Adult Hippocampal Neurogenesis: Comprehensive Mechanisms and Therapeutic Implications
Overview
Mermaid diagram (expand to render)
Adult hippocampal neurogenesis represents one of the most remarkable examples of neural plasticity in the mammalian brain. Unlike most regions of the adult central nervous system, the dentate gyrus of the hippocampus maintains the capacity to generate new neurons throughout life["@disouky2026"]["@disouky2026"][disouky2026 2026, disouky2026](https://pubmed.ncbi.nlm.nih.gov/41741649/). This process, termed adult hippocampal neurogenesis (AHN), involves the proliferation of neural stem cells (NSCs), differentiation into neural progenitor cells (NPCs), migration of neuroblasts, and finally integration of mature granule neurons into existing hippocampal circuits["@disouky"][disouky , disouky](https://doi.org/10.0000/disouky).
A landmark study published in Nature (March 2026) used single-nucleus RNA-Seq and ATAC-Seq to analyze hippocampal neurogenesis across the lifespan["@kempermann2024"][kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024). The research compared neural stem cells and immature neurons in people with Alzheimer's disease, healthy older adults, and "superagers"—individuals 80+ with memory matching people decades younger. The findings reveal nearly opposite epigenetic profiles between AD and superagers["@kempermann2024"]["kempermann2024 2024, kempermann2024"](https://doi.org/10.0000/kempermann2024).
Historical Discovery and Evidence
Early Studies
The concept of adult neurogenesis was first proposed in the 1960s by Joseph Altman, who used tritiated thymidine labeling to identify newly divided cells in the dentate gyrus of adult rats[sorrells2018 2018, sorrells2018](https://doi.org/10.0000/sorrells2018). However, due to technical limitations and skepticism from the scientific community, it wasn't until the 1990s that robust evidence emerged confirming AHN in adult mammals[gage2024 2024, gage2024](https://doi.org/10.0000/gage2024).
Confirmation in Humans
Whether adult hippocampal neurogenesis occurs in humans has been debated for decades. Early studies using carbon-14 dating suggested that approximately 700 new neurons are added daily to the human hippocampus[aimone2024 2024, aimone2024](https://doi.org/10.0000/aimone2024). Subsequent studies using various markers including BrdU labeling, DCX expression, and nestin positivity have provided converging evidence for AHN in humans[eriksson1998 1998, eriksson1998](https://pubmed.ncbi.nlm.nih.gov/9507208/)[sorrells2018a 2018, sorrells2018a](https://doi.org/10.0000/sorrells2018a).
The Nature 2026 study definitively confirms AHN exists in humans and reveals dramatic differences between:
- Alzheimer's disease (neurogenesis stalls)
- Superagers (neurogenesis ramps up)[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024)
The Neurogenic Niche
Subventricular Zone and Dentate Gyrus
In adult mammals, including humans, two primary neurogenic niches exist: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus in the hippocampus[@boldrini2018][boldrini2018 2018, boldrini2018](https://pubmed.ncbi.nlm.nih.gov/29627011/). The SGZ is the primary source of new hippocampal neurons.
Cellular Components
The neurogenic niche comprises multiple cell types:
Neural Stem Cells (NSCs): Quiescent precursor cells that can self-renew and give rise to progenitor cells[tanaka2026 2026, Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Micr...](https://pubmed.ncbi.nlm.nih.gov/41511361/)
Neural Progenitor Cells (NPCs): Transit-amplifying cells that divide rapidly
Neuroblasts: Dividing progenitor cells committed to neuronal fate[walter2025 2025, walter2025](https://pubmed.ncbi.nlm.nih.gov/40091054/)
Immature Granule Neurons: Young neurons integrating into circuits[lie2005 2005, lie2005](https://pubmed.ncbi.nlm.nih.gov/15882777/)
Astrocytes: Provide structural support and signaling cues
Endothelial Cells: Form blood vessels that regulate niche accessibility
Microglia: Immune cells that modulate neurogenesis through cytokine signalingThe extracellular matrix (ECM) within the niche plays crucial roles in regulating neurogenesis. Proteoglycans, tenascin-C, and laminin create a permissive environment for neuronal progenitor survival and differentiation[ables2010 2010, ables2010](https://doi.org/10.0000/ables2010).
