Aβ₁₋₄₂ stimulates adult SVZ neurogenesis through the p75 neurotrophin receptor

Sotthibundhu, Areechun, Li, Qiao-Xin, Thangnipon, Wipawan and Coulson, Elizabeth J. (2009) Aβ₁₋₄₂ stimulates adult SVZ neurogenesis through the p75 neurotrophin receptor. Neurobiology of Aging, 30 12: 1975-1985. doi:10.1016/j.neurobiolaging.2008.02.004

Author Sotthibundhu, Areechun
Li, Qiao-Xin
Thangnipon, Wipawan
Coulson, Elizabeth J.
Title Aβ₁₋₄₂ stimulates adult SVZ neurogenesis through the p75 neurotrophin receptor
Journal name Neurobiology of Aging   Check publisher's open access policy
ISSN 0197-4580
Publication date 2009-12
Year available 2008
Sub-type Article (original research)
DOI 10.1016/j.neurobiolaging.2008.02.004
Volume 30
Issue 12
Start page 1975
End page 1985
Total pages 11
Editor Paul D. Coleman
Place of publication Philadelphia, PA, United States
Publisher Elsevier
Collection year 2009
Language eng
Subject C1
110902 Cellular Nervous System
060103 Cell Development, Proliferation and Death
060110 Receptors and Membrane Biology
730104 Nervous system and disorders
Formatted abstract
The generation of amyloid-beta peptide (Aβ) and its accumulation in amyloid plaques are generally recognized as key characteristics of Alzheimer's disease. A number of reports have indicated that Aβ can regulate the proliferation of neural precursor cells and adult neurogenesis, suggesting that this may underpin the cognitive decline and compromised olfaction also associated with the condition. Here we report that Aβ1–42 treatment both in vitro and in vivo, as well as endogenous generation of Aβ in C100 and APP/PS1 transgenic models of Alzheimer's disease, stimulate neurogenesis of young adult subventricular zone precursors. The neurogenic effect of Aβ1–42 was found to require expression of the p75 neurotrophin receptor (p75NTR) by the precursor cells, and activation of p75NTR by metalloprotease cleavage. However, precursors from 12-month-old APP/PS1 mice failed to respond to Aβ1–42. Our results suggest that overstimulation of p75NTR-positive progenitors during early life might result in depletion of the stem cell pool and thus a more rapid decline in basal neurogenesis. This, in turn, could lead to impaired neurogenic function in later life. 
Keyword Amyloid-beta peptide
Alzheimer's disease
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 41 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 43 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Thu, 26 Mar 2009, 11:47:39 EST by Debra McMurtrie on behalf of Queensland Brain Institute