Laura K. Hamilton

TL;DR: A fatty acid-mediated mechanism suppressing endogenous NSC activity in Alzheimer's disease is uncovered, whereby AD-induced perturbation of niche fatty acid metabolism suppresses the homeostatic and regenerative functions of NSCs.

TL;DR: Important similarities and differences are identified between the central canal ependymal zone and the forebrain subventricular zone (SVZ), a well-characterized niche of neural stem cells, and it is suggested that dorsal ependedymal cells possess the potential for stem cell activity.

TL;DR: It is shown that mammalian target of rapamycin (mTOR) signaling is pivotal in determining proliferation versus quiescence in the adult forebrain neural stem cell (NSC) niche, and mTORC1 activity and progenitor proliferation decline within the quiescent NSC niche of the aging brain.

TL;DR: The findings indicate that AD‐associated mutations suppress neurogenesis early during disease development, which suggests that deficits in adult neuroGenesis may mediate premature cognitive decline in AD.

TL;DR: In this article, the authors assessed the spatiotemporal dynamics of ependymal cell proliferation for up to 35 days in three models of spinal pathologies: contusion SCI using the Infinite Horizon impactor, focal demyelination by intraspinal injection of lysophosphatidylcholine (LPC), and autoimmune-mediated multi-focal demyeling using the active experimental autoimmune encephalomyelitis (EAE) model of MS.