The question in that French title sounds almost like the premise of a science fiction novel: can we really grow new brain cells as adults? Maybe you remember childhood lessons about the brain being “hard-wired” and neurons being permanently lost when they die. Over the last few decades, neuroscience has pushed back on that idea and replaced it with a far more dynamic picture. Adult neurogenesis — the birth of new neurons in the mature brain — is now a lively field that mixes rigorous evidence, heated debate, promising implications for health, and a fair amount of complexity. In this article I’ll walk you through the history, the evidence, the controversies, and the practical stakes, step by step, in an accessible conversational style. Grab a cup of coffee, and let’s explore whether we can truly create new neurons at adult ages.

Why this question matters

This isn’t just an academic argument. If new neurons can be generated and integrated into adult circuits, that opens doors for understanding learning, memory, mood regulation, recovery from injury, and even neurodegenerative disease. If, on the other hand, adult neurogenesis is rare or absent in humans, that changes how we think about therapies and recovery. For patients, families, clinicians and researchers the outcome changes priorities: should we focus on protecting existing neurons, stimulating neurogenesis, or enhancing plasticity in other ways?

A short history: from dogma to discovery

For most of the twentieth century, the reigning dogma in neuroscience was that neurons do not divide after development — the brain had a fixed number of cells. That started to change in the 1960s and 1970s when researchers found evidence of dividing cells in the adult brains of rodents. Stronger, more reproducible findings accumulated in the 1980s and 1990s, including demonstration that new neurons are born in adult rodents’ hippocampus and olfactory bulb and that they can integrate functionally into neural circuits.

Once the phenomenon was established in animals, the big question became: does the same thing happen in adult humans? Over the last 20 years evidence has accumulated for and against, and the debate reached public attention with high-profile studies using different methods and reaching different conclusions.

Where adult neurogenesis has been seen: regions and species

Not all parts of the brain are equally likely to generate new neurons in adulthood. Two regions are central to the discussion:

• Subgranular zone (SGZ) of the hippocampal dentate gyrus — widely reported in rodents and many other species; linked to learning, memory and mood.
• Subventricular zone (SVZ) — in rodents it supplies new neurons migrating to the olfactory bulb; in humans this SVZ-to-olfactory-bulb pathway appears much reduced or different.

Different species exhibit different patterns. Rodents show robust adult neurogenesis in both the hippocampus and olfactory bulb. Non-human primates show hippocampal neurogenesis but at lower levels than rodents, and the olfactory pathway seems diminished. Human studies are the most contentious, particularly regarding the extent of hippocampal neurogenesis across the lifespan.

Quick comparative table

How scientists detect new neurons

Detecting neurogenesis is technically challenging. Researchers use several complementary methods, each with strengths and limitations. Understanding these helps explain why studies sometimes disagree.

Major experimental approaches

• Thymidine analogs (e.g., BrdU): These get incorporated into the DNA of dividing cells, allowing later identification of newborn cells. Highly informative but requires controlled administration (often in animals) and raises ethical problems in humans.
• Endogenous markers (e.g., doublecortin, DCX; Ki67): Proteins expressed transiently by immature neurons or dividing cells. Useful in post-mortem tissue, but expression windows can be short and markers sometimes label cells that won’t become mature neurons.
• Carbon-14 dating: A clever approach exploiting nuclear bomb tests that raised atmospheric C-14 levels during the mid-20th century. Cells born after those tests incorporated more C-14; measuring C-14 in neuronal DNA can estimate neuron “birthdates.” This method provided influential evidence for adult-born human neurons in some studies.
• Lineage tracing and transgenic labeling in animals: Genetic methods that indelibly tag dividing progenitors and follow their fate over time. Powerful in animals but not possible in humans for ethical reasons.
• Single-cell RNA sequencing and molecular profiling: Newer and increasingly informative, these methods can identify cells at transcriptional stages consistent with immature neurons.

