Dementia patients' memories could be restored with injection that suppresses specific enzymes, study on mice suggests
Mice who had dementia had their memories restored after receiving an injection which managed to suppress specific enzymes, revealed a new study. Researchers have shared that the results could have groundbreaking implications for human beings.
According to researchers, the findings potentially make it possible to counter memory loss, which is a significant marker of the illness at a much later stage.
After they injected the rodents with dementia, the University of Buffalo scientists observed a "dramatic" shift in the rodents' recognition memory, spatial memory, and working memory. These findings were published in the journal 'Brain', as reported by Daily Mail.
The results suggest that focusing on gene changes which are caused by things other than DNA sequences, made it possible to reverse memory decline in an animal model of Alzheimer's.
Senior author Professor Zhen Yan from the University at Buffalo shared, "In this paper, we have not only identified the epigenetic factors that contribute to the memory loss, but also found ways to temporarily reverse them in an animal model of Alzheimer's Disease."
The experiment and research were conducted on mice which had genetic mutations for familial Alzheimer's which is when more than one member of the family has the disease. It was also conducted on post-mortem brain tissues from Alzheimer's patients.
The disease can come as a result of both genetic as well as environmental factors like aging. This combines to result in epigenetic changes which lead to gene expression changes though not much is known about how exactly that occurs.
According to professor Yan, the epigenetic changes in Alzheimer's tend to happen in the later stages when patients are unable to retain any new or recently learned information.
Yan added that one of the main reasons for this kind of a cognitive decline is the loss of the glutamate receptors which are the key to learning as well as short term memory.
Yan shared, "We found that in Alzheimer's disease, many subunits of glutamate receptors in the frontal cortex are downregulated, disrupting the excitatory signals, which impairs working memory." This loss of glutamate receptors is known as repressive histone modification which gets heightened in Alzheimer's.
Yan shared that the histone modifiers change the structure of chromatin which controls how genetic material has access to a cell's transcriptional machinery.
"This Alzheimer's-linked abnormal histone modification is what represses gene expression, diminishing glutamate receptors, which leads to loss of synaptic function and memory deficits. Our study not only reveals the correlation between epigenetic changes and Alzheimer's, but also found we can correct the cognitive dysfunction by targeting the epigenetic enzymes to restore glutamate receptors."
When the rodents were injected with compounds to inhibit the enzyme, the researchers saw a 'dramatic' shift in their memory. "We were quite surprised to see such dramatic cognitive improvement. At the same time, we saw the recovery of glutamate receptor expression and function in the frontal cortex," Yan added.