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Home: Papers of the Week
Annotation


Park JH, Gimbel DA, GrandPre T, Lee JK, Kim JE, Li W, Lee DH, Strittmatter SM. Alzheimer precursor protein interaction with the Nogo-66 receptor reduces amyloid-beta plaque deposition. J Neurosci. 2006 Feb 1;26(5):1386-95. PubMed Abstract

Comments on Paper and Primary News
  Comment by:  Li-Huei Tsai
Submitted 4 February 2006  |  Permalink Posted 4 February 2006
  I recommend this paper

  Comment by:  Andre Delacourte
Submitted 6 February 2006  |  Permalink Posted 6 February 2006
  I recommend this paper

  Comment by:  Paul Coleman, ARF Advisor
Submitted 4 February 2006  |  Permalink Posted 6 February 2006
  I recommend this paper

This paper provides an additional aspect to the story of altered neuroplasticity in the AD brain. Although dendritic (e.g., Buell and Coleman, 1979) and GAP-43 data (Coleman et al., 1992) indicate reduced plasticity in AD brain, localized increased neuritic proliferation around plaques has been demonstrated (e.g., Masliah et al., 1991). The present paper suggests that the localized sprouting around plaques may be related to the association of NgR and APP, although the association is complicated by the effect of NgR on Aβ production.

References:
Buell, S.J. and P.D. Coleman. (1979) Dendritic growth in aged human brain and failure of growth in senile dementia. Science 206:854-856. Abstract

Coleman, P.D., A.M. Kazee, L. Lapham, T. Eskin and K. Rogers. (1992) Reduced GAP-43 message levels are associated with increased neurofibrillary tangle density in frontal association cortex area 9 in Alzheimer’s disease. Neurobiol. Aging, 13:631-639. Abstract

Masliah E. Mallory M. Hansen L. Alford M. Albright T. DeTeresa R. Terry R. Baudier J. Saitoh T. Patterns of aberrant sprouting in Alzheimer's disease. Neuron. 6(5):729-39, 1991. Abstract

View all comments by Paul Coleman


  Comment by:  Tommaso Russo, ARF Advisor
Submitted 6 February 2006  |  Permalink Posted 6 February 2006
  I recommend this paper
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REAGENTS/MATERIAL:

Anti-NgR (AF1440) antibody was from R & D Systems, the 369 anti-C-terminal-APP antibody was a generous gift from S. S. Sisodia (University of Chicago, Chicago, IL). The anti-N-terminal-APP 5228 antibody, the anti-Ab1–17 6E10 antibody, and the anti-C-terminal-APP 5352 antibody were obtained from Chemicon (Temecula, CA). The anti-Ab 4G8 antibody and the anti-C-terminal-APP 51–2700 antibodies were from Signet Laboratories (Dedham, MA) and Zymed Laboratories (South San Francisco, CA), respectively. The anti-secretet APP (SAPP)swe-specific 6A1 antibody was from Immunobiological Laboratories (Gunma, Japan).

Transgenic APPswe/PSEN-1(dE9) mice were from The Jackson Laboratory (Bar Harbor, ME) (stock #04462).

Ab ELISA assays were performed according to the instructions of the manufacturer (Biosource, Camarillo, CA). Neuritic dystrophy was visualized by staining with monoclonal-anti-synaptophysin antibodies (Sigma, St. Louis, MO) in parasagittal paraffin-embedded sections.

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