Neurogenesis

Neurogenesis is the process by which neural stem cells generate new neurons. In mammalian development, neurogenesis is widespread and accounts for the production of nearly all neurons in the central nervous system before birth. In adult mammals, neurogenesis is largely restricted to two specific regions of the brain: the subgranular zone of the dentate gyrus of the hippocampus (producing granule neurons that integrate into hippocampal memory circuits) and the subventricular zone lining the lateral ventricles (producing neurons that migrate to the olfactory bulb in rodents, with much-reduced activity in humans). Adult neurogenesis in rodents and non-human primates is well-established; whether it persists at functionally significant levels in adult humans has been one of the most actively contested questions in neuroscience over the past three decades.

The first direct evidence for adult human hippocampal neurogenesis came from Eriksson and colleagues (1998) in Nature Medicine. They examined postmortem brain tissue from cancer patients who had received bromodeoxyuridine (BrdU, a thymidine analog) for tumor staging during life. BrdU is incorporated into the DNA of dividing cells, so any cell that divided during the treatment window could be identified later by immunostaining. Eriksson and colleagues found BrdU-positive neurons in the dentate gyrus of adult humans (oldest subject 72 years), establishing that new neurons can be generated in the adult human hippocampus. Subsequent work by Spalding and colleagues (2013) at the Karolinska Institutet used carbon-14 dating (exploiting the atmospheric 14C spike from 1950s-60s nuclear weapons testing) to estimate that approximately 700 new neurons are added to the human hippocampus per day, with modest decline during aging.

The contemporary literature is more complicated. In 2018, two high-profile papers reached opposite conclusions about whether adult hippocampal neurogenesis persists into late adulthood. Boldrini and colleagues (2018) in Cell Stem Cell reported that neurogenesis persists throughout life into the eighth decade. Sorrells and colleagues (2018) in Nature reported the opposite: that adult hippocampal neurogenesis drops to undetectable levels by adolescence. The dispute reflected methodological differences in tissue processing, marker selection (DCX/PSA-NCAM), and quantification approaches. Subsequent work including Moreno-Jiménez et al. (2019) in Nature Medicine, the Dumitru et al. (2025) Frisén-lab paper in Science using single-nucleus RNA sequencing with machine learning, and the Lazarov et al. (2026) multiomic paper in Nature has substantially shifted the field toward the persists-into-adulthood view, while ongoing methodological discussions remain.

Adult neurogenesis matters at three substantive levels, though the strength of the evidence varies across them.

For hippocampal memory function. In rodents, adult hippocampal neurogenesis is required for several specific memory operations, particularly pattern separation (distinguishing similar but distinct experiences) and certain forms of contextual learning. Newly generated dentate granule cells have distinctive electrophysiological properties for a limited window after their birth that make them especially well-suited for these functions. The functional role of adult neurogenesis in human memory is harder to establish directly, since the experimental manipulations possible in rodents (genetic ablation of neurogenesis, irradiation to suppress proliferation) cannot be performed in humans. The 2026 Lazarov et al. Nature paper found a distinctive neurogenesis-related “resilience signature” in SuperAgers (adults 80+ with memory performance matching adults in their 50s-60s), suggesting that preserved neurogenesis may contribute to maintained cognitive function in healthy aging, though sample sizes were modest and the causal direction is not yet established.

For Alzheimer's disease and other neurodegenerative conditions. The hippocampal dentate gyrus is one of the earliest-affected regions in Alzheimer's disease, and several studies have reported reductions in markers of adult neurogenesis in AD relative to age-matched controls. Moreno-Jiménez and colleagues (2019) reported a sharp decline in adult hippocampal neurogenesis in AD compared to neurologically healthy subjects of similar age. The 2026 Lazarov et al. work identified disease-specific alterations in chromatin accessibility in neurogenic cell populations from individuals with preclinical AD, with more pronounced changes in established AD. Whether reduced neurogenesis contributes to AD pathology or is a downstream consequence of it remains an open question, but the AD-neurogenesis link is one of the more consistent findings in the contested literature.

