Memory loss caused by Alzheimer's disease can be restored: study

New York: The researchers have developed a new approach that could one day reverse the memory loss caused by Alzheimer's disease.

The team, led by scientists at the University of Buffalo, discovered that by focusing on genetic modifications caused by influences other than DNA sequences, called epigenetics, it was possible to reverse the decline of memory in an animal model of Alzheimer's.

"We have not only identified the epigenetic factors that contribute to memory loss, but we have also found ways to temporarily reverse them in an animal model of Alzheimer's disease," said Zhen Yan, a professor at the University of California. University of Buffalo, United States.

The research, published in the journal Brain, was conducted on murine models carrying genetic mutations for familial Alzheimer's disease – where more than one family member has the disease – and on post-mortem brain tissue from patients with Alzheimer's disease.

Alzheimer's disease is caused by genetic and environmental risk factors, such as aging, that combine to cause epigenetic changes, resulting in changes in gene expression, but little is known about about how this happens.

Epigenetic changes in Alzheimer's disease occur mainly in the late stages, when patients are unable to retain the newly acquired information and exhibit the most dramatic cognitive decline, Yan said. The loss of glutamate receptors, essential for learning and short-term memory, is one of the leading causes of cognitive decline.

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.

"Our study not only reveals the correlation between epigenetic changes and Alzheimer's disease, but we have also found that we can correct cognitive dysfunction by targeting epigenetic enzymes to restore glutamate receptors," Yan said. Alzheimer's animals were injected three times with compounds designed to inhibit the enzyme that controls the repressive modification of the histone.

In animals receiving the enzyme inhibitor, cognitive function was restored and confirmed by evaluations of recognition memory, spatial memory and working memory.

The improvements lasted a week. Future research aims to develop compounds that penetrate the brain more efficiently and last longer, the researchers say.