Each method has caveats. For example, DCX expression can be downregulated during long maturation periods, BrdU labeling requires prior injection, and carbon-14 provides population-level timing but not detailed location or function. The combination of methods strengthens confidence when results converge.

What the strongest human evidence says

Let’s look at some of the headline human studies and their findings so you can see how the debate emerged.

• Positive evidence: Several studies using markers like DCX, BrdU (in rare clinical contexts), and carbon-14 found immature neurons in the adult human hippocampus, suggesting ongoing neurogenesis, although at a declining rate with age. These studies linked neurogenesis to learning and mood regulation in ways analogous to animal models.
• Negative evidence: Other high-profile analyses, examining carefully preserved post-mortem tissue from adult humans, reported very low or negligible markers of new neurons in older adults, concluding that hippocampal neurogenesis in humans sharply declines and may be rare or absent in adulthood.

Why the differences? They come down to technical issues (tissue preservation, time between death and fixation of tissue), marker choice, age and health of donors, and interpretive frameworks. Some studies analyzed hippocampi from surgical resections with immediate fixation, while others used post-mortem samples with longer delays that can degrade protein markers like DCX. Different labs also counted cells differently and used different thresholds for what qualifies as a new neuron. The field continues to refine methods and reconcile findings.

Timeline and maturation: new neurons are not instantly functional

Even when adult-born neurons are generated, they follow a multi-week to multi-month maturation trajectory. In rodents, immature neurons are highly plastic and may temporarily support certain kinds of learning. In primates and humans, maturation could take longer, potentially months to years before full integration. That means the functional consequences of newborn neurons depend not only on birth but on survival, maturation, synaptic integration, and activity-driven plasticity.

Functional roles proposed for adult neurogenesis

Why would the brain keep making neurons in adulthood? Researchers have proposed several complementary roles, especially for hippocampal neurogenesis:

• Pattern separation: New neurons may help distinguish similar experiences or contexts, reducing memory interference.
• Mood regulation: In animal models, reduced hippocampal neurogenesis is associated with depressive-like behavior and antidepressants can increase neurogenesis; this suggests a link but not a simple cause–effect relationship.
• Memory flexibility: New neurons might support the updating or forgetting of old memories, promoting behavioral adaptability.
• Network repair and plasticity: After injury, some neurogenic processes could aid rewiring, although this is limited.

Importantly, functional links are stronger in animal models than in humans. Translating roles observed in rodents to human cognition remains an active research challenge.

What affects adult neurogenesis?

Across species, environmental, physiological and molecular factors influence rates of new neuron birth, survival and integration. Some factors promote neurogenesis; others suppress it.

Positive influences

• Physical exercise — especially aerobic exercise like running — robustly increases hippocampal neurogenesis in rodents and associates with better cognitive outcomes in humans.
• Environmental enrichment — complex, stimulating environments boost neurogenesis and learning in animals.
• Learning itself can enhance survival of newborn neurons when tasks are appropriate in timing and difficulty.
• Some drugs, including certain antidepressants (e.g., SSRIs), are associated with increased neurogenesis in animal studies.

Negative influences

• Stress and elevated glucocorticoids — chronic stress reduces neurogenesis in animal models and is linked to mood disorders.
• Inflammation and aging — both reduce cell proliferation and survival.
• Poor diet, sleep loss, and certain toxins — also detrimental.

These relationships suggest that lifestyle and environment can modulate neurogenic capacity — if that capacity exists significantly in humans.

Neurogenesis and mental health: potential and limits

One of the most enticing implications of adult neurogenesis is for mental health. Studies in animals suggest a link between neurogenesis and depression-like behaviors, and that boosting neurogenesis can be part of how antidepressants work. That doesn’t mean depressed humans lack new neurons or that simply increasing neurogenesis is a magic cure.

