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Neurons are not the only cells implicated in memory-related processes. Mouse studies point to memory-linked astrocytes and chemical signaling at neuronal connections, while a laboratory study found that cultured human cells responded differently to spaced and simultaneous chemical pulses. These findings add possible pieces to the picture—but they do not reveal a single missing mechanism or explain how human memories are stored as a whole.
What do these studies mean by memory?
The word “memory” refers to different outcomes in these experiments. In mice, researchers measured recall-related freezing behavior or changes associated with memory formation. In cultured cells, they measured activation of a gene associated with memory—not recollection or conscious experience. Those results are related questions, but they are not interchangeable evidence.
| Research strand | Cells and setting | What researchers examined | What the result supports |
|---|---|---|---|
| Astrocyte ensembles | Astrocytes in mice undergoing fear conditioning | Learning-associated cells, neuronal connections and recall-related behavior | Astrocytes can participate in memory-circuit activity and retrieval in these mice |
| Spaced chemical pulses | Human nerve-tissue-derived and kidney-derived cells grown in a laboratory | A memory-associated gene reporter after spaced or simultaneous chemical stimulation | Stimulus timing can shape a molecular response in cultured cells |
| Lipid signaling | Neurons and their connections in mice | DDHD2, myristic acid and protein changes associated with memory formation | A lipid-signaling pathway contributes to memory-related changes in mice |
How might astrocytes take part in memory circuits?
Astrocytes are non-neuronal cells in the brain. In a 2024 Nature study described by Baylor College of Medicine on 6 November 2024, researchers used fear conditioning in mice and developed tools to identify astrocytes associated with learning. A subset expressed c-Fos during learning and was physically close to neuronal engram cells—neurons associated with a particular experience.
The team reported functional coupling between the learning-associated astrocytes and their corresponding neuronal ensemble: activating the astrocytes stimulated synaptic activity or communication in that neuronal group. In a different context, activating the astrocyte ensemble could prompt freezing behavior, a response used to assess recall in the experiments.
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The researchers also examined NFIA, a protein whose levels rose in astrocytes activated during learning. Preventing NFIA production in those astrocytes suppressed recall of the associated memory, while the mice could still recall other memories. This points to a role for astrocyte ensembles in specific memory-circuit function and retrieval. It does not show that astrocytes independently hold a complete memory, and the findings described here are from mice, not people.
Can cells outside the brain respond to learning-like signals?
A 2024 study published in Nature Communications, “The massed-spaced learning effect in non-neural human cells” (DOI 10.1038/s41467-024-53922-x), tested two types of human cells grown in a laboratory: cells derived from nerve tissue and cells derived from kidney tissue. Researchers exposed the cells to chemical-signal patterns modeled on neurotransmitter activity. The cells had also been engineered to produce a glowing protein when a memory-associated gene was active.
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When researchers delivered the chemical signals in spaced pulses, the gene response was stronger and lasted longer than when the same treatment was delivered all at once. The result suggests that stimulus timing can affect a learning-associated molecular response in cultured cells. It does not demonstrate that kidney or nerve-tissue cells have autobiographical memories, consciousness or the ability to recall experiences.
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The study was led by Nikolay V. Kukushkin, identified in a Medical Xpress report using NYU-provided material dated 8 November 2024 as a clinical associate professor of life science at NYU Liberal Studies and a research fellow at NYU’s Center for Neural Science. The finding concerns cells in a dish; it is not evidence that chemical pulses make a person learn or remember better.
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What role could fat signaling play at neuronal connections?
A separate line of mouse research concerns lipid chemistry at the points where neurons connect. In a University of Queensland report dated 18 June 2025, researchers led by Professor Frédéric Meunier described how the enzyme DDHD2 releases myristic acid, a saturated fatty acid. The acid chemically tags proteins at neuronal connections. Blocking this signaling pathway in mice prevented protein changes associated with memory formation.
An earlier University of Queensland report, dated 6 February 2024, discussed PLA1 and STXBP1 in the formation and targeting of saturated fatty acids during neuronal communication. In mouse models lacking the PLA1 gene, levels of saturated free fatty acids were lower before memory impairment appeared. The researchers interpreted those results as evidence that the enzyme and fatty acids play a role in memory acquisition.
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Together, these reports identify molecular pathways for further study; they do not show that eating particular fats improves memory. Nor do they establish a treatment. The University of Queensland said clinical applications remained a long way off in its 2025 report.
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Do these findings reveal the missing piece of memory?
No single study here completes an explanation of memory. The Baylor work concerns astrocytes linked with neuronal ensembles and recall-related behavior in mice. The cell-culture study measures a gene response to stimulus timing, not an organism remembering an event. The Queensland reports examine lipid pathways and memory-related changes in mice. They address distinct parts of the problem, and the cited sources do not establish how much any of them contributes to everyday human memory or whether the mechanisms work together.
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The useful shift is narrower: memory research need not focus only on neurons. Support cells and chemical signaling may also matter, depending on the process being studied. Whether these findings lead to a safe way to treat memory disorders—or to control memory—has not been demonstrated. As University of Queensland co-author Nathalie Dehorter cautioned in the 2025 report, clinical applications are still a long way off, and attempts to control memory would raise ethical questions.
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