Scientists have identified new genes capable of modulating the toxicity of beta-amyloid protein, associated with the development of Alzheimer’s.
Based on molecular biology, genomics and bioinformatics techniques, 238 protective or activating genes against neurodegenerative disease were identified.
Among them, the Surf4 gene stands out, which is involved in the control of intracellular calcium and, by increasing the toxicity of the protein, contributes to the disease.
The results were published in the journal International Journal of Molecular Sciences.
Every year, 10 million new cases of dementia are diagnosed worldwide, according to estimates by the World Health Organization (WHO). Of these, 7 out of 10 are due to Alzheimer’s.
The disease develops with advancing age, when the beta-amyloid protein – released by neurons – begins to unfold and aggregate within the brain, eventually having a harmful effect on the organ. There is currently no effective treatment to prevent this protein-related process.
In the study, the researchers identified, in yeast – a type of fungus, 238 genes, similar to those of humans, that regulate Alzheimer’s disease. Of these, 81 increased beta-amyloid protein toxicity and 157 were shown to be protective against this cellular toxicity.
Analysis details
Through a bioinformatics analysis, it was discovered that most of the 238 genes identified were involved in three mechanisms: activity of mitochondria, which are structures related to cellular respiration; translation of proteins and regulation of calcium present in cells.
According to the study, in this last process, where most of the identified genes are involved, the Surf4 gene stands out, whose protein regulates the entry of calcium into the cell and has resulted in increased toxicity of beta-amyloid, contributing to the Alzheimer’s.
“Calcium is one of the most important messengers that transfer information from the outside to the inside of cells. It is involved in almost all cellular functions. That is why when the Surf4 protein is overexpressed, which prevents the entry of calcium and aborts the cellular processes that depend on it, the neurons cannot function and become very sensitive to amyloid toxicity”, explains the study coordinator, Francisco J Muñoz, in a statement.
The identification of Surf4 as an accelerator of damage caused by beta-amyloid protein toxicity opens the door to the discovery of new therapeutic targets that act precisely on the reduction of amyloid toxicity in patients with neurodegenerative disease.
To identify the genes that regulate Alzheimer’s disease, a collection of 5,154 samples with genetic modifications of yeast was analyzed. Saccharomyces cerevisiae – that share high similarity with the human genome – in which the expression of a gene has been knocked out.
Each of these ‘mutants’ was crossed with other yeasts of the same strain that overexpress the human beta-amyloid protein. Then, the viability of these cells was analyzed over several days. In addition, an algorithm analysis was performed to identify other genes related to the regulation of dementia-associated protein toxicity.
The study had the participation of specialists from Pompeu Fabra University and the Barcelona Institute of Science and Technology, from Spain, and from Koç University, from Turkey.
Source: CNN Brasil
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