Mental health is multifactorial. Adult-born neurons, if present and functional, may contribute to mood regulation among many other mechanisms — neurotransmitter systems, synaptic plasticity, circuit dynamics, and psychosocial factors all matter. Clinical interventions that also target inflammation, stress resilience, sleep, exercise, and cognitive engagement likely influence brain health via multiple pathways, neurogenesis among them.

Therapeutic approaches: where might new neurons help?

If neurogenesis can be safely and effectively enhanced in humans, where might that help?

• Depression and mood disorders — as an adjunct to other therapies.
• Cognitive aging — preserving or restoring hippocampal function to support memory.
• Recovery after brain injury — limited regenerative capacity might be supported by stimulating progenitors or transplant strategies.
• Neurodegenerative disease — theoretically valuable, but diseases like Alzheimer’s involve widespread network dysfunction and protein pathology that make simple neuron replacement insufficient.

Real-world translation is challenging. Stimulating neurogenesis indiscriminately could have unintended consequences — improper integration could disrupt circuits or increase excitability. Any therapeutic strategy must balance promotion of healthy integration, control of inflammation, and avoidance of oncogenic risk (uncontrolled cell proliferation).

Open questions and controversies

Even after decades of research, adult neurogenesis remains a field with major unresolved questions. Here are the principal controversies:

1. Extent in humans: Do adult humans meaningfully produce functional new neurons in the hippocampus? Some data say yes; some say negligible. Ongoing work is clarifying methods and sampling to settle this.
2. Functional importance: If neurogenesis is present, how essential is it for human cognition and mood? Correlational and causal links in humans are hard to prove.
3. Maturation timelines: Are newly born human neurons slower to mature than in rodents, and if so, what are the implications for timing of interventions?
4. Species differences: How well can we generalize from rodents to humans? Behavioral repertoires and cortical expansion in humans complicate direct translation.
5. Therapeutic feasibility: Can we safely and effectively harness neurogenesis (or substitute forms of plasticity) for therapy?

These open questions make the field exciting and a little messy — the hallmark of active science where methods and ideas are evolving.

Illustrative experimental designs to resolve debates

Scientists propose and pursue several experimental strategies to reduce ambiguity:

• Standardized tissue-handling protocols for post-mortem human hippocampus to reduce variability in marker detection.
• Multiplexed marker strategies combining DCX, NeuN, Ki67, and lineage-specific RNAs to better classify immature neurons versus non-neuronal cells.
• In vivo imaging proxies — though direct imaging of newborn neurons in humans remains technically out of reach, advances in MRI and PET tracers might offer indirect evidence of neurogenic activity in the future.
• Single-cell multi-omics on human tissue to determine transcriptional signatures of cells at different maturation stages.

Practical takeaways right now

Regardless of the final verdict on the exact level of adult neurogenesis in humans, several practical conclusions are reasonable and actionable:

• Lifestyle matters: Exercise, a stimulating environment, good sleep, healthy diet, and stress management support brain plasticity broadly, and likely support neurogenic processes where they exist.
• Antidepressant effects are multifactorial: Neurogenesis may be one mechanism among many; treatment decisions should remain evidence-based and individualized.
• Prevention and protection of existing neurons is crucial: Reducing vascular risk factors, controlling inflammation, and protecting against head trauma remain top priorities for brain health.
• Be skeptical of simplistic claims: Promises of “brain cell regeneration” from supplements or quick fixes are premature without rigorous clinical evidence.

Case studies and landmark experiments

To bring things to life, here are a few landmark experiments and what they taught us:

• Rodent running studies: Mice allowed voluntary running show dramatic increases in hippocampal cell proliferation and improved performance on spatial tasks. These studies linked behavior, environment, and neurogenesis.
• Antidepressant–neurogenesis link: Experiments where neurogenesis was selectively blocked in rodents showed that certain behavioral effects of antidepressants were lost, supporting a mechanistic role for neurogenesis in some responses.
• Carbon-14 dating in humans: By measuring C-14 in hippocampal neurons, researchers inferred ongoing neuron generation in adult humans, providing population-level birthdating evidence that adult neurogenesis does occur.
• Contradictory post-mortem analyses: Other teams examining hippocampal tissue reported minimal DCX-positive cells in adults, challenging earlier interpretations and highlighting methodological sensitivities.

