Abstract
Neurogenesis persists throughout adulthood in the hippocampus and contributes to specific cognitive functions. In Alzheimer’s disease (AD), the hippocampus is affected by pathology and functional impairment early in the disease. Human AD patients have reduced adult hippocampal neurogenesis (AHN) levels compared to age-matched healthy controls. Similarly, rodent AD models show a decrease in AHN before the onset of the classical hallmarks of AD pathology. Conversely, enhancement of AHN can protect against AD pathology and ameliorate memory deficits in both rodents and humans. Therefore, impaired AHN may be a contributing factor of AD-associated cognitive decline, rather than an effect of it. In this review we outline the regulation and function of AHN in healthy individuals, and highlight the relationship between AHN dysfunction and cognitive impairments in AD. The existence of AHN in humans and its relevance in AD patients will also be discussed, with an outlook toward future research directions.
Highlights
Adult hippocampal neurogenesis occurs in the brains of mammals including humans.
Adult hippocampal neurogenesis is reduced in Alzheimer’s disease in humans and animal models.
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This post is Copyright: Joris N. Geigenmüller,
Atefe R. Tari,
Ulrik Wisloff,
Tara L. Walker | August 21, 2024