For mood disorders and antidepressant mechanism. A substantial rodent literature implicates adult hippocampal neurogenesis in mood regulation and in the mechanism of action of common antidepressants. Chronic stress reduces hippocampal neurogenesis in rodents, while antidepressant treatment (SSRIs, ECT, exercise) increases it. The translation of these findings to humans has been complicated by the dispute over whether adult neurogenesis occurs at sufficient levels to have functional significance. Boldrini and colleagues' 2009 work in Neuropsychopharmacology reported increased neural progenitor cells in human hippocampus following antidepressant treatment, supporting the rodent-to-human translation. The mood-neurogenesis link remains an active research area, with the contemporary picture more strongly supporting an association than the 2018 controversy initially suggested.

The dogma that the adult mammalian brain produces no new neurons was orthodox neuroscience for most of the 20th century, traceable to Santiago Ramón y Cajal's influential 1928 statement that “in adult centres the nerve paths are something fixed, ended, immutable. Everything may die, nothing may be regenerated.” This view persisted for decades despite scattered evidence to the contrary.

The first systematic challenge came from Joseph Altman's work in the early 1960s using tritiated thymidine to label dividing cells in rat brains. Altman and Das (1965) reported new neurons in the adult rat dentate gyrus, but the finding was largely ignored or dismissed by the broader field for two decades. The work of Fernando Nottebohm in the 1980s on song-learning birds, demonstrating extensive seasonal neurogenesis tied to behavioral function, contributed to gradually reopening the question. By the early 1990s, Elizabeth Gould's work and others had re-established adult hippocampal neurogenesis as a real phenomenon in rodents.

The pivotal human study was Eriksson, Perfilieva, Björk-Eriksson, Alborn, Nordborg, Peterson, and Gage (1998) in Nature Medicine. The methodological opportunity was unusual: cancer patients in Sweden had been given BrdU injections during life for tumor-staging purposes, and after their deaths the researchers were able to examine postmortem brain tissue for BrdU-positive neurons. The finding of BrdU+ NeuN+ cells in the dentate gyrus of adult humans (the oldest subject was 72 years) established that adult human neurogenesis was not merely a rodent phenomenon. The study was limited (five brains, ethical impossibility of replication using the same BrdU approach in healthy adults), but it opened the field.

A decade and a half later, Spalding, Bergmann, Alkass, and colleagues (2013) at the Karolinska Institutet provided a quantitative estimate using a different methodology. The 1950s and 1960s nuclear weapons tests produced an atmospheric spike in carbon-14, which was incorporated into the DNA of cells dividing during that period. By measuring 14C concentrations in genomic DNA isolated from postmortem hippocampal neurons across 55 individuals, the Frisén lab inferred birth dates for those neurons. The result: substantial neurogenesis throughout adult life, with approximately 700 new neurons added per day, and only a modest decline during aging. The Spalding study used a quantitative, independent methodology and is widely regarded as the strongest evidence for adult human hippocampal neurogenesis prior to the contemporary single-cell sequencing work.

The field then encountered a substantial controversy. In early 2018, Sorrells, Paredes, Cebrian-Silla, and colleagues (2018) from the Alvarez-Buylla lab at UCSF published a paper in Nature titled “Human hippocampal neurogenesis drops sharply in children to undetectable levels in adults.” They examined N=17 postmortem control samples and N=12 surgical resection samples from epilepsy patients (ages 18-77) and reported that young neurons were not detected in the dentate gyrus of adults. The proposed mechanism was that humans differ from rodents in that the subgranular neurogenic niche fails to coalesce during development, and that putative “adult neurogenesis” in earlier reports reflected methodological artifacts. The paper got substantial media attention as evidence that adult human neurogenesis was effectively absent.

Less than a month later, Boldrini, Fulmore, Tartt, and colleagues (2018) at Columbia published a paper in Cell Stem Cell titled “Human hippocampal neurogenesis persists throughout aging.” They examined hippocampal tissue from N=28 individuals (ages 14-79) using stereological quantification methods and reported preserved neurogenesis into the eighth decade of life. The two papers used overlapping markers (DCX, PSA-NCAM) but reached opposite conclusions. The dispute reflected methodological differences in tissue processing (postmortem interval, fixation), sample populations (epilepsy patients in Sorrells; control populations in Boldrini), marker validation, and quantitative analysis. Subsequent letters in Cell Stem Cell (Paredes et al., Tartt et al.) clarified the methodological positions of both groups without resolving the dispute.

