A common feature of neurodegenerative disorders, in particular Alzheimer's disease (AD), is a chronic neuroinflammation associated with aberrant neuroplasticity. Development of neuroinflammation affects efficacy of stem and progenitor cells proliferation, differentiation, migration, and integration of newborn cells into neural circuitry. However, precise mechanisms of neurogenesis alterations in neuroinflammation are not clear yet. It is well established that expression of NLRP3 inflammasomes in glial cells marks neuroinflammatory events, but less is known about contribution of NLRP3 to deregulation of neurogenesis within neurogenic niches and whether neural stem cells (NSCs), neural progenitor cells (NPCs) or immature neuroblasts may express inflammasomes in (patho)physiological conditions. Thus, we studied alterations of neurogenesis in rats with the AD model (intra-hippocampal injection of Aβ1-42). We found that in Aβ-affected brain, number of CD133+ cells was elevated after spatial training in the Morris water maze. The number of PSA-NCAM+ neuroblasts diminished by Aβ injection was completely restored by subsequent spatial learning. Spatial training leads to elevated expression of NLRP3 inflammasomes in the SGZ (subgranular zones): CD133+ and PSA-NCAM+ cells started to express NLRP3 in sham-operated, but not AD rats. Taken together, our data suggest that expression of NLRP3 inflammasomes in CD133+ and PSA-NCAM+ cells may contribute to stimulation of adult neurogenesis in physiological conditions, whereas Alzheimer’s type neurodegeneration abolishes stimuli-induced overexpression of NLRP3 within the SGZ neurogenic niche.

神经退行性疾病，特别是阿尔茨海默病 (AD) 的一个共同特征是与异常神经可塑性相关的慢性神经炎症。神经炎症的发展会影响干细胞和祖细胞增殖、分化、迁移和新生细胞整合到神经回路中的功效。然而，神经炎症中神经发生改变的确切机制尚不清楚。众所周知，神经胶质细胞中 NLRP3 炎性体的表达标志着神经炎症事件，但关于 NLRP3 对神经源性生态位内神经发生失调的贡献以及神经干细胞 (NSC)、神经祖细胞 (NPC) 或未成熟成神经细胞是否可能在（病理）生理条件下表达炎症小体。因此，我们研究了 AD 模型大鼠神经发生的改变（海马内注射 Aβ1-42）。我们发现，在受 Aβ 影响的大脑中，在 Morris 水迷宫中进行空间训练后，CD133+ 细胞的数量增加。通过随后的空间学习完全恢复了通过 Aβ 注射减少的 PSA-NCAM+ 成神经细胞的数量。空间训练导致 SGZ（颗粒下区）中 NLRP3 炎症小体的表达升高：CD133+ 和 PSA-NCAM+ 细胞开始在假手术大鼠中表达 NLRP3，但在 AD 大鼠中不表达。总之，我们的数据表明 NLRP3 炎症小体在 CD133+ 和 PSA-NCAM+ 细胞中的表达可能有助于在生理条件下刺激成人神经发生，而阿尔茨海默病型神经变性消除了 SGZ 神经原性生态位内刺激诱导的 NLRP3 过度表达。