Specific niche signals play a vital role in supporting the proliferation and differentiation of neural stem cells (NSCs) throughout neural development and neural regeneration. Glial cells, including astrocytes and microglia, are key components of the stem cell niche. However, their interactions with NSCs remain poorly understood. To explore these interactions, primary NSCs isolated from rat embryos were cultured in either glial cell-derived conditioned medium (CM) or co-cultured with mixed glial cells via Transwell inserts. NSC viability, proliferation, differentiation, and the underlying mechanism involving BMP4 signaling were evaluated. Results showed that microglia and astrocytes were closely localized with NSCs in the subventricular zone (SVZ) of rat brains at postnatal day 14. After being cultured with CM or glial co-culture, NSC viability and astrocytic differentiation were significantly enhanced, while cell proliferation and neuronal differentiation were reduced. BMP4 secretion by both astrocytes and microglia as well as Smad1/5/8 and Stat3 phosphorylation in NSCs was also elevated, indicating that the BMP4–Smad1/5/8 signaling pathway was involved in the effects of the glial cell niche on NSC behaviors. These findings suggest that glial cells regulate NSCs’ fate through BMP4-mediated signaling, providing potential targets for future therapeutic strategies in neurogenesis and regeneration.

Background: To study the age‐dependent relationship between body mass index (BMI) and cognitive impairment in rural population aged 40 years and above. Method: From October 2014 to March 2015, people aged 40 years and above, lived in two natural villages in Huyi district of Xi'an, were selected as the research subjects. General demographic information, lifestyle, medical history, family history, physical examination, and biochemical examination were collected. Mini‐mental state examination (MMSE) assessed global cognitive function, with cognitive impairment defined as a score below the cutoff. The age‐dependent relationship between BMI and cognitive impairment was analyzed using stratified analysis, restricted cubic spline (RCS), and multivariate logistic regression. Result: A total of 1792 subjects were included in the analysis, of which 230 were diagnosed with cognitive impairment. There were 726 males (40.5%); the average age was 55.53±9.92 years, ranging from 40‐85 years, 1193 subjects aged 40‐59 years (66.6%), and 599 subjects aged ≥60 years (33.4%); the average BMI was 25.29±3.14 kg/m ² . In the total population, logistic regression, adjusting for confounders, showed a significant correlation between BMI and cognitive impairment ( P _overall =0.023), with a nonlinear trend ( P _nonlinear =0.097); the specific relationship was that, for BMI <25 kg/m ² , the odds ratio (OR) value increased as BMI decreased, while BMI ≥25 kg/m ² showed no significant change. The population was divided into two subgroups according to age (40‐59 years vs ≥60 years). Stratified analysis showed that in the ≥60 years old subgroup, the risk of cognitive impairment with BMI index was similar to that of the overall population ( P _overall =0.038, P _nonlinear =0.097); but in the 40‐59 years old subgroup, BMI index was not significantly associated with cognitive impairment ( P _overall =0.722, P _nonlinear =0.738). Conclusion: The relationship between BMI and cognitive impairment was affected by age. No significant association was found in the middle‐aged population of 40‐59 years old; while there may be a nonlinear association in the elderly population over 60 years old. Specifically, with BMI = 25 kg/m2 as the boundary, as BMI decreased, the risk of cognitive impairment gradually increased; and as BMI further increased, the risk of cognitive impairment did not change significantly even if it reached the obesity level.