![]() ![]() Our previous study proved that aging specifically reduces proliferation of active neural progenitors (Romine et al., 2015). Neurogenesis comprises several critical steps, including neural stem/progenitor cell (NSC) proliferation, immature neuron survival, dendrite development, maturation, and functional integration (Ming & Song, 2005). Hippocampal neurogenesis and synaptic plasticity, which are involved in cognitive functions, are both greatly affected by the aging process (Rao et al., 2006). However, the molecular and cellular mechanisms of age‐dependent cognitive decline remain elusive, impeding the development of an effective clinical treatment. A treatment approach is urgently needed to target aging‐related cognition disorders. Census Bureau, by 2050, the older population, which is over 65‐year‐old, is estimated to reach 83.7 million, accounting for around 20% of the total population (Ortman et al., 2014). As we grow older, we can experience memory loss and cognitive decline, including processing speed decrease, working memory deficits and episodic memory encoding dysfunctions, which can interfere with our daily routines (Hedden & Gabrieli, 2004). DHF‐promoted dendrite development of newborn neurons in the hippocampus may enhance their function in the aging animal leading to a possible improvement in cognition.Īging is a process in which overall body functions fall over time. We found that systemically administration of 7, 8‐dihydroxyflavone ( DHF), a small molecule imitating brain‐derived neurotrophic factor ( BDNF), significantly enhanced dendrite length in the newborn neurons, while it did not promote survival of immature neurons, in the hippocampus of 12‐month‐old mice. ![]() Currently, no effective approach is available to increase neurogenesis or promote dendrite development of newborn neurons in the aging brain. Here, we further find that aging impaired dendrite development of newborn neurons. Through our previous research, we discovered that active neural progenitor cells selectively become more quiescent in response to aging, thus leading to the decline of neurogenesis in the aged hippocampus. The molecular and cellular mechanisms leading to age‐related cognitive decline are still not fully understood. All aging individuals will develop some degree of decline in cognitive capacity as time progresses. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |