Most people have experienced the unsettling moment after a sleepless night when an important name, face, or appointment simply vanishes from memory.
A new study suggests that what feels like forgetting may not be forgetting at all. The memories are not erased — they are hidden somewhere in the brain, inaccessible but intact. Animal experiments have shown that both light stimulation and drug treatment can unlock them.
The findings, published in the June 2026 issue of Science Advances, come from a research team led by professor Robbert Havekes at the University of Groningen in the Netherlands. The team examined how sleep deprivation affects long-term social recognition memory and identified the neuroscientific mechanisms that could reverse the damage.
Sleep loss makes the brain forget social bonds
The research team focused on social memory — the ability to recognize specific individuals and maintain relationships with them. This function is essential to social life, and its breakdown is a hallmark of conditions such as Alzheimer's disease.
In the experiment, mice were allowed to interact with an unfamiliar mouse for 10 minutes. Half were then kept awake for six hours. When all the mice were reintroduced to the same individual 24 hours later, the two groups behaved very differently.
The well-rested mice recognized the mouse they had met the previous day and spent less time investigating it. The sleep-deprived mice explored it just as intently as before, as though encountering it for the first time. On the surface, the memory appeared to be gone.
To test whether the memory had truly been erased, the research team ran two separate experiments aimed at recovering it.
Switching memory cells back on with light
The clusters of neurons that store a specific experience are known as engrams, or memory cells. The concept holds that cells activated together during an experience become jointly responsible for encoding that memory.
The research team tagged the memory cells active during the original social encounter with a fluorescent marker, then used optogenetics — a technique that uses light to stimulate specific neurons — to reactivate those cells later.
When the memory cells of sleep-deprived mice were reactivated with light, the mice recognized the individual they had met the day before. The memory had not been erased; it had been stored in the brain all along, simply beyond reach.
The results grew more striking still. A single pulse of light stimulation was enough: when the mice were tested six days later, they still recognized the individual.
The researchers offered this analogy: the contents of a drawer were always there, but the key had been lost. The light stimulation forced the drawer open once, and after that the mice could open it on their own.
An existing drug unlocks the same blocked memories
The research team also tested a pharmacological approach that could be applied in clinical settings.
The drug in question was roflumilast, already approved by the US Food and Drug Administration for treatment of chronic obstructive pulmonary disease. It works by preventing the breakdown of a signaling molecule inside cells that is required for memory formation.
Administering the drug to sleep-deprived mice prevented memory impairment from developing. Even in mice that had already lost the memory, a dose given 30 minutes before a recall test restored it temporarily.
The research team interpreted the result as the drug reopening the neural pathway that sleep deprivation had blocked.
Distinct memories are stored separately
The study also revealed that when mice encountered two different individuals on consecutive days in the same space, the brain stored each memory separately.
The research team labeled the memory cells activated during each encounter with different colored fluorescent markers. The two sets of cells overlapped by only about 30 percent, and that proportion held regardless of whether the mice had been sleep-deprived.
When only the memory cells from the first encounter were stimulated with light, the mice recognized only the first individual. Selective retrieval of a specific memory was possible. Sleep deprivation did not affect the initial formation of memory cells.
New clues for treating sleep disorders and dementia
The pattern of memories appearing lost while in fact remaining inaccessible has been reported in animal models of early-stage Alzheimer's disease as well, suggesting the phenomenon may extend beyond sleep deprivation.
Because roflumilast is already FDA-approved for use in humans, the findings open the door to potential applications in treating memory decline caused by sleep disorders or aging.
"This could become a new medical clue for treating memory decline caused by sleep disorders, aging, and related conditions," the research team said.
However, the team acknowledged a limitation: the experiments were conducted exclusively on male mice, and further validation will be needed before the findings can be applied to humans.
Reference
DOI: 10.1126/sciadv.adu9805
Adithya Sarma et al., "Restoring access to long-term social recognition memories disrupted by sleep deprivation." Sci. Adv. 12, eadu9805 (2026).
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