencies such as the FDA, researchers say sargramostim should not be used outside of already approved indications.
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