A clue to why memory deteriorates with age has been found by US researchers.
Experiments on mice suggested low levels of a protein in the brain may be responsible for memory loss.
It is hoped the discovery could lead to treatments to reverse forgetfulness, but it is a big leap from the mouse to a human brain.
The study, published in the journal Science Translational Medicine, said age-related memory loss was a separate condition to Alzheimer's disease.
The team at Columbia University Medical Centre started by analysing the brains of eight dead people, aged between 22 and 88, who had donated their organ for medical research.
They found 17 genes whose activity level differed with age. One contained instructions for making a protein called RbAp48, which became less active with time.
Memory boostYoung mice genetically engineered to have low RbAp48 levels performed as poorly as much older mice in memory tests.
Using a virus to boost RbAp48 in older mice appeared to reverse the decline and boosted their memory.
One of the researchers, Prof Eric Kandel, said: "The fact that we were able to reverse age-related memory loss in mice is very encouraging.
"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 with Alzheimer's, there is no significant loss of neurons."
It is still not know what impacted adjusting levels of RbAp48 in the far more complex human brain or even it if is possible to manipulate levels safely.
Dr Simon Ridley, from Alzheimer's Research UK, said: "While the findings may seem clear cut from these studies, in reality people reaching older age may well have a combination of changes happening in the brain - both age-related and those involved in the early stages of Alzheimer's.
"Separating early changes in Alzheimer's from age-related memory decline in the clinic still presents a challenge, but understanding more about the mechanisms of each process will drive progress in this area."
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