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Neurogenesis means making new neurons. Neuroplasticity is the broader ability of the brain and nervous system to adapt by changing cells, connections, and activity. Neurogenesis can be one contribution to plasticity, but most plastic changes do not require adding new neurons.
That distinction matters when interpreting claims about learning, memory, recovery after injury, or “boosting” brain growth. Neural plasticity is an established general property of the nervous system. How much new-neuron formation persists in the adult human hippocampus, and what it does, remains an active scientific debate.
Neurogenesis and neuroplasticity at a glance
| Question | Neurogenesis | Neuroplasticity |
|---|---|---|
| What changes? | New neurons are formed from precursor or stem-like cells, then mature and may integrate into circuits. | The nervous system adapts through changes to existing neurons, synapses, circuits, myelin, activity, and sometimes new neurons. |
| How broad is the term? | A specific biological process. | An umbrella term covering many forms of structural and functional adaptation. |
| Where is the adult-human question focused? | Especially the dentate gyrus of the hippocampus; widespread neuron production throughout the adult brain is not established. | Across the nervous system, including learning, rehabilitation, sensory adaptation, and responses to injury. |
| Evidence status | The extent and functional importance of adult human hippocampal neurogenesis remain disputed. | The capacity of neural systems to adapt is well established, although its limits vary by age, region, health, and type of change. |
| What can you infer? | Evidence of new neurons does not by itself prove a consumer intervention works. | Evidence that the brain is plastic does not show that it is producing new neurons. |
The National Institute on Deafness and Other Communication Disorders defines neural plasticity as the “ability of the brain and/or certain parts of the nervous system to adapt to new conditions, such as an injury.” NIDCD glossary
The two words therefore answer different questions. Neurogenesis asks, “Are additional neurons being generated?” Neuroplasticity asks, “How is the nervous system changing its organization or operation?” A study can demonstrate one without demonstrating the other.
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What neurogenesis means
Neurogenesis is the formation of neurons. In an adult-neurogenesis model, precursor cells divide, some daughter cells commit to a neuronal fate, and the resulting immature neurons mature. A subset may establish connections with neighboring cells and become part of an existing circuit. The term therefore describes more than a cell appearing: researchers also examine differentiation, survival, maturation, and functional integration.
Those stages are important because a precursor cell, an immature neuron, and a mature neuron integrated into a working circuit are not interchangeable findings. A tissue sample might contain a marker associated with cell division or neuronal immaturity, yet that observation alone may not establish how many cells survive, whether they become functional neurons, or what they contribute to behavior.
Developmental and adult neurogenesis are different questions
Neurogenesis is prominent during nervous-system development, when the brain is building much of its cellular architecture. Adult neurogenesis is a narrower question about whether precursor cells continue to generate neurons after development and, if so, in which regions and at what level. Evidence from one developmental stage or species cannot simply be transferred to another.
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In discussions of adult humans, the hippocampus—particularly the dentate gyrus—is the central focus. It is inaccurate to describe adults as routinely generating large numbers of neurons throughout the brain. Proposed adult sites are limited and may differ greatly between species. The adult and aging brain chapter in the NCBI Bookshelf likewise treats neurogenesis as a region- and age-dependent biological topic rather than a process occurring uniformly across all brain tissue. NCBI Bookshelf overview
Region matters functionally as well as anatomically. A finding in the dentate gyrus cannot be described as evidence that the cortex, spinal cord, or every brain region is continuously replacing neurons. It also does not show that a particular cognitive skill is being improved.
New neurons are not the same as stronger connections
A learner can improve because existing neurons change their synapses, firing patterns, or coordination. That is plasticity, even if no new neuron is added. Conversely, finding immature neurons would establish a cellular process, not automatically prove that memory, mood, or learning improved.
What neuroplasticity includes
Plasticity describes adaptation at several levels. A circuit can alter the strength of communication between existing cells; dendrites and axons can remodel; inhibitory and excitatory balance can shift; networks can change their activity patterns; and supporting cells and myelin can adjust how signals travel. After injury, neighboring or parallel networks may assume functions that were previously handled by damaged tissue. Practice, sensory experience, and rehabilitation can likewise change how circuits are organized and recruited.