Future directions: where the field is heading

Exciting developments are on the horizon. Advances in single-cell technologies, spatial transcriptomics, and molecular imaging promise to refine our understanding of cell types and maturation states in the human hippocampus. Better post-mortem and clinical sampling standards will reduce variability among studies. Novel PET tracers could one day allow non-invasive measurement of neurogenesis-related molecular activity in living humans. Finally, clinical trials informed by a deeper molecular understanding may test whether targeted interventions (lifestyle, pharmacological, or bioengineering approaches) can safely promote beneficial plasticity.

At the same time, brain repair strategies may adopt complementary angles: rather than relying solely on generating new neurons, therapies might focus on enhancing synaptic plasticity, rewiring surviving networks, modulating inflammation, or using stem-cell-derived transplants with careful integration controls. The field stands at the intersection of curiosity-driven basic science and translational urgency.

A simple checklist for evaluating claims about adult neurogenesis

• What species is the claim based on? Rodent data are helpful but not definitive for humans.
• What methods were used? Look for converging approaches (molecular markers, birthdating, single-cell sequencing).
• What is the age and health status of the subjects or donor tissues?
• Are functional outcomes demonstrated, or only molecular signatures?
• Is the claim overstated relative to the data? Be cautious about clinical extrapolation.

Common misconceptions

Given the complexity, several misconceptions circulate:

• “Neurogenesis means you can regrow your brain.” Not exactly — even if neurogenesis exists, regenerating complex circuits and reversing neurodegenerative disease is far more complex.
• “If you exercise, you’ll get new neurons immediately.” Exercise supports conditions that favor neurogenesis but does not guarantee immediate or large-scale neuron birth and integration.
• “All neurons are the same.” Newborn neurons go through unique maturation stages and might have distinct roles compared with embryonically born neurons.

Ethical and societal considerations

As research progresses, ethical questions emerge. If interventions can increase neurogenesis (or mimic its effects), who should have access? Could boosting plasticity have cognitive or behavioral side effects that alter identity or risk? Is it ethical to pursue aggressive regenerative strategies in patients with severe neurodegeneration when outcomes are uncertain? Thoughtful dialogue among scientists, clinicians, ethicists, and the public will be necessary.

Summary of evidence and balanced interpretation

To summarize where the science stands: animal models provide strong, reproducible evidence for adult neurogenesis in the hippocampus and olfactory system, and that these new neurons can affect behavior. In humans, the evidence is mixed but suggestive: many studies indicate hippocampal neurogenesis occurs at least into early adulthood, and possibly at lower levels across the lifespan, while other rigorous studies find very little signal in older adults. Discrepancies largely reflect methodological differences and the difficulty of working with human tissue. The functional relevance in humans is plausible but not definitively proven. Thus, the cautious conclusion is that adult neurogenesis is a real biological phenomenon in many species and likely contributes to human brain plasticity, but its magnitude and exact roles in adult human cognition and disease remain active areas of research.

Conclusion

Yes, the brain is more dynamic than the old “fixed” model suggested: adult neurogenesis is a verified phenomenon in many animals and likely contributes to learning, memory, and mood in species that employ it robustly. In humans the picture is nuanced — evidence supports some level of hippocampal neuron birth in adulthood, especially earlier in life, but rates seem to decline with age and vary by individual and health status. Methodological differences have fueled debate, and the field is steadily refining tools to resolve open questions. Meanwhile, practical steps that promote brain health — exercise, cognitive stimulation, good sleep, stress management and healthy living — remain wise, whether they act partly by supporting neurogenesis or by strengthening other forms of plasticity. The promise of harnessing neuron birth for therapies is real but will require careful, evidence-based advances to move from exciting possibility to safe clinical reality.