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Home: Papers of the Week
Annotation


Blurton-Jones M, Kitazawa M, Martinez-Coria H, Castello NA, Müller FJ, Loring JF, Yamasaki TR, Poon WW, Green KN, Laferla FM. Neural stem cells improve cognition via BDNF in a transgenic model of Alzheimer disease. Proc Natl Acad Sci U S A. 2009 Aug 11;106(32):13594-9. PubMed Abstract

  
Comments on Related News
  Related News: Honolulu: Neuroregeneration Taps Glia, Neurotrophins

Comment by:  Christian Hoelscher
Submitted 12 August 2010  |  Permalink Posted 13 August 2010

The effects of BDNF on neuronal protection and synapse preservation are most impressive, similar to those shown by NGF. As they do not cross the blood-brain barrier (BBB), new methods are tested, such as the stem cell injection or genetic vector transfer of genes that induce increased release of BDNF or NGF. Clearly, that limits the application of these growth factors.

If I may draw attention to the fact that there are other growth factors out there that actually cross the BBB and show exactly the same protective effects: I presented a poster at the meeting on the effects of the incretin GLP-1 analogue Liraglutide. Incretins are well known as novel treatments for type 2 diabetes, but really are growth factors that have numerous other properties in addition to regulating insulin signaling. Liraglutide not only crosses the BBB, but also protects memory in APP/PS1 mice, protects LTP, and reduces plaques and the associated inflammation response in the brain (as assessed by measurement of activated microglia) when injected peripherally. Interestingly enough, the drug is already on...  Read more

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REAGENTS/MATERIAL:
ELISA: Aß sandwich ELISAs were performed following standard protocols as previously described (13). BDNF ELISA was performed following the manufacturers protocol (Promega).
Immunofluorescent Labeling and Primary Antibodies: Specificity of primary antibodies was confirmed by Western blot or conformation-sensitive ELISA (A11 and OC), and primary antibody omission controls. The following primary antibodies were used: mouse monoclonal anti-Aß, aa 1-16 (6E10) (Signet); rabbit anti-oligomeric Aß (A11) and rabbit anti-fibrillar Aß (OC) (gifts of C. Glabe, University of California, Irvine); anti-tau (HT7) (Innogenetics); rabbit anti-phospho-Tau, Ser 199/202 (Invitrogen); mouse monoclonal anti-tau (PHF-1) (gift of P. Davies, Albert Einstein College of Medicine, Bronx, NY); anti-synaptophysin (Sigma); mouse monoclonal anti-ß-actin (Sigma); anti-BDNF and anti-Doublecortin (Santa Cruz Biotechnology); anti-Pro-BDNF (gift of D. Cribbs, University of California, Irvine); anti-GFAP (Dako); anti-ß-III-tubulin (Millipore); anti-GFP (Millipore); mouse monoclonal anti-GalC (mGalC) (Millipore) and and mouse monoclonal anti-CNPase (11-5B) (Millipore).

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