Research by scientists of the DZNE and The Salk Institute show the protein “lamin B1” to be involved in declining neurogenesis.
Throughout life, an area of the brain called “hippocampus” keeps growing new neurons – even in adulthood. This “adult neurogenesis” contributes to brain plasticity, i. e. to the brain’s ability to change and adapt. However, neurogenesis declines in the aging brain and this reduction is assumed to be implicated in cognitive and emotional impairments. The mechanisms underlying this recession have still remained elusive. Now, based on a study in mice, researchers from the DZNE’s Dresden site including Dr. Tomohisa Toda, and colleagues from The Salk Institute for Biological Studies present new insights into this phenomenon. Their findings are published in “The EMBO Journal”.
In the brain, new neurons develop from a reservoir of so-called adult neural stem cells. It was these stem cells that the scientists focused on in the current study. Based on previous evidence that the nuclear membrane protein “lamin B1” might play roles in neurogenesis and cellular aging, they studied expression levels and found that lamin B1 is abundant in stem cells of young wild-type mice. However, these levels drop with age, coinciding with the timing of reduced adult neurogenesis.
Additional studies in transgenic mice in which expression of lamin B1 could be modulated by treatment, revealed that lamin B1 has a critical role in the mantainance of neurogenesis and that a lack of this protein induces age-related anxiety-like behavior.
“Summarizing, our findings indicate that lamin B1 affects stem cell aging and mood regulation”, Toda said. “Lamin B1 is likewise expressed in the human brain. Thus, it is quite possible that our findings also apply to humans. Acting on lamin B1 might therefore be a potential target for future therapies aimed at alleviating effects of the aging brain.”