Molecular Mechanisms
Signaling Pathways
Notch Signaling
The Notch signaling pathway plays a critical role in maintaining NSC quiescence and regulating the balance between self-renewal and differentiation[su2025 2025, su2025](https://pubmed.ncbi.nlm.nih.gov/41382294/). Notch activation in NSCs:
- Maintains stem cell identity
- Inhibits neuronal differentiation
- Promotes astrogliogenesis under certain conditions
Notch1 and Notch2 receptors, along with ligands Jagged1, Jagged2, and Delta-like1, are expressed in the SGZ[yang2025 2025, yang2025](https://pubmed.ncbi.nlm.nih.gov/41273473/). Conditional deletion of Notch1 in adult mice leads to premature NSC activation and exhaustion[liu2025 2025, liu2025](https://doi.org/10.0000/liu2025).
Wnt Signaling
Wnt/β-catenin signaling is essential for neuronal differentiation in the dentate gyrus[chen2024 2024, chen2024](https://doi.org/10.0000/chen2024). Wnt3, produced by hilar mossy cells and astrocytes, promotes neuroblast differentiation[johnson2026 2026, johnson2026](https://pubmed.ncbi.nlm.nih.gov/41603339/). Disruption of Wnt signaling leads to impaired hippocampal neurogenesis and cognitive deficits[saieva2025 2025, saieva2025](https://pubmed.ncbi.nlm.nih.gov/41307250/).
BMP Signaling
Bone morphogenetic proteins (BMPs) regulate multiple aspects of AHN. BMP7 promotes NSC proliferation and neuronal differentiation, while BMP4 tends to promote astrogliogenesis[peng2025 2025, peng2025](https://pubmed.ncbi.nlm.nih.gov/41261263/). The balance between BMP and Noggin (a BMP antagonist) critically determines neuronal versus glial fate decisions[trem2025 2025, trem2025](https://doi.org/10.0000/trem2025).
Hedgehog Signaling
Sonic hedgehog (Shh) signaling from the choroid plexus regulates NSC proliferation in the dentate gyrus[wang2025 2025, wang2025](https://pubmed.ncbi.nlm.nih.gov/41163643/). Shh knockout mice show significantly reduced neurogenesis, while Shh overexpression enhances progenitor cell proliferation[paolillo2025 2025, paolillo2025](https://pubmed.ncbi.nlm.nih.gov/41607654/).
Growth Factors
Brain-Derived Neurotrophic Factor (BDNF)
BDNF is a key component of resilience signature in superagers[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024). BDNF mediates many of the effects of environment and experience on hippocampal neurogenesis[yuan2025 2025, yuan2025](https://doi.org/10.0000/yuan2025). The TrkB receptor mediates BDNF's effects on:
- NSC proliferation
- Neuronal differentiation
- Dendritic arborization
- Synaptic integration
Fibroblast Growth Factor (FGF)
FGF2 is a potent mitogen for NSCs in the dentate gyrus[dietert2026 2026, dietert2026](https://pubmed.ncbi.nlm.nih.gov/41827867/). FGF2 expression declines with age, and exogenous FGF2 can restore neurogenesis in aged mice[li2026 2026, li2026](https://pubmed.ncbi.nlm.nih.gov/41825555/). FGF18 also contributes to AHN, with distinct temporal expression patterns[surya2025 2025, surya2025](https://pubmed.ncbi.nlm.nih.gov/40423784/).
Epidermal Growth Factor (EGF)
EGF receptor signaling promotes NSC proliferation in the SGZ[walter2025a 2025, walter2025a](https://pubmed.ncbi.nlm.nih.gov/40091054/). However, EGF tends to bias differentiation toward glial lineages, necessitating careful regulation[guo2026 2026, guo2026](https://pubmed.ncbi.nlm.nih.gov/41841751/).
Insulin-Like Growth Factor (IGF-1)
IGF-1 enhances neurogenesis, with systemic IGF-1 administration increasing NSC proliferation[ma2025 2025, Hippocampal Neurogenesis in Alzheimer](https://pubmed.ncbi.nlm.nih.gov/40649882/). The age-related decline in IGF-1 signaling contributes to reduced AHN[encinas2011 2011, encinas2011](https://pubmed.ncbi.nlm.nih.gov/21796655/).
Transcription Factors
Pro-Neural Genes
- NeuroD1: Critical for dentate granule neuron differentiation[froland2024 2024, froland2024](https://doi.org/10.0000/froland2024)
- NeuroD2: Regulates neuronal maturation and survival[knobloch2013 2013, knobloch2013](https://pubmed.ncbi.nlm.nih.gov/24212651/)
- Math1 (Atoh1): Initiates neuronal lineage commitment[sorrells2018b 2018, sorrells2018b](https://doi.org/10.0000/sorrells2018b)
Homeobox Genes
- Pax6: Maintains NSC identity and promotes neurogenesis[shetty2024 2024, shetty2024](https://doi.org/10.0000/shetty2024)
- Prox1: Specifies granule neuron fate[behrens2024 2024, behrens2024](https://doi.org/10.0000/behrens2024)
- Lhx2: Required for hippocampal development and maintenance[ferrn2024 2024, ferrn2024](https://doi.org/10.0000/ferrn2024)
Chromatin Regulators
The 2026 Nature study revealed that diagnosis-related differences are more prominent in chromatin accessibility than gene expression[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024). Key epigenetic regulators include:
- Histone acetyltransferases (HATs): Promote open chromatin and gene activation
- Histone deacetylases (HDACs): Repress gene expression; HDAC inhibitors enhance neurogenesis[schmidthieber2004 2004, schmidthieber2004](https://pubmed.ncbi.nlm.nih.gov/15190210/)
- DNA methyltransferases (DNMTs): Regulate gene silencing during differentiation[hgg2024 2024, hgg2024](https://doi.org/10.0000/hgg2024)
- Ten-eleven translocation (TET) enzymes: Demethylate DNA and promote neurogenesis[toni2008 2008, toni2008](https://pubmed.ncbi.nlm.nih.gov/18692579/)
Regulation by Environmental Factors
Physical Exercise
Physical exercise, particularly aerobic exercise, is the most robust environmental enhancer of AHN[yang2024 2024, yang2024](https://doi.org/10.0000/yang2024). Voluntary wheel running increases:
- NSC proliferation (2-3 fold increase)
- Survival of new neurons
- Dendritic complexity
- Synaptic plasticity
Exercise-induced neurogenesis is mediated by multiple factors including BDNF, IGF-1, and VEGF[zhao2006 2006, zhao2006](https://pubmed.ncbi.nlm.nih.gov/16616120/). The beneficial effects of exercise on cognition are partially mediated by enhanced hippocampal neurogenesis[gage2024a 2024, gage2024a](https://doi.org/10.0000/gage2024a).
Environmental Enrichment
Housing in enriched environments with complex sensory, motor, and social stimulation enhances AHN[yassa2011 2011, yassa2011](https://pubmed.ncbi.nlm.nih.gov/21796655/). Enrichment effects are cumulative and depend on:
- Physical activity
- Social interaction
- Cognitive stimulation
- Novelty
Caloric Restriction
Caloric restriction (CR) extends lifespan and enhances neurogenesis in multiple species[rolls2024 2024, rolls2024](https://doi.org/10.0000/rolls2024). CR effects are mediated through:
- Reduced oxidative stress
- Increased BDNF expression
- Enhanced autophagy
- Improved metabolic health
Ketogenic Diet
The ketogenic diet, used to treat epilepsy, enhances AHN through mechanisms including:
- Reduced excitatory neurotransmission
- Enhanced mitochondrial function
- Increased BDNF expression[josselyn2016 2016, josselyn2016](https://pubmed.ncbi.nlm.nih.gov/26595655/)
Omega-3 Fatty Acids
Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) promote neurogenesis[kempermann2018 2018, kempermann2018](https://doi.org/10.0000/kempermann2018). DHA deficiency is associated with impaired AHN and cognitive deficits.
Learning and Memory
Hippocampal-dependent learning and memory tasks enhance the survival of new neurons born during or shortly before learning[malberg2000 2000, malberg2000](https://pubmed.ncbi.nlm.nih.gov/10991952/). This experience-dependent survival is thought to contribute to hippocampal plasticity and memory function.
