Adult hippocampal neurogenesis plays a critical role in learning and memory and is significantly affected in Alzheimer's disease (AD). The hippocampus, a key brain region for memory, is vulnerable to damage in AD, and altered neurogenesis in the adult hippocampus is an early event in AD progression. Key molecules involved in AD pathogenesis influence neurogenesis, either positively or negatively. Functional changes in neurogenesis contribute to structural plasticity and network maintenance, and dysfunctional neurogenesis may worsen neuronal vulnerability and memory impairment, while enhanced neurogenesis may represent a compensatory repair mechanism. Recent studies show that neurogenesis-based diagnostics and therapies may offer new approaches for AD treatment. The adult hippocampus continuously generates new neurons from neural stem cells (NSCs) in the subgranular zone (SGZ). These NSCs differentiate into neuroblasts that migrate to the granule cell layer and become dentate granule cells (DGCs). New neurons integrate into existing circuits and contribute to hippocampus-dependent learning and memory. However, in AD, neurogenesis is impaired, with reduced proliferation and survival of new neurons. AD-related mutations, such as in presenilin 1 (PS1) and amyloid precursor protein (APP), disrupt neurogenesis, leading to cognitive impairments. Some studies show that AD-related proteins like AICD impair neurogenesis, while sAPPα may promote it. In AD mouse models, neurogenesis is altered, with some showing reduced neurogenesis and others increased. These discrepancies may be due to differences in genetic backgrounds, disease stages, and experimental methods. Environmental enrichment and physical exercise can enhance neurogenesis and improve cognitive function in AD models, suggesting that neurogenesis may be a target for therapeutic interventions. However, the relationship between neurogenesis and AD pathogenesis is complex, with some studies showing that neurogenesis may be a compensatory mechanism, while others suggest it may exacerbate disease. Overall, neurogenesis is an important aspect of AD pathology, with alterations occurring early in the disease process. Understanding the molecular mechanisms underlying these changes may lead to new diagnostic and therapeutic strategies for AD. Further research is needed to clarify the role of neurogenesis in AD and to develop effective interventions.Adult hippocampal neurogenesis plays a critical role in learning and memory and is significantly affected in Alzheimer's disease (AD). The hippocampus, a key brain region for memory, is vulnerable to damage in AD, and altered neurogenesis in the adult hippocampus is an early event in AD progression. Key molecules involved in AD pathogenesis influence neurogenesis, either positively or negatively. Functional changes in neurogenesis contribute to structural plasticity and network maintenance, and dysfunctional neurogenesis may worsen neuronal vulnerability and memory impairment, while enhanced neurogenesis may represent a compensatory repair mechanism. Recent studies show that neurogenesis-based diagnostics and therapies may offer new approaches for AD treatment. The adult hippocampus continuously generates new neurons from neural stem cells (NSCs) in the subgranular zone (SGZ). These NSCs differentiate into neuroblasts that migrate to the granule cell layer and become dentate granule cells (DGCs). New neurons integrate into existing circuits and contribute to hippocampus-dependent learning and memory. However, in AD, neurogenesis is impaired, with reduced proliferation and survival of new neurons. AD-related mutations, such as in presenilin 1 (PS1) and amyloid precursor protein (APP), disrupt neurogenesis, leading to cognitive impairments. Some studies show that AD-related proteins like AICD impair neurogenesis, while sAPPα may promote it. In AD mouse models, neurogenesis is altered, with some showing reduced neurogenesis and others increased. These discrepancies may be due to differences in genetic backgrounds, disease stages, and experimental methods. Environmental enrichment and physical exercise can enhance neurogenesis and improve cognitive function in AD models, suggesting that neurogenesis may be a target for therapeutic interventions. However, the relationship between neurogenesis and AD pathogenesis is complex, with some studies showing that neurogenesis may be a compensatory mechanism, while others suggest it may exacerbate disease. Overall, neurogenesis is an important aspect of AD pathology, with alterations occurring early in the disease process. Understanding the molecular mechanisms underlying these changes may lead to new diagnostic and therapeutic strategies for AD. Further research is needed to clarify the role of neurogenesis in AD and to develop effective interventions.