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NEW YORK (Reuters Health) – Mice with dementia have recovered memory after receiving an injection to inhibit an enzyme, a new study found.
The researchers say this discovery may have unprecedented effects on humans, which could reverse the memory loss that is characteristic of advanced dementia.
Shortly after the injection of demented rodents, researchers at the University of Buffalo saw a dramatic change in rodent memory, spatial memory, and working memory.
The findings, published in the journal Brain, suggest that by focusing on genetic changes caused by effects other than DNA sequences, memory degradation could be reversed in an animal model of the disease d & # 39; Alzheimer's.
"In this article, we have not only discovered genetic factors that contribute to memory loss, but also found ways to temporarily reverse them in an animal model of Alzheimer's disease," said Professor Chen Yan from the University of Buffalo.
Research has been conducted on rat models carrying genetic mutations of Alzheimer's disease in the family, where more than one family member has the disease, and models carrying brain tissue after the death of Alzheimer's disease.
The results showed that Alzheimer's disease, caused by genetic and environmental risk factors, such as aging, resulted in changes in gene expression, but little is known about how it happens.
Dr. Jan said that genetic changes in Alzheimer's disease occur mainly in the later stages of the disease, when patients are unable to retain the information they've recently learned and show dramatic cognitive decline. .
The loss of glutamate receptors, essential for learning and short-term memory, is the leading cause of cognitive decline.
"We found that in Alzheimer's disease, many subunits of the glutamate receptor are separated in the frontal cortex, thus disrupting the abnormal signal, thus weakening the working memory," Jan said.
The researchers discovered that the loss of glutamate receptors is the result of a genetic process called histone damage, which occurs in Alzheimer's disease.
They found in animal models studied and in post-mortem tissues of patients with Alzheimer's disease.
Yan explained that histone levels alter the composition of chromatin, which controls how the genetic material reaches the copier in the cell.
"An abnormal alteration of histones associated with Alzheimer's disease is what inhibits gene expression and reduces glutamate receptors, leading to memory deficits," said Professor Yan.
He explained that understanding this process revealed potential targets for drugs, including controlling or modifying the degradation of histones by enzymes.
Rodents have injected three times with Alzheimer's disease compounds designed to prevent the enzyme that controls histone modification. "We were very surprised to see this incredible improvement, before."
The improvements continued for a week, but future studies will focus on developing compounds that penetrate the brain more efficiently and last longer.
Source: Daily Mail
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