Brain image University of Cambridge
"In this report we have not only identified the epigenetic factors that contribute to the memory, but we also find ways to reverse them into animal models," said author Zhen Yan, a researcher at the university.
The team found that focusing on the genetic changes caused by influences, apart from the sequences of DNA, called epigenetics, it was possible to reverse the memory of the mice.
The research was done with mouse models with family mutations of Alzheimer's family, where more than one member of a family suffers from disease and with brain fabrics of dead human patients.
The epigenetic changes of Alzheimer's disease occur mainly when patients can not retain new learning information and show accentuated news.
A key reason for the decisive decision is the loss of glutamous receptors, which are essential for the learning and the short-term memory.
"We found that in Alzheimer's disease, many subunites of glutamous receptors in the frontal cruise regulate down, interrupting the shocking signals that effect the memory," said Yan.
The researchers have discovered that the loss of glutamous receptors is the result of an epigenetic process known as a repressive histone modification that is raised in patients with Alzheimer's.
The modification suppresses genetic expression
According to the authors, this "abnormal" modification of histone linked to Alzheimer's is what suppresses genetic expression, decreasing glutamous receptacles, which leads to loss of synapt function and memory deficits.
After this disfiguration was detected, they injected compounds designed to stop the enzyme that controls the repressive histone modification three times in the sick mice.
"When we have given the animals of Alzheimer's disease this inhibitor of enzymes, we have seen the rescue of the cognitive function confirmed by the assessment of memory recognition, space memory and work memory," said the researcher.
"We were completely surprised to see such a drastic improvement improvement," added Yan.
At the same time, the authors confirmed the recovery of the expression and function of the glutamate receptor in the frontal cruise.
These improvements lasted for a week, so future studies will focus on developing compounds that more effectively penetrate the brain and, therefore, are more permanent. Efefuture