By Martin N. Rossor (auth.), Markus Tolnay, Alphonse Probst (eds.)
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Extra info for Neuropathology and Genetics of Dementia
Ann Neurol45: 270-271. Goedert M, Spillantini MG, Crowther RA et al. (1999) Tau gene mutation in familial progressive subcortical gliosis. Nat Med 5: 454-457. Mirra SS, Murrell JR, Gearing M et al. (