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Functional plasticity
Functional plasticity is a change in how existing networks operate. Repeated practice can make a task more efficient, while rehabilitation can teach the nervous system to use alternative pathways. These changes can occur without neurogenesis. A person may show a different pattern of activation or improved coordination even when the number of neurons remains constant.
Structural plasticity
Structural plasticity involves physical changes such as synapse formation or elimination, altered dendritic branches, and remodeling of axons or myelin. It is still broader than neurogenesis because it modifies existing cellular hardware rather than necessarily creating new neurons. Structural changes can support functional changes, but a scan or behavioral test that suggests reorganization is not a direct count of newly generated cells.
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Plasticity after injury
Adaptation after stroke, trauma, or sensory loss illustrates why “plasticity” should not be treated as a synonym for neuron production. Recovery may involve uninjured regions changing their activity, new training strategies, altered connectivity, and compensation. The NIDCD definition explicitly uses injury as an example of a new condition to which the nervous system can adapt.
Plasticity can also be maladaptive. Reorganized circuits may contribute to persistent pain or other unwanted patterns, depending on the condition. Thus, “more plasticity” is not automatically the same as “better brain function”; the relevant question is what changed, in which direction, and with what outcome.
Is neurogenesis a type of neuroplasticity?
Usually, yes: neurogenesis can be considered one cellular route by which a nervous system changes, so it can contribute to plasticity. The relationship is one-way, however. Plasticity does not require neurogenesis. Changes in synapses, circuit activity, dendrites, axons, glia, or myelin are plastic changes even when the number of neurons stays constant.
A useful test is to ask what the claim measures. If it measures altered performance, connectivity, or synaptic strength, it is evidence of plasticity but not necessarily neurogenesis. If it measures newly formed and correctly identified neurons, it addresses neurogenesis, but it still does not establish the behavioral importance of those cells.
The terms can overlap in a paper without being synonyms. A review may discuss new neurons as one mechanism that changes circuit behavior, while another section describes plasticity caused by remodeling existing synapses. Reading the methods and the authors’ definition of each term prevents a broad conclusion from being drawn from a narrow measurement.
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Does neurogenesis happen in adult humans?
The responsible answer is that the extent and importance of adult human hippocampal neurogenesis are unresolved. Reviews have reported evidence both supporting persistence and questioning whether commonly used methods can demonstrate robust production in adults and older people.
Why the literature conflicts
A 2018 review by Gerd Kempermann, Jonas Frisén, and Fred H. Gage describes opposing findings and emphasizes that human tissue studies differ in how samples are collected and analyzed. Marker selection matters: a label used to identify dividing or immature cells may not be specific enough on its own. Postmortem delay also affects tissue quality and the detectability of markers. These methodological differences can produce apparently different results without one short summary resolving the dispute. Kempermann, Frisén and Gage, Human adult neurogenesis: evidence and remaining questions (2018)
Human studies are especially difficult because researchers cannot routinely observe the birth, maturation, and integration of individual neurons in a living person. Investigators must combine indirect methods, carefully preserved tissue, chemical markers, imaging or isotope approaches, and comparisons across ages. Each method answers a somewhat different question and has its own limitations. A disagreement may therefore reflect differences in sampling, timing, marker interpretation, or the biological heterogeneity of the people studied.
What the newer review says
A 2023 review by Gabriele Zanirati, Padmashri A. Shetty, and Ashok K. Shetty summarizes a substantial body of evidence supporting persistence of hippocampal neurogenesis during adulthood and aging, while stating that robust neurogenesis in the adult and aged human hippocampus has yet to be confirmed and calling for further validation. Zanirati, Shetty and Shetty (2023) review abstract
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These positions are not equivalent to “adult humans definitely make no neurons” or “the rate is known.” They mean that the field is still evaluating how much neurogenesis occurs, in which people and conditions, and whether the cells make a measurable functional contribution. Age, health, medication, environmental conditions, and the precise hippocampal subregion could all matter, but the current evidence does not justify assigning a settled rate to every adult.
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What about the often-quoted daily estimate?
The 2018 review discusses a carbon-14 study of 55 individuals that estimated approximately 700 new neurons were added per day in each dentate gyrus. That is a published estimate from a particular analysis, not an uncontested daily rate for every adult. It should not be presented as a routine measurement readers can apply to themselves, especially because other human studies and methods have produced conflicting conclusions.