The contemporary picture has been substantially shaped by more recent work. Moreno-Jiménez and colleagues (2019) in Nature Medicine reported abundant neurogenesis in neurologically healthy adults up to the ninth decade of life, with sharp decline in Alzheimer's disease. Tobin and colleagues (2019) in Cell Stem Cell independently reported neurogenesis persistence in aged adults and AD patients. The Frisén lab returned with Dumitru et al. (2025) in Science, using single-nucleus RNA sequencing with Ki67 antibody staining and machine learning algorithms to identify proliferating neural progenitor cells in adult human hippocampus. Most recently, Lazarov and colleagues (2026) in Nature used multiomic single-cell sequencing (snRNA-seq + snATAC-seq) on 355,997 nuclei from young adults, healthy agers, preclinical AD, AD patients, and SuperAgers, identifying neural stem cells, neuroblasts, and immature granule neurons across cohorts. The current preponderance of evidence supports the persists-into-adulthood view, though methodological debates continue and the precise rate of neurogenesis in adult humans remains uncertain.

Adult hippocampal neurogenesis proceeds through identifiable stages, well-characterized in rodents and increasingly mapped in humans through single-cell transcriptomic studies.

1. Neural stem cells (NSCs). Quiescent or slowly proliferating cells in the subgranular zone of the dentate gyrus with stem-cell properties: self-renewal, multipotency, and capacity for asymmetric division. NSCs express markers including GFAP, nestin, and Sox2. They give rise to transit-amplifying progenitors (Type-2 cells) that proliferate rapidly. NSCs typically remain quiescent for most of adulthood; specific signals (exercise, antidepressants, environmental enrichment in rodents) increase their activation.
2. Intermediate neural progenitors (INPs) and neuroblasts. Transit-amplifying cells that expand the population of committed neural precursors. They express markers including doublecortin (DCX) and PSA-NCAM in immature forms. This is the population that the 2018 Boldrini and Sorrells papers attempted to quantify with different conclusions; subsequent single-cell sequencing studies have provided more direct molecular characterization.
3. Immature granule neurons. Newly generated neurons that have begun to extend dendrites and integrate into the dentate gyrus circuit. They express DCX during this phase (typically 1-3 weeks post-birth in rodents). Immature granule neurons have distinctive electrophysiological properties — lower threshold for activation, higher excitability, and reduced GABAergic inhibition — that make them well-suited for pattern separation functions.
4. Mature granule neurons. Fully integrated dentate granule cells with mature morphology, synaptic connections, and electrophysiological properties indistinguishable from developmentally generated granule cells. The maturation process from neuroblast to mature granule cell takes approximately 4-8 weeks in rodents, with the exact timeline in humans not fully established.

The functional integration of adult-born neurons into hippocampal circuits is the critical question for their behavioral significance. In rodents, adult-born neurons during their immature phase make distinctive contributions to dentate gyrus computation: they support pattern separation (distinguishing similar but distinct events), contribute to memory updating and flexibility, and may be involved in the temporal organization of experience. Adult-born neurons that fail to integrate are eliminated by apoptosis — a substantial fraction of newly generated cells do not survive to maturation.

The regulators of adult neurogenesis include intrinsic and extrinsic factors that have been extensively mapped in rodents and are increasingly characterized in humans. Positive regulators include exercise (one of the most robust enhancers of rodent neurogenesis), environmental enrichment, learning, antidepressants (SSRIs, electroconvulsive therapy), and several neurotrophic factors (BDNF, IGF-1, VEGF). Negative regulators include chronic stress (via glucocorticoid effects on NSCs), aging, sleep deprivation, inflammation, and certain drugs of abuse. The 2026 Lazarov et al. Nature paper identified specific transcription factor networks (eRegulons) that distinguish neurogenesis in young adults, healthy agers, preclinical AD, AD, and SuperAgers, including BDNF and CALB1 upregulation in immature neurons from SuperAgers as part of a putative resilience signature.

