Sleep plays a major role in consolidating memories, helping the brain stabilise and strengthen experiences from the day. A new study suggests the brain may decide which experiences are worth remembering before we even go to sleep.
Researchers writing in PLOS Biology studied how memories formed during the day are selected for later strengthening during sleep. They found that memories which benefited most from sleep were associated, at the time of learning, with slow wave brain activity [1].
You can think of it as an electrical bookmark. During the day, the brain may be placing a tag on certain experiences that says: come back to this later. Sleep then appears to do some of the filing.
The researchers found that people who showed more theta activity—a slow, rhythmic pattern of brain activity associated with learning and memory—also showed stronger coordination between two important patterns of brain activity during sleep: slow oscillations, which are large, regular rises and falls in the brain’s electrical activity linked to deep sleep, and sleep spindles, which are brief bursts of faster activity. This coordination has repeatedly been linked to memory consolidation—the process by which new, fragile memories are strengthened and connected to information we already know [2,3]. This is one reason sleep is not simply a period when the brain switches off.
The sleeping brain is active. It appears to replay, reorganise and strengthen information acquired while we were awake. Some memories become more durable. Others fade.
But there is an obvious complication if alcohol enters the picture. Sleep can only strengthen a memory that was encoded properly in the first place.
Memory formation depends heavily on glutamate, one of the brain’s major neurotransmitters. Glutamate acts through receptors in the hippocampus, a brain region crucial for forming episodic memories: what happened, where, with whom and in what order.
Alcohol interferes with this system. Acute alcohol consumption suppresses glutamate signalling [4,5]. At sufficiently high doses, this can produce a blackout. A blackout is not the same as passing out. Someone who passes out loses consciousness. Someone experiencing an alcohol blackout may still talk, walk, order another drink and interact with other people. What has failed is the recording system.
A blackout means that the hippocampus has not properly encoded experiences into a memory that can later be retrieved [4]. This explains something that can otherwise seem rather strange: a person may appear awake and functional at a party, yet the following morning have no memory of a conversation that lasted twenty minutes.
The memory was not hidden somewhere and then lost. In important respects, it was never properly made. That gives us an interesting contrast with the new sleep research.
The PLOS Biology study suggests that the brain may tag some experiences during waking life for further processing during sleep. Alcohol, especially at higher doses, can interfere earlier in the chain by disrupting the chemistry needed to build a stable memory trace in the first place. If sleep is when the brain files the day’s important experiences, alcohol can leave some of the folders empty.
There is another side to the glutamate story.
With heavy alcohol exposure, the brain adapts to alcohol’s persistent suppression of excitatory signalling. Glutamate activity can become upregulated to compensate. When alcohol is then removed, this increased activity is no longer being held down by alcohol, creating what researchers call a hyperglutamatergic state [6].
This is part of why a hangover can involve agitation, anxiety or ‘hangxiety’. So alcohol can disturb the same signalling system in two different directions: suppressing it during intoxication, then encouraging compensatory overactivity after repeated heavy use.
None of this means a glass of wine with dinner will erase your memories. Dose matters enormously. But it does explain why drinking heavily before bed is a particularly poor bargain for the brain. Alcohol can interfere with the creation of memories while you are awake and disrupt the sleep that helps consolidate them afterwards.
We tend to think of memory as something the brain simply stores. It is much more dynamic than that. First an experience has to be encoded. Then the brain has to decide that it matters. Then sleep helps strengthen and integrate it. Alcohol can interfere at more than one stage of that process.
Perhaps the most useful thing to remember is this: sleep cannot preserve a memory that alcohol prevented you from making.
—Professor David Nutt
References
[1] Denis, D., Chen, Z., Kaur, M., Clayden, B., Schreiner, T., & Cairney, S. A. “Theta oscillations tag episodic memories for sleep-dependent consolidation.” PLOS Biology, 24(8): e3003938, 2026.
[2] Diekelmann, S., & Born, J. “The memory function of sleep.” Nature Reviews Neuroscience, 11, 114–126, 2010.
[3] Schreiner, T., Petzka, M., Staudigl, T., & Staresina, B. P. “Endogenous memory reactivation during sleep in humans is clocked by slow oscillation-spindle complexes.” Nature Communications, 12:3112, 2021.
[4] Mennerick, S., & Izumi, Y. “Acute and Chronic Effects of Ethanol on Learning-Related Synaptic Plasticity.” Alcohol, 48(1), 1–17, 2014.
[5] Nutt, D. J. “Alcohol and the brain: pharmacological insights for psychiatrists.” British Journal of Psychiatry, 175, 114–119, 1999.
[6] Quelch, D., Lingford-Hughes, A., John, B., Nutt, D., Bradberry, S., & Roderique-Davies, G. “Promising strategies for the prevention of alcohol-related brain damage through optimised management of acute alcohol withdrawal: A focussed literature review.” Journal of Psychopharmacology, 2025.