Carbon-14 dating is useful for estimating the timing of cell birth over a person’s lifetime, but an estimate from that method still depends on assumptions, sample characteristics, and the biological interpretation of the measured signal. Quoting the number without those qualifications turns a debated population estimate into a false personal promise.
Why animal findings cannot be applied directly to people
Rodent studies have made adult neurogenesis experimentally useful: investigators can label cells, manipulate their development, and test effects on circuits or behavior. Such work can suggest mechanisms involving learning, memory, stress, mood, or pattern separation. It does not, by itself, establish that the same process occurs at the same scale in humans or that changing it will improve a person’s health.
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1Fix the driver behind crashes, sound loss and screen glitches2Repair Windows errors before they cause bigger problems3Scan for outdated or missing drivers - takes under a minuteSpecies differ in hippocampal organization, lifespan, environment, baseline cell production, and experimental conditions. A result in a controlled animal model is therefore a hypothesis about human biology, not a guarantee about a supplement, exercise plan, brain-training device, or treatment. Even within an animal study, an effect may depend on when cells were born, how long they survived, and which circuit was tested.
Animal evidence remains valuable for identifying mechanisms and generating testable questions. The translation step requires human studies that measure a relevant biological signal and a meaningful outcome, with appropriate controls and safety monitoring. Until that chain is demonstrated, language such as “may influence” is more accurate than “proven to increase.”
What neurogenesis and plasticity might have to do with learning and memory
Plasticity is directly relevant to learning because acquiring a skill changes how neural networks respond and coordinate. Synaptic strengthening and weakening, altered inhibition, and network reorganization can all support learning without adding neurons. Practice can make responses more efficient, recruit different pathways, or change the timing between regions.
New neurons, if and where they are produced in adult humans, could provide another form of flexibility. In animal models, immature neurons have distinctive properties and may influence how similar experiences are separated or encoded. Human reviews discuss possible links to memory and other functions, but the evidence does not establish a simple rule such as “more neurogenesis equals better memory.” A biological process can be real yet have effects that depend on timing, location, cell survival, and the surrounding circuit.
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Consequently, a memory test, attention score, or brain-activity scan can indicate a functional change without identifying its cellular cause. Conversely, a cellular observation can be biologically interesting without producing a detectable improvement on a particular test. Strong conclusions require both kinds of evidence to align.
Can you increase neurogenesis?
No consumer method has been established as a guaranteed way to increase new-neuron formation in a person. The reviewed human evidence does not justify recommending a supplement, device, or commercial brain-training product for that purpose.
How to read lifestyle claims
Exercise, enrichment, sleep, stress, and other conditions are studied in animal models and sometimes associated with markers of brain plasticity in people. An association with improved performance or altered brain activity is not the same as a demonstrated increase in human neurogenesis. When a claim cites an animal result, ask whether human neuron formation was actually measured, whether the study was randomized, and whether the outcome was a validated health benefit.
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Also check whether the study measured plasticity broadly rather than neurogenesis specifically. Changes in connectivity, task performance, or a blood-based marker may be useful findings, but none is automatically a count of new hippocampal neurons. Marketing often collapses these distinct outcomes into the single phrase “brain growth.”
What is reasonable to do anyway
Activities that support general health—regular physical activity appropriate to your condition, adequate sleep, medical care, and sustained learning—can be sensible for overall brain function and may engage plasticity. They should not be advertised or understood as proven ways to manufacture a specified number of new hippocampal neurons. Anyone with a medical condition should discuss exercise, sleep problems, or supplements with a qualified clinician rather than relying on a neurogenesis claim.
Common misconceptions
“Plasticity means the brain can do anything.”
Plasticity is capacity for adaptation, not unlimited repair. Age, injury severity, disease, practice, motivation, sensory input, and available pathways constrain what changes are possible.
“If the brain learns, new neurons must have formed.”
Learning can be supported by changes in existing circuits. Improved performance is not a neurogenesis measurement.
“Adult neurogenesis is either proven everywhere or completely absent.”
The human debate concerns extent, persistence, methods, and function, especially in the hippocampus. It does not support either extreme statement.
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Plasticity is broader than neuron production. A claim about attention, reaction time, connectivity, or training does not demonstrate new neurons, and a claim about new neurons requires credible human evidence.
“A single marker settles the question.”
