In adult brain, new neurons are generated throughout adulthood in the subventricular zone and the dentate gyrus; this process is commonly known as adult neurogenesis. The regulation or modulation of adult neurogenesis includes various intrinsic pathways (signal transduction pathway and epigenetic or genetic modulation pathways) or extrinsic pathways (metabolic growth factor modulation, vascular, and immune system pathways). Altered neurogenesis has been identified in Alzheimer’s disease (AD), in both human AD brains and AD rodent models. The exact mechanism of the dysregulation of adult neurogenesis in AD has not been completely elucidated. However, neuroinflammation has been demonstrated to alter adult neurogenesis. The presence of various inflammatory components, such as immune cells, cytokines, or chemokines, plays a role in regulating the survival, proliferation, and maturation of neural stem cells. Neuroinflammation has also been considered as a hallmark neuropathological feature of AD. In this review, we summarize current, state-of-the art perspectives on adult neurogenesis, neuroinflammation, and the relationship between these two phenomena in AD. Furthermore, we discuss the potential therapeutic approaches, focusing on the anti-inflammatory and proneurogenic interventions that have been reported in this field.

BackgroundAtrial flutter (AFL) has been identified to be equivalent to atrial fibrillation (AF) in terms of preventing ischemic stroke, although differences exist in atrial rate, substrate, and electrophysiological mechanisms. This study aimed to investigate differences in clinical outcomes between nonvalvular AF and AFL.Methods and Results AF and AFL patients without any prescribed anticoagulation were enrolled from a 13‐year national cohort database. Under series exclusion criteria, ischemic stroke, heart failure hospitalization, and all‐cause mortality were compared between the groups in real‐world conditions and after propensity score matching. We identified 175 420 patients in the AF cohort and 6239 patients in the AFL cohort, and the prevalence of most comorbidities and frequency of medications were significantly higher in the AF group than the AFL group. In the real‐world setting the AF patients had higher incidence rates of ischemic stroke, heart failure hospitalization, and all‐cause mortality than the AFL patients (all P<0.001). After propensity score matching, the incidence rate of ischemic stroke in the AF cohort was 1.63‐fold higher than in the AFL cohort (P<0.001), the incidence rate of heart failure hospitalization in the AF cohort was 1.70‐fold higher than in the AFL cohort (P<0.001), and the incidence rate of all‐cause mortality in the AF cohort was 1.08‐fold higher than in the AFL cohort (P=0.002).ConclusionsThere were differences between AF and AFL in comorbidities and prognosis with regard to ischemic stroke, heart failure hospitalization, and all‐cause mortality.

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