New research has unlocked some reasons why memories weaken as we age – and more intriguingly, it suggests that the process can be reversed.
According to a study published in the journal Nature, a large part of this decline is due to the chemical environment of neurons in the prefrontal cortex (PFC), an area of the frontal lobe that plays a large part in maintaining working memory – the ability to keep an idea, sound, or image “in mind” while we’re not directly perceiving it in our environment.
As we age, a chemical called cyclic adenosine monophosphate (cAMP), which normally is involved in intracellular signaling, piles up in the prefrontal cortex to the point that it actually slows the firing of a certain type of neurons, known as ‘DELAY’ neurons, which help maintain working memory.
But by introducing cAMP-blocking chemicals into the prefrontal cortices of macaques, a team led by Amy Arnsten of Yale’s Kavli Institute for Neuroscience were able to bring back these neurons’ youthful firing speeds:
PFC persistent firing with advancing age … can be rescued by restoring an optimal neurochemical environment. … Recordings showed an age-related decline in the firing rate of DELAY neurons, [but] the memory-related firing of aged DELAY neurons was partially restored to more youthful levels by inhibiting cAMP signalling.
This is still very early research, but the results are encouraging: inhibiting cAMP – or blocking the ion channels it uses – may become a promising treatment for people suffering from forgetfulness:
One of the compounds that enhanced neuronal firing was guanfacine, a medication that is already approved for treating hypertension in adults, and prefrontal deficits in children, suggesting that it may be helpful in the elderly as well.
Though neuroscientists – and plenty of other people – have known for centuries that age leads to a decline in various types of memory, the neurochemical basis for this decline remained poorly understood until very recently.
However, as scientists began to understand the connections between the PFC and working memory decline, they realized that the problem was closely linked with DELAY neurons’ firing rate – DELAY neurons in younger subjects fired more quickly during working memory tasks, while those in older subjects were much slower, which made them far less efficient in transmitting their messages.
This study marks the first definite evidence of a specific molecular problem underlying this slowness, and also the first strong indication that an effective treatment may be possible. The only caution, Arnsten points out, is that the treatment is unlikely to be effective for those suffering from Alzheimer’s or other forms of senile dementia, where neurological damage is often much more severe and widespread.
Even so, Arnsten says the treatment is already preparing to move to the clinical trial stage, meaning that aging patients may soon have a second shot at youth – at least as far as memory is concerned.