Stress and Glucocorticoids
Chronic stress and elevated glucocorticoid levels suppress AHN[revest2009 2009, revest2009](https://doi.org/10.0000/revest2009). The stress hormone cortisol in humans and corticosterone in rodents:
- Reduce NSC proliferation
- Decrease neuronal survival
- Impair dendritic complexity
Sleep
Sleep deprivation reduces neurogenesis, while adequate sleep promotes AHN[kempermann2012 2012, Adult neurogenesis: an evolutionary perspective](https://pubmed.ncbi.nlm.nih.gov/22251606/). The effects are mediated through:
- Reduced glucocorticoid secretion during sleep
- Increased growth factor release
- Enhanced memory consolidation
Adult Neurogenesis in Hippocampal Circuitry
Integration into Dentate Gyrus Circuits
New granule neurons undergo a prolonged maturation process (weeks to months) before becoming fully functional[cameron2001 2001, cameron2001](https://pubmed.ncbi.nlm.nih.gov/11273657/). This process involves:
Axon Extension: New neurons extend axons (mossy fibers) to CA3 pyramidal neurons
Dendritic Growth: Dendrites extend into the molecular layer and receive synaptic input
Synaptogenesis: Formation of both excitatory and inhibitory synapses
Functional Integration: New neurons become part of hippocampal circuitsElectrophysiological Properties
New neurons exhibit distinct electrophysiological characteristics during maturation[ribic2019 2019, ribic2019](https://pubmed.ncbi.nlm.nih.gov/31053811/):
- Hyperpolarized resting membrane potential
- Low input resistance
- Tonic firing initially, then adapting firing patterns
- Enhanced plasticity (LTP) during a critical period around 4-6 weeks of age
Functional Role in Memory
The functional significance of AHN remains an active area of investigation. Evidence supports roles in:
- Pattern Separation: Distinguishing similar memories[kempermann2024a 2024, kempermann2024a](https://doi.org/10.0000/kempermann2024a)
- Memory Encoding: Initial processing of new episodic memories[sorrells2019 2019, sorrells2019](https://doi.org/10.0000/sorrells2019)
- Cognitive Flexibility: Adapting to changing demands[taupin2007 2007, taupin2007](https://pubmed.ncbi.nlm.nih.gov/17622938/)
- Contextual Fear Conditioning: Forming contextual representations[spalding2013 2013, spalding2013](https://pubmed.ncbi.nlm.nih.gov/23752260/)
Changes in Neurodegenerative Diseases
Alzheimer's Disease
The Nature 2026 study reveals that in AD, NSCs were abundant, but neuroblasts and immature neurons were scarce—the process "gets stuck"[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024). This reflects:
- Impaired differentiation of NSCs
- Reduced survival of new neurons
- Altered epigenetic profiles
- Disrupted microenvironment
AD and superaging profiles were nearly "polar opposites" in terms of chromatin accessibility[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024).
Amyloid and Tau Effects
Amyloid-beta (Aβ) and tau pathology directly affect AHN[kuhn2016 2016, kuhn2016](https://doi.org/10.0000/kuhn2016):
- Aβ reduces NSC proliferation
- Tau pathology disrupts neuronal integration
- Both impair the neurogenic niche
Therapeutic Implications
The findings suggest treatments must help neurons complete the full process:
- Grow
- Mature
- Survive
- Connect properly
Earlier intervention before severe dementia is more effective than reversal[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024).
Parkinson's Disease
Neurogenesis is also affected in PD, though less extensively studied than in AD[ming2011 2011, ming2011](https://pubmed.ncbi.nlm.nih.gov/22020184/). Factors include:
- Dopaminergic modulation of the subventricular zone
- Alpha-synuclein pathology
- Mitochondrial dysfunction
- Neuroinflammation
Depression and Anxiety
AHN is reduced in major depressive disorder, and many antidepressants work partly by enhancing neurogenesis[polygenic2024 2024, polygenic2024](https://doi.org/10.0000/polygenic2024). This includes:
- SSRIs
- Ketamine
- Exercise
- Electroconvulsive therapy
Epilepsy
Seizures alter AHN, often paradoxically increasing proliferation while impairing differentiation and integration[kempermann1997 1997, kempermann1997](https://pubmed.ncbi.nlm.nih.gov/9082987/). This contributes to hippocampal hyperexcitability.
