Researchers from Columbia University Medical Centre have found that age-related memory loss is linked to a deficiency of a protein called RbAp48.
You walk into the kitchen. You know you went to get something, but can't remember what it is. You go back to the lounge, only to remember when your derrière brushes the couch - if you remember at all.
This begins to happen more frequently as you get older. You get worried, and start researching Alzheimer's disease.
Researchers from Columbia University Medical Centre have found that age-related memory loss is linked to a deficiency of a protein called RbAp48 in the hippocampus region of the brain, noting that it is a "significant contributor" to memory loss.
The good news is that this deficiency is treatable, and is separate from Alzheimer's.
The research, which was published in Science Translational Medicine on August 28, centres on the hippocampus, an area in the brain involved in memory formation.Located near the brain stem, the hippocampus looks like a sea horse, which is where its name [Greek for "coiled horse"] comes from.
"It was initially thought that age-related memory loss is an early manifestation of Alzheimer's, but mounting evidence suggests that it is a distinct process that affects the dentate gyrus, a subregion of the hippocampus," the university said.
Team leader and Nobel laureate Eric Kandel, co-director of Columbia's Mortimer B Zuckerman Mind Brain Behaviour Institute, said: "Our study provides compelling evidence that age-related memory loss is a syndrome in its own right, apart from Alzheimer's."
The researchers examined post-mortem brain cells from the dentate gyruses of eight brain-disease-free people between 33 and 88 years old.
They compared them with cells from the entorhinal cortex, which links to the hippocampus but is not affected by ageing.
They analysed 17 genes which might contribute to ageing and found that the expression of the RbAp48 gene steadily declined with ageing.
"The first question was whether RbAp48 is down regulated [the expression of the gene is reduced] in aged mice," said Dr Elias Pavlopoulos, research scientist at the centre.
"And, indeed, that turned out to be the case."
When RbAp48 was inhibited in younger mice they exhibited the same memory loss as old mice. This was determined through object recognition and maze tests.
When the expression of RbAp48 was reactivated, the young mice's memory returned to normal, the university said.
This memory revitalisation also occurred when RbAp48 expression was increased in the dentate gyrus of older mice.
"We were astonished that not only did this improve the mice's performance on the memory tests, but their performance was comparable to that of young mice," Pavlopoulos said.
However, Kandel noted that there may be other changes in the dentate gyrus that contribute to age-related memory loss.
"But at the very least, it shows that this protein is a major factor, and it speaks to the fact that age-related memory loss is due to a functional change in neurons of some sort. Unlike Alzheimer's, there is no significant loss of neurons," he said.
Globally, there are millions of people suffering from brain diseases, including Alzheimer's, and this number is set to increase as improvements in medicine en-able people to live longer.
Alzheimer's, which is thought to be linked to plaque on the brain, is the most common form of dementia, and there is no cure.