Adult neurogenesis is measured through several complementary methods, each with characteristic strengths and limitations. Methodological choice has been at the center of the contemporary disputes about whether adult human neurogenesis exists.

Thymidine analog incorporation (BrdU, IdU, CldU). The gold-standard rodent method, also used in the foundational Eriksson et al. (1998) human study. Dividing cells incorporate the analog into DNA, which can be detected immunohistochemically. Limitations: requires injection of the analog during life (only possible in humans in rare clinical contexts), and detects only cells that divided during the labeling window. Not feasible for routine adult human neurogenesis studies.

Carbon-14 dating. The Frisén lab's method, used in Spalding et al. (2013). Exploits the atmospheric 14C spike from 1950s-60s nuclear weapons tests, which was incorporated into the DNA of cells dividing during that period. By measuring 14C concentrations in genomic DNA from isolated nuclei of specific cell types, researchers can infer when those cells were born. Strengths: quantitative, retrospective, works on archival postmortem tissue, independent of cell-marker assumptions. Limitations: depends on accurate atmospheric 14C modeling, requires large pooled samples, gives population-level rather than individual-cell information.

Immunohistochemistry with neurogenic markers (DCX, PSA-NCAM, Ki67, Sox2, nestin). The most widely used method for human postmortem studies. Different markers identify different stages of the neurogenic lineage. DCX (doublecortin) marks immature neurons; PSA-NCAM marks migrating and immature neurons; Ki67 marks proliferating cells; Sox2 marks neural stem cells. The 2018 Boldrini and Sorrells papers both used DCX/PSA-NCAM but reached opposite conclusions, illustrating that marker-based methods are sensitive to tissue processing (postmortem interval, fixation duration), marker validation, and quantification approach. The marker-based dispute drove much of the 2018-2024 controversy.

Single-nucleus RNA sequencing (snRNA-seq). The contemporary state-of-the-art method. Sequences the transcriptomes of individual cell nuclei isolated from postmortem tissue, allowing identification of cell types by gene expression signature rather than single-marker immunostaining. Dumitru et al. (2025) combined snRNA-seq with Ki67 antibody staining and machine learning algorithms to identify proliferating neural progenitors in adult hippocampus. The 2026 Lazarov et al. Nature paper combined snRNA-seq with snATAC-seq (chromatin accessibility) for multiomic characterization. These methods have substantially clarified the field by providing molecular signatures less ambiguous than single-marker immunostaining.

Magnetic resonance spectroscopy (MRS). Indirect in vivo method using a metabolite signal proposed to reflect neural progenitor cell activity. Manganas and colleagues (2007) identified a 1.28 ppm lipid signal as a putative biomarker. The method has not become a standard for human neurogenesis quantification due to specificity concerns and the difficulty of validating MRS-based estimates against histological methods.

What the LBL Brain Lab tools capture. The Brain Age Index and Cognitive Reserve Estimator use cognitive performance and risk-factor inputs to estimate biological brain age and cognitive reserve respectively, drawing on the broader cognitive aging literature including neurogenesis-related research. These tools do not directly measure neurogenesis (which would require neuroimaging or postmortem analysis) but the cognitive domains they assess overlap with hippocampally-supported functions including episodic memory and pattern separation. For users specifically interested in neurogenesis research, contemporary measurement remains an active research area rather than a routine clinical assessment.

Neurogenesis sits at the intersection of developmental neuroscience, stem cell biology, and aging research. Several adjacent concepts are commonly conflated.

