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A study has shown that a new approach to Alzheimer's Disease (AD) could eventually help address memory loss, characteristic of the disease at its advanced stages.
The study was published in the journal Brain.
The research, led by the University of Buffalo, revealed that by focusing on genetic modifications caused by influences other than DNA sequences, called epigenetic, it was possible to reverse the decline of memory in an animal model of AD.
Speaking of which, the main author Zhen Yan said: "In this article, we have not only identified the epigenetic factors that contribute to memory loss, we have also found ways to temporarily reverse them in a model. MA animal. "
The research was conducted on murine models carrying genetic mutations for familial AD – where more than one family member has the disease – and on post-mortem brain tissue from AD patients.
Yan added, "We found that in Alzheimer's disease, many subunits of glutamate receptors in the frontal cortex are negatively regulated, disrupting excitatory signals, thereby impairing working memory."
The researchers discovered that the loss of glutamate receptors is the result of an epigenetic process called repressive modification of the histone, which is high in Alzheimer's disease. They found it in both the animal models studied and in the post-mortem tissues of AD patients.
Yan explained that histone modifiers alter the structure of chromatin, which controls the access of genetic material to the transcription mechanism of a cell.
"This alteration of the abnormal histone-related AD is what represses gene expression, decreasing glutamate receptors, resulting in loss of synaptic function and memory deficits," he said. said Yan.
Understand that this process has revealed potential drug targets because the repressive modification of histone is controlled or catalyzed by enzymes, she said.
"Our study not only reveals the correlation between epigenetic changes and AD, but we also found that we can correct cognitive dysfunction by targeting epigenetic enzymes to restore glutamate receptors," said Yan.
The study showed three AD animals injected three times with compounds designed to inhibit the enzyme that controls the repressive modification of histone.
After receiving enzyme inhibitors, the researchers found that cognitive function had been saved. It has been confirmed by evaluations of the recognition memory, the spatial memory and the working memory. "At the same time, we witnessed the recovery of expression and function of glutamate receptors in the frontal cortex," said Yan.
The improvements lasted a week. Future studies will focus on developing compounds that penetrate the brain more efficiently and last longer, said Yan.
(This story has not been changed by Business Standard staff and is generated automatically from a syndicated feed.)
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