Wednesday , June 16 2021

Restore memory in mice with future Alzheimer's EFE



Image of the brain. University of Cambridge

"In this report, we have not only identified the epigenetic factors that contribute to the loss of memory, but we also find ways to temporarily transform them into an animal model," said lead author Zhen Yan, a researcher at the University.

The team found that by focusing on genetic changes caused by influences other than DNA sequences called epigenetics, it is possible to reverse memory impairment in mice.

The study was performed with mouse models with familial gene mutations of Alzheimer'swhere more than one family member suffers from the disease, and brain tissue from dead patients.

Epigenetic changes in Alzheimer's disease occur mainly when patients can not retain newcomers and show a marked cognitive decline.

The main reason for the cognitive decline is the loss of glutamate receptors, which are essential for learning and short-term memory,

"We have found that in Alzheimer's disease many glutamate receptors in the anterior crust are downward, interrupting the excitatory signals that affect memory," Yan said.

The researchers found that loss of glutamate receptors was the result of an epigenetic process known as repressive histone modification that was elevated in Alzheimer's patients.

Modification suppresses gene expression

According to the authors, this "abnormal" modification of histone associated with Alzheimer's disease is what inhibits gene expression by reducing glutamate receptors, resulting in loss of synaptic function and memory deficiency.

Once this dysfunction has been detected, they inject compounds designed to inhibit the enzyme that controls replication histone modification three times in diseased mice.

"When we give the animals Alzheimer's disease to this enzyme inhibitor, we have seen that cognitive function rescue is confirmed by the recognition of memory recognition, spatial memory and memory," said the researcher.

"We were quite surprised to see such a drastic cognitive improvement," Jan added.

At the same time, the authors confirm the recovery of the expression and function of the glutamate receptor in the anterior cortex.

These improvements continued for a week, so future research will focus on developing compounds that penetrate more effectively into the brain and are therefore more durable. EFEfuturo

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