• vs. neuroplasticity (broader concept). Neuroplasticity is the brain's capacity for structural and functional change in response to experience, learning, injury, or training. Neurogenesis is one specific form of neuroplasticity — the generation of entirely new neurons. Other forms of plasticity include synaptic strengthening and weakening, dendritic remodeling, axonal sprouting, and myelination changes, none of which require new neurons. Adult neurogenesis is one of several mechanisms underlying neuroplasticity, not the whole of it.
• vs. gliogenesis. Gliogenesis is the generation of new glial cells (astrocytes, oligodendrocytes, microglia). Adult gliogenesis occurs throughout the brain, including regions where neurogenesis is absent. Oligodendrogenesis (production of myelinating glia) is particularly active in adulthood and contributes to white-matter changes with learning and aging. Adult gliogenesis is much less contested than adult neurogenesis and is documented across many brain regions.
• vs. embryonic and developmental neurogenesis. The vast majority of neurons in the adult mammalian brain were generated during embryonic and early postnatal development. Developmental neurogenesis is widespread, robust, and uncontested. The contested question is specifically about whether neurogenesis continues at meaningful levels into adulthood and aging — not whether neurogenesis happens at all in mammals.
• vs. neuroregeneration. Neuroregeneration refers to the regrowth of damaged neurons or neural tissue after injury. The adult mammalian brain has very limited neuroregenerative capacity outside the neurogenic niches; damaged cortical neurons are not replaced. Some species (zebrafish, salamanders) have substantially greater neuroregenerative capacity, sometimes proposed as targets for biomimetic therapeutic strategies. Adult neurogenesis is constitutive (ongoing under normal conditions), while neuroregeneration is reactive (in response to injury); the two operate via partially distinct mechanisms.
• vs. cognitive reserve. Cognitive reserve is the capacity to maintain cognitive function despite age-related or pathological brain changes. Preserved hippocampal neurogenesis is one of several factors that may contribute to cognitive reserve, particularly for hippocampal memory functions in aging. The Lazarov et al. 2026 SuperAger work suggests that distinctive neurogenesis signatures may underlie some cases of exceptional cognitive aging, though the causal direction is not yet established.
• vs. brain age. Brain age refers to biological brain age relative to chronological age, often estimated from neuroimaging features. Adult neurogenesis is one of many cellular processes that change with brain aging; reduced hippocampal volume and structural integrity in older adults may partly reflect reduced neurogenesis along with other aging-related changes. Brain-age estimation does not directly measure neurogenesis but the two concepts intersect at the hippocampal aging literature.
• vs. default mode network. The DMN includes the medial temporal lobe (hippocampus and parahippocampal regions) as one of its subsystems. Hippocampal neurogenesis may support some DMN-related functions (autobiographical memory, future thinking, mental scene construction) but the relationship is mediated by hippocampal contribution to those cognitive operations rather than direct neurogenesis-DMN coupling. The two concepts operate at different levels of analysis.

Example 1 — The marathon training year

A 47-year-old software engineer takes up marathon training after a decade of sedentary work. Over six months he progresses from 2-mile walk-runs to consistent 15-mile training runs and competes in his first marathon. He reports subjectively that his concentration and memory feel sharper, his sleep is better, and his mood is more stable. Some popular sources would attribute these benefits to “exercise-induced neurogenesis,” pointing to the rodent literature showing that voluntary running substantially increases hippocampal neurogenesis.

The honest scientific picture is that exercise is one of the most robust enhancers of adult hippocampal neurogenesis in rodents, with multiple studies showing 2-3x increases in newly generated dentate granule cells in runners compared to sedentary controls. Human translation is harder to establish directly. Cross-sectional studies show that fit middle-aged adults have larger hippocampal volumes than unfit peers, and longitudinal exercise interventions show hippocampal volume increases in older adults. Whether these volume changes reflect increased neurogenesis specifically, or other forms of plasticity, or vascular changes, or some combination, is not directly resolvable with current human methods. The honest claim is that exercise supports hippocampal health through multiple mechanisms that almost certainly include some contribution from neurogenesis, while the popular framing of “exercise grows new brain cells” oversimplifies what the human evidence supports.

Example 2 — The antidepressant response

A 34-year-old teacher with a recent major depressive episode begins SSRI treatment. She notices initial improvement in physical symptoms (sleep, appetite) within 2-3 weeks, but mood improvement is more gradual, becoming clinically meaningful around the 4-6 week mark. This delay-of-onset has been one of the puzzles of antidepressant pharmacology: SSRIs increase serotonin transmission within hours, but mood improvement takes weeks.