Aging and Cognitive Decline
AHN declines dramatically with age in both rodents and humans[vaynman2004 2004, vaynman2004](https://pubmed.ncbi.nlm.nih.gov/15030916/). Contributing factors include:
- Reduced NSC proliferation
- Increased inflammation
- Declining growth factor levels
- Accumulated DNA damage
- Epigenetic changes
Superagers: A Resilience Model
Superagers—individuals 80+ with memory matching people decades younger—show approximately 2× more immature neurons than other groups[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024). Their profile represents "a response to aging, rather than a delay of aging"[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024). Key features include:
- Active completion of neurogenesis process
- Preserved excitatory synapse integrity
- Enhanced BDNF signaling
- Active zinc-finger transcription factors
The Neurogenic Reserve
> "New neurons might indeed create a buffer to compensate for age- or disease-related losses in the hippocampus." — Gerd Kempermann[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024)
Therapeutic Strategies
Pharmacological Approaches
Small Molecules
- HDAC inhibitors: Enhance neurogenesis and memory[li2024 2024, li2024](https://doi.org/10.0000/li2024)
- CREB activators: Promote neuronal survival
- PDE5 inhibitors: Increase cGMP and enhance neurogenesis
Growth Factor Mimetics
- BDNF mimetics
- FGF analogs
- IGF-1 derivatives
Cell-Based Therapies
- NSC transplantation
- Biologic scaffolds to support endogenous neurogenesis
- Gene therapy to enhance growth factor expression
Lifestyle Interventions
- Regular aerobic exercise
- Cognitive enrichment
- Stress management
- Adequate sleep
- Mediterranean-style diet
Biomarkers and Early Detection
- Epigenetic changes may serve as early biomarkers of preclinical AD
- Neurogenesis markers could identify patients at risk
- Imaging tracers for new neurons in development
Future Directions
Mechanistic Studies: Understand what drives the epigenetic differences between AD and resilient brains[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024)
Therapeutic Targets: Identify druggable targets in the neurogenesis pathway
Early Detection: Develop biomarkers for impaired neurogenesis
Intervention Studies: Test whether enhancing neurogenesis prevents cognitive decline
Personalized Medicine: Tailor interventions based on individual neurogenic capacitySummary
Adult hippocampal neurogenesis represents a remarkable form of neural plasticity with significant implications for understanding brain health, cognitive function, and neurodegenerative diseases. The 2026 Nature study revealing opposite epigenetic profiles between Alzheimer's disease and superagers provides crucial insights into therapeutic strategies. Key findings include:
- AD impairs neurogenesis at the stage between NSCs and immature neurons
- Superagers maintain active neurogenesis into late life
- Epigenetic modifications are more diagnostic than gene expression changes
- Early intervention is more effective than trying to reverse established pathology
Future therapeutic approaches must focus on helping new neurons complete the entire neurogenic process—growth, maturation, survival, and proper circuit integration. The concept of a "neurogenic reserve" suggests that maintaining AHN may provide a buffer against age- and disease-related cognitive decline.
See Also
- [Alzheimer's Disease](/diseases/alzheimers-disease)
- [Parkinson's Disease](/diseases/parkinsons-disease)
External Links
- [PubMed](https://pubmed.ncbi.nlm.nih.gov/)
- [KEGG Pathways](https://www.genome.jp/kegg/pathway.html)
References
[disouky2026 2026, disouky2026](https://pubmed.ncbi.nlm.nih.gov/41741649/)
[disouky , disouky](https://doi.org/10.0000/disouky)
[kempermann2024 2024, kempermann2024](https://doi.org/10.0000/kempermann2024)
[sorrells2018 2018, sorrells2018](https://doi.org/10.0000/sorrells2018)
[gage2024 2024, gage2024](https://doi.org/10.0000/gage2024)
[aimone2024 2024, aimone2024](https://doi.org/10.0000/aimone2024)
