A new research study has found that mutations in the progranulin gene (develops the progranulin protein and helps brain neurons), led to the development of frontotemporal lobar degeneration (FTLD) type of dementia. However, those individuals with a progranulin mutation who had copies of the protective TMEM106B allele did not develop FTLD immediately.
Reference:
N. Finch, M.M. Carrasquillo, M. Baker, N.J. Rutherford, G. Coppola, M. Dejesus-Hernandez, R. Crook, T. Hunter, R. Ghidoni, L. Benussi, J. Crook, E. Finger, K.J. Hantanpaa, A.M. Karydas, P. Sengdy, J. Gonzalez, W.W. Seeley, N. Johnson, T.G. Beach, M. Mesulam, G. Forloni, A. Kertesz, D.S. Knopman, R. Uitti, C.L. White III, R. Caselli, C. Lippa, E.H. Bigio, Z.K. Wszolek, G. Binetti, I.R. Mackenzie, B.L. Miller, B.F. Boeve, S.G. Younkin, D.W. Dickson, R.C. Petersen, N.R. Graff-Radford, D.H. Geschwind, R. Rademakers. TMEM106B regulates progranulin levels and the penetrance of FTLD in GRN mutation carriers. Neurology,
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