Mapping It out: A Novel Signaling Pathway Linking Aβ-PrPc-Fyn Complex to Cognitive Impairment in Alzheimer’s Disease

Abstract

Understanding the signaling cascade that leads to the rapid memory and cognitive breakdown in Alzheimer’s disease is the key to finding a potential treatment method for the disease. Recently, Larson et al. connect the roles of major proteins implicated in the disease progression and propose targeting of cellular prion protein (PrPc) as a way of someday rescuing synaptic plasticity in humans with Alzheimer’s, as it has been done on mice.


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Wang, Y. and Xue, L. (2014) Mapping It out: A Novel Signaling Pathway Linking Aβ-PrPc-Fyn Complex to Cognitive Impairment in Alzheimer’s Disease. Advances in Alzheimer's Disease, 3, 20-23. doi: 10.4236/aad.2014.31003.

Conflicts of Interest

The authors declare no conflicts of interest.

References

[1] Shankar, G.M., Li, S., Mehta, T.H., Garcia-Munoz, A., Shepardson, N.E., Smith, I., Brett, F.M., Farrell, M.A., Rowan, M.J., Lemere, C.A., Regan, C.M., Walsh, D.M., Sabatini, B.L., and Selkoe, D.J. (2008) Amyloid β-Protein Dimers Isolated Directly from Alzheimer Brains Impair Synaptic Plasticity and Memory. Nature Medicine, 8, 837-842. http://dx.doi.org/10.1038/nm1782
[2] Laurén, J., Gimbel, D.A., Nygaard, H., Gilbert, J.W. and Strittmatter, S.M. (2009) Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-Beta Oligomers. Nature, 457, 1128-1132. http://dx.doi.org/10.1038/nature07761
[3] Hoover, B.R., Reed, M.N., Su, J., Penrod, R.D., Kotilinek, L.A., Grant, M.K., Pitstick, R., Carlson, G.A., Lanier, L.M., Yuan, L.L., Ashe, K.H. and Liao, D. (2010) Tau Mislocalization to Dendritic Spines Mediates Synaptic Dysfunction Independently of Neurodegeneration. Neuron, 68, 1067-1081.
http://dx.doi.org/10.1016/j.neuron.2010.11.030
[4] Roberson, E.D., Halabisky, B., Yoo, J.W., Yao, J., Chin, J., Yan, F., Wu, T., Hamto, P., Devidze, N., Yu, G.Q., Palop, J.J., Noebels, J.L. and Mucke, L. (2011) Amy-loid-Beta/Fyn-Induced Synaptic, Network, and Cognitive Impairments Depend on Tau Levels in Multiple Mouse Models of Alzheimer’s Disease. The Journal of Neuroscience, 31, 700 -711. http://dx.doi.org/10.1523/JNEUROSCI.4152-10.2011
[5] Larson, M., Sherman, M.A., Amar, F., Nuvolone, M., Schneider, J.A., Bennett, D.A., Aguzzi, A. and Lesné, S.E. (2012) The Complex PrPc-Fyn Couples Human Oligomeric Aβ with Pathological Tau Changes in Alzheimer’s Disease. The Journal of Neuroscience, 32, 16857-16871.
http://dx.doi.org/10.1523/JNEUROSCI.1858-12.2012
[6] Calella, A.M., Farinelli, M., Nuvolone, M., Mirante, O., Moos, R., Falsig, J., Mansuy, I.M. and Aguzzi, A. (2010) Prion Protein and Abeta-Related Synaptic Toxicity Impairment. EMBO Molecular Medicine, 2, 306 -314. http://dx.doi.org/10.1002/emmm.201000082
[7] Balducci, C., Beeg, M., Stravalaci, M., Bastone, A., Sclip, A., Biasini, E., Tapella, L., Colombo, L., Manzoni, C., Borsello, T., Chiesa, R., Gobbi, M., Salmona, M. and Forloni, G. (2010) Synthetic Amyloid-β Oligomers Impair Long-Term Memory Independently of Cellular Prion Protein. Proceedings of the National Academy of Sciences, 107, 2295- 2300. http://dx.doi.org/10.1073/pnas.0911829107

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