The words, ‘losing your mind’ can send a chill down anyone’s spine. Even temporary loss of memory such as that word which escapes us can result in frustration. The concern is strong enough to translate across to fiction where it has become an effective plot device: perhaps someone is given a spiked drink, leaving a hole in their evening and lack of a critical alibi. Other story lines use retrograde amnesia like the successful Bourne Identity series. Whatever the incident, we all know that memories can slip our mind, but just what causes memory loss?
Back in 2006, Todd Sacktor, a neurologist and pharmacologist, was credited with a discovery considered to be one of the most important for that year, although his work stretches back into the 1990s. What was the discovery? Sacktor found a chemical that completely wipes memory, and this told us a lot about how memory works in the brain. He called it ZIP, or in long form, zeta inhibitory peptide.
This tiny protein interferes with long-term memory, including getting rid of fears, spatial- and muscle-based memory, taste-aversion and other sensory-based memories. Although initial experiments focused on mice rather than getting into the ethical quicksand of human experimentation, we all appear to have the same memory-based brain chemistry. Basically, we are talking about a cascade. ZIP stops the action of another protein, PKMzeta (for short), which is needed to lock memory into place.
How does this work? The 'plasticity' of the brain allows nerves to activate, swell and change so that they become a preferred pathway. But this preference needs to be supported, including each time we remember. Why? If our brain did not become plastic again when we remember things, we might never change what we know or unlearn things. The upshot is that consolidating and retaining memories requires the full support of the nerve cells involved. If their capacity to fuel the activation is interrupted then the memory disappears. It all seems rather fragile really.
But concern about ZIP is something of a fantasy because it needs to be injected straight into the brain. Far more concerning are the medications in everyday life which interrupt the chemical cascade.
Drugs that shut down noradrenaline (released during stress and fight or flight), such as propranolol, a beta blocker used in treating high blood pressure, can affect memory consolidation.
Medication that messes with the neurotransmitter acetylcholine (anticholinergic drugs) is also of concern. A study published in BMJ in 2018 links use to increased incidence of dementia for many classes. Each drug is given a score from 1 to 3 for its Anticholinergic Cognitive Burden (ACB), with 3 having the highest effect. Medications include antihistamines, antispasmodics, antidepressants and many more. Lists and calculators are available. Although it appears possible to reduce the risk with strategic prescription.
Even statin therapy is now recognised as a danger to memory, upping the risk of impairment 4-fold within the first 30 days. Again though, there are alternative drugs or approaches available to discuss with medical practitioners.
Importantly, no one should modify a medical regime or stop taking medications without first consulting a medical practitioner.
Such drugs are not all bad news though. One such drug class, after tweaking to improve its targeting, has been found to act in the opposite way, bringing back memory for age or stress-damaged brains. This drug is currently heading towards clinical trials so we may see it available in a few years.
There is also a physical path to memory loss. Everyone has heard about the dangers of a blow to the head, which rips apart delicate links in the brain or causes fluid to build up and crush regions. But recent research reported by David Celermajer, of the Heart Research Institute in Australia, suggests this danger may be a lot closer to home than previously considered.
The culprit can be our own blood pressure. When this is high and coupled with a stiffening of neck arteries, so that they no longer absorb the shock waves, brain tissue may suffer. Plaques in the brain, seen in many cases of dementia and associated memory loss, may be a response to such damage, rather than a primary cause. Thankfully, a solution is under investigation which aims to return elasticity to the vessel walls, although we will have to wait a few years for it to pass clinical trials.
So, what causes memory loss? Could it be as vague as anything that interrupts the fragile chemical or physical machinery of long-term potentiation? If so, perhaps a better question is, what can we do to protect this machinery? The list is fairly well known. Assessing medication for risk, providing a good diet, reducing chronic stress (see previous blog on coping with stress), challenging the brain through use, and keeping blood pressure under control are all thought to be important for maintaining a healthy memory.
Till next time – B.W. Cribb