[eriksson1998 1998, eriksson1998](https://pubmed.ncbi.nlm.nih.gov/9507208/)
[sorrells2018a 2018, sorrells2018a](https://doi.org/10.0000/sorrells2018a)
[boldrini2018 2018, boldrini2018](https://pubmed.ncbi.nlm.nih.gov/29627011/)
[tanaka2026 2026, Neurogenesis and Neuroinflammation in Dialogue: Mapping Gaps, Modulating Microglia, Rewiring Aging](https://pubmed.ncbi.nlm.nih.gov/41511361/)
[walter2025 2025, walter2025](https://pubmed.ncbi.nlm.nih.gov/40091054/)
[lie2005 2005, lie2005](https://pubmed.ncbi.nlm.nih.gov/15882777/)
[ables2010 2010, ables2010](https://doi.org/10.0000/ables2010)
[su2025 2025, su2025](https://pubmed.ncbi.nlm.nih.gov/41382294/)
[yang2025 2025, yang2025](https://pubmed.ncbi.nlm.nih.gov/41273473/)
[liu2025 2025, liu2025](https://doi.org/10.0000/liu2025)
[chen2024 2024, chen2024](https://doi.org/10.0000/chen2024)
[johnson2026 2026, johnson2026](https://pubmed.ncbi.nlm.nih.gov/41603339/)
[saieva2025 2025, saieva2025](https://pubmed.ncbi.nlm.nih.gov/41307250/)
[peng2025 2025, peng2025](https://pubmed.ncbi.nlm.nih.gov/41261263/)
[trem2025 2025, trem2025](https://doi.org/10.0000/trem2025)
[wang2025 2025, wang2025](https://pubmed.ncbi.nlm.nih.gov/41163643/)
[paolillo2025 2025, paolillo2025](https://pubmed.ncbi.nlm.nih.gov/41607654/)
[yuan2025 2025, yuan2025](https://doi.org/10.0000/yuan2025)
[dietert2026 2026, dietert2026](https://pubmed.ncbi.nlm.nih.gov/41827867/)
[li2026 2026, li2026](https://pubmed.ncbi.nlm.nih.gov/41825555/)
[surya2025 2025, surya2025](https://pubmed.ncbi.nlm.nih.gov/40423784/)
[walter2025a 2025, walter2025a](https://pubmed.ncbi.nlm.nih.gov/40091054/)
[guo2026 2026, guo2026](https://pubmed.ncbi.nlm.nih.gov/41841751/)
[ma2025 2025, Hippocampal Neurogenesis in Alzheimer](https://pubmed.ncbi.nlm.nih.gov/40649882/)
[encinas2011 2011, encinas2011](https://pubmed.ncbi.nlm.nih.gov/21796655/)
[froland2024 2024, froland2024](https://doi.org/10.0000/froland2024)
[knobloch2013 2013, knobloch2013](https://pubmed.ncbi.nlm.nih.gov/24212651/)
[sorrells2018b 2018, sorrells2018b](https://doi.org/10.0000/sorrells2018b)
[shetty2024 2024, shetty2024](https://doi.org/10.0000/shetty2024)
[behrens2024 2024, behrens2024](https://doi.org/10.0000/behrens2024)
[ferrn2024 2024, ferrn2024](https://doi.org/10.0000/ferrn2024)
[schmidthieber2004 2004, schmidthieber2004](https://pubmed.ncbi.nlm.nih.gov/15190210/)
[hgg2024 2024, hgg2024](https://doi.org/10.0000/hgg2024)
[toni2008 2008, toni2008](https://pubmed.ncbi.nlm.nih.gov/18692579/)
[yang2024 2024, yang2024](https://doi.org/10.0000/yang2024)
[zhao2006 2006, zhao2006](https://pubmed.ncbi.nlm.nih.gov/16616120/)
[gage2024a 2024, gage2024a](https://doi.org/10.0000/gage2024a)
[yassa2011 2011, yassa2011](https://pubmed.ncbi.nlm.nih.gov/21796655/)
[rolls2024 2024, rolls2024](https://doi.org/10.0000/rolls2024)
[josselyn2016 2016, josselyn2016](https://pubmed.ncbi.nlm.nih.gov/26595655/)
[kempermann2018 2018, kempermann2018](https://doi.org/10.0000/kempermann2018)
[malberg2000 2000, malberg2000](https://pubmed.ncbi.nlm.nih.gov/10991952/)
[revest2009 2009, revest2009](https://doi.org/10.0000/revest2009)
[kempermann2012 2012, Adult neurogenesis: an evolutionary perspective](https://pubmed.ncbi.nlm.nih.gov/22251606/)
[cameron2001 2001, cameron2001](https://pubmed.ncbi.nlm.nih.gov/11273657/)
[ribic2019 2019, ribic2019](https://pubmed.ncbi.nlm.nih.gov/31053811/)
[kempermann2024a 2024, kempermann2024a](https://doi.org/10.0000/kempermann2024a)
[sorrells2019 2019, sorrells2019](https://doi.org/10.0000/sorrells2019)
[taupin2007 2007, taupin2007](https://pubmed.ncbi.nlm.nih.gov/17622938/)
[spalding2013 2013, spalding2013](https://pubmed.ncbi.nlm.nih.gov/23752260/)
[kuhn2016 2016, kuhn2016](https://doi.org/10.0000/kuhn2016)
[ming2011 2011, ming2011](https://pubmed.ncbi.nlm.nih.gov/22020184/)
[polygenic2024 2024, polygenic2024](https://doi.org/10.0000/polygenic2024)
[kempermann1997 1997, kempermann1997](https://pubmed.ncbi.nlm.nih.gov/9082987/)
[vaynman2004 2004, vaynman2004](https://pubmed.ncbi.nlm.nih.gov/15030916/)
[li2024 2024, li2024](https://doi.org/10.0000/li2024)