German researchers that studied  mice at different stages in life found that the older mice had some changes in the proteins regulating the genes in their brains, more specifically in a process called histone H4K12 acetylation, which showed that it slowed their ability to learn.
The discovery suggests that, changesover time in the way our genes are expressed may lead to impaired learning & memory. That sudden deregulation of H4K12 acetylation could be the early warning sign of a brain that is starting to decline.
Medicines that are known to help regulate such changes in the brain, known as histone deacetylase (HDAC) inhibitors, are at this time being developed by drug makers such as Merck & Co for the treatment of some cancers.
Andre Fischer of the European Neuroscience Institute in Goettingen, who has been involved in the mouse study, said he believes more targeted versions of these types of  medicines can be developed to treat dementia or Alzheimer's patients.
He told Reuters in a telephone interview,"We have finished the first phase, the pre-clinical phase, now it's time for the pharmaceutical industry to really try and drive it into application,"
Dementia affects some 35 million people around the globe and the number is expected to skyrocket as our populations continue to age. Experts have commented that this study and said it could have enormous implications.
Despite decades of research, doctors still only have very few weapons that are effective against Alzheimer's and Dementia, which are the most common forms of the brain-killing disease.
Alzheimer's International predicts that the number of sufferers of all types of Dementia will almost double every 20 years -- to 66 million in 2030 and more than 115 million in 2050, globally.
This drug has been found to restore the ability to learn in mice.
In this study, Fischer and his colleagues gave various learning tasks to groups of mice that were aged 3 months, 8 months and 16 months so they could see when age started to hamper their mental ability.
After they identified that the 16-month-old mice were the slowest learners, the studied the mice brains and found that their H4K12 acetylation function had completely failed.
The result is that the 16-month-old mice were unable to properly regulate levels of genes associated with memory and learning, the scientists found, the 16 month old mice were unable to use the same key brain functions as the younger mice did to learn things.
When scientists gave the mice a medication which restored their H4K12 acetylation which enabled the learning genes to be turned on again, the 16 month-old mice were able to learn and store memories again.
David Sweatt of the neurobiology department at the University of Alabama, Birmingham, in the U.S., said scientists "may now be one step closer to understanding age-related memory loss, and to developing a medication that might help boost memory".Studies in our lab and elsewhere strongly suggested that these drugs could potentially reverse aging-associated memory dysfunction."