No isolated label should be treated as proof of a complete neurogenesis process. Researchers need to consider marker specificity, tissue handling, cell maturity, survival, and integration, along with appropriate controls.
Independent reader supportYour contribution helps us test, update, and keep practical guides available for everyone.How to evaluate a claim about new neurons
- Identify the species. A mouse or rat result is not a human intervention result.
- Check the brain region. Adult-human discussion usually concerns the hippocampal dentate gyrus, not the whole brain.
- Look for direct measures. Behavioral improvement or a scan of activity is not equivalent to counting newly formed, identified neurons.
- Read the methods. Marker specificity, tissue handling, postmortem delay, sample size, and controls affect interpretation.
- Ask what stage was measured. Evidence of dividing precursors is different from evidence of mature neurons that survived and integrated into a circuit.
- Separate mechanism from outcome. Even confirmed cell formation would not automatically prove better memory, mood, or recovery.
- Check the wording. “May contribute,” “associated with,” and “under investigation” are materially different from “proven to increase.”
- Look for independent replication. A single study or dramatic headline should not outweigh later work with different methods and samples.
Why the distinction matters in medicine and technology
Neuroplasticity is a useful framework for designing rehabilitation and learning: clinicians can repeatedly train a task, adjust sensory feedback, and build strategies that recruit available networks. It also helps explain why recovery is variable and why practice must be specific and sustained.
Neurogenesis is a narrower biological question that may eventually inform therapies, but translating a cellular finding into a safe treatment requires evidence at several stages: reproducible human biology, a controllable mechanism, demonstrated benefit, known risks, and appropriate clinical trials. Until those links are established, “supports plasticity” should not be treated as proof of neuron growth.
The distinction also protects patients from overstated technology claims. A device that changes stimulation, connectivity, or task performance may be studying plasticity without generating neurons. Conversely, a laboratory method that detects a cell marker may have no demonstrated therapeutic effect. The biological mechanism, the measured outcome, and the safety profile must each be described separately.
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Bottom line: different terms, connected biology
Neurogenesis is the formation and possible integration of new neurons. Neuroplasticity is the nervous system’s broader ability to adapt, often by modifying cells and connections that already exist. Neurogenesis can fit inside that larger concept, but plasticity does not imply neuron production.
For adults, especially humans, the amount and functional role of hippocampal neurogenesis remain unsettled. Reviews from 2018 and 2023 describe both supporting evidence and important methodological limits. Treat animal findings and commercial “brain growth” claims as hypotheses or marketing unless rigorous human evidence demonstrates the specific effect being promised.
Frequently Asked Questions
Is neurogenesis the same as neuroplasticity?
No. Neurogenesis is the specific formation of new neurons. Neuroplasticity is the broader ability of the nervous system to adapt through changes in synapses, activity, dendrites, axons, myelin, supporting cells, circuits, and sometimes new neurons.
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Researchers continue to debate the extent and functional importance of adult human hippocampal neurogenesis, especially in the dentate gyrus. Reviews report evidence supporting persistence as well as methodological limits, so neither a known universal rate nor complete absence is established.
Can learning occur without making new neurons?
Yes. Learning can result from changes in synaptic strength, network activity, inhibition, connectivity, and other forms of plasticity that leave the number of neurons unchanged.
Is the estimate of 700 new neurons per day a proven personal rate?
No. The 2018 review discusses a carbon-14 study of 55 people that estimated about 700 new neurons per day in each dentate gyrus. It is a debated estimate from one analysis, not a routine measurement that applies to every adult.
Can a supplement or brain-training device increase neurogenesis?
No consumer product has been established as a guaranteed way to increase new-neuron formation in people. Animal findings and broad plasticity measures do not prove that a supplement or device creates functional human neurons.
How should I interpret a claim that an intervention “boosts plasticity”?
Ask what was actually measured. Changes in performance, connectivity, or brain activity may indicate plasticity, but they do not by themselves demonstrate neurogenesis. Look for direct human evidence, appropriate controls, and clear wording about uncertainty.
The Bottom Line
Neurogenesis is new-neuron formation; neuroplasticity is the nervous system’s wider capacity to adapt. Neurogenesis may contribute to plasticity, but plasticity commonly occurs through changes in existing cells and connections. Adult human hippocampal neurogenesis remains an open, methodologically difficult question, and no consumer product is proven to increase it.
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