The neurogenesis hypothesis of antidepressant action, advanced by groups including Hen and Santarelli starting in the early 2000s, proposes that the therapeutic effect requires upregulation of adult hippocampal neurogenesis, which takes 3-4 weeks to produce a meaningful population of functionally integrated new neurons. Rodent studies have shown that chronic SSRI treatment increases hippocampal neurogenesis and that ablation of neurogenesis (via irradiation or genetic manipulation) blocks the behavioral effects of SSRIs in some paradigms. The 2009 Boldrini et al. work in Neuropsychopharmacology reported increased neural progenitor cells in human hippocampus from individuals who had received antidepressant treatment. The translation from rodent to human is supported but not definitively established; the contemporary view treats neurogenesis as one of several mechanisms contributing to antidepressant action, alongside synaptic plasticity changes, neuroinflammation reduction, and broader neuroplastic effects. The 4-6 week delay of clinical response is consistent with a neurogenesis-related mechanism but does not by itself prove it.

Adult human neurogenesis has been one of the most actively contested questions in neuroscience over the past three decades. Several real qualifications are worth naming.

• The 2018 Boldrini-Sorrells dispute was real and the field is not yet fully unified. The two papers reached opposite conclusions using overlapping methods. Subsequent work (Moreno-Jiménez 2019, Tobin 2019, Dumitru 2025, Lazarov 2026) has substantially tilted the field toward “persists in adults,” but the methodological discussions that drove the 2018 dispute (tissue processing effects, marker specificity, quantification approaches) remain active research questions. Anyone presenting adult human neurogenesis as a fully settled finding is overstating what the literature supports; anyone presenting it as still completely disputed is understating the substantial recent evidence in favor of persistence.
• The rate of adult human neurogenesis is uncertain. Spalding et al. 2013's estimate of ~700 new neurons per day in the adult hippocampus is widely cited but represents one quantification method (carbon-14 dating with mathematical modeling). Other estimates range substantially higher or lower depending on method. The contemporary single-cell sequencing studies have characterized neurogenic cell populations but generally have not provided quantitative rate estimates comparable to the Spalding work. Confidence in the existence of adult human neurogenesis has grown faster than confidence in its precise rate.
• Functional significance for human cognition is hard to establish. Rodent studies can directly manipulate neurogenesis (genetic ablation, irradiation, exercise) and observe effects on memory tasks. The corresponding human experiments are ethically impossible. Inference from rodent to human depends on assuming functional homology, which the literature on hippocampal pattern separation supports but does not definitively establish. Claims that adult human neurogenesis is “required” for specific human cognitive functions extrapolate from rodent data more than direct human evidence supports.
• Marker-based methods have known limitations. DCX, PSA-NCAM, and similar markers were developed in rodent contexts and may have different specificity profiles in human tissue. DCX positivity does not necessarily mean “adult-born neuron” in all contexts; some inhibitory interneurons retain DCX expression into adulthood, contributing to the methodological disputes about how to interpret immunohistochemical signals. The 2025 and 2026 single-cell sequencing studies have provided molecular signatures less ambiguous than single-marker immunostaining, but tissue-processing effects (postmortem interval, fixation duration) still affect detection across studies.
• The popular framing often outruns the evidence. Self-help and popular science sources sometimes present adult neurogenesis as a straightforward target for lifestyle intervention, with claims like “exercise grows new brain cells.” The honest scientific picture is more constrained. Exercise robustly enhances hippocampal neurogenesis in rodents; human evidence supports exercise-related hippocampal volume and cognitive benefits but cannot directly isolate the neurogenesis contribution. Antidepressant-neurogenesis links are similarly supported but not as definitive as popular framing suggests. The honest claim is that adult human neurogenesis exists and is responsive to lifestyle factors, while the precise causal contribution to specific cognitive or mood outcomes is harder to establish than popular sources typically convey.
• Sample sizes and inter-individual variability remain substantial challenges. Even the most recent multiomic studies typically have N=6-10 per group, reflecting the difficulty of obtaining well-characterized postmortem human brain tissue with appropriate cognitive characterization and rapid processing. Inter-individual variability in neurogenesis-related markers is high, partly reflecting genuine biological variation and partly reflecting differences in tissue quality across donors. Findings from individual studies need to be interpreted with awareness of these sample-size and variability constraints.
• Causal direction in Alzheimer's findings remains unclear. Multiple studies have reported reduced neurogenesis markers in AD compared to age-matched controls. Whether reduced neurogenesis contributes to AD pathology (and could therefore be a therapeutic target) or is a downstream consequence of AD-related neurodegeneration (and would therefore not be an intervention point) is not yet established. The 2026 Lazarov et al. finding of altered chromatin accessibility in neurogenic cells in preclinical AD is suggestive of an early role for neurogenesis disruption, but causal interpretation requires longitudinal data and intervention studies not yet available.

The LBL Brain Age Index uses cognitive performance and risk-factor inputs to estimate biological brain age relative to chronological age. The Cognitive Reserve Estimator uses educational, occupational, and lifestyle inputs to estimate cognitive reserve. Neither tool directly measures neurogenesis (which would require neuroimaging or postmortem analysis) but both assess cognitive domains supported by hippocampal function. For users interested in the broader picture of brain health and cognitive aging, these tools provide complementary assessments of the downstream cognitive consequences of cellular processes including neurogenesis. For users specifically interested in neurogenesis research, contemporary measurement methods including single-cell sequencing remain active research tools rather than routine clinical assessments.

Neurogenesis is the process by which neural stem cells generate new neurons. In adult mammals, neurogenesis is largely restricted to the subgranular zone of the hippocampal dentate gyrus and the subventricular zone. Whether adult human hippocampal neurogenesis persists at functionally significant levels has been one of the most actively contested questions in neuroscience over the past three decades. The first direct evidence came from Eriksson et al. (1998) in Nature Medicine, who found BrdU-positive neurons in the dentate gyrus of adult humans. Spalding et al. (2013) at the Karolinska Institutet used carbon-14 dating to estimate ~700 new neurons per day across 55 individuals with modest decline during aging. In 2018, Boldrini et al. in Cell Stem Cell reported neurogenesis persistence into the eighth decade, while Sorrells et al. in Nature reported the opposite — that adult neurogenesis drops to undetectable levels by adolescence. The dispute reflected methodological differences in tissue processing, marker selection, and quantification. Subsequent work including Moreno-Jiménez et al. (2019) in Nature Medicine, the Frisén lab's Dumitru et al. (2025) single-nucleus RNA sequencing study in Science, and the Lazarov et al. (2026) multiomic study in Nature has substantially shifted the field toward the persists-into-adulthood view, while ongoing methodological discussions remain active. Adult neurogenesis is implicated in hippocampal memory functions (particularly pattern separation), in Alzheimer's disease pathophysiology, and in mood regulation and antidepressant action. The popular framing of neurogenesis as a straightforward lifestyle target often outruns what the evidence directly supports, while the underlying biological process is real, responsive to lifestyle factors, and one of several contributing mechanisms to brain health across the lifespan.

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LifeByLogic. (2026). Neurogenesis: Adult Human Hippocampus Evidence. https://lifebylogic.com/glossary/neurogenesis/

LifeByLogic. "Neurogenesis: Adult Human Hippocampus Evidence." LifeByLogic, 14 May 2026, https://lifebylogic.com/glossary/neurogenesis/.

LifeByLogic. 2026. "Neurogenesis: Adult Human Hippocampus Evidence." May 14. https://lifebylogic.com/glossary/neurogenesis/.

@misc{lblneurogenesis2026,
  author = {{LifeByLogic}},
  title = {Neurogenesis: Adult Human Hippocampus Evidence},
  year = {2026},
  month = {may},
  publisher = {LifeByLogic},
  url = {https://lifebylogic.com/glossary/neurogenesis/},
  note = {Accessed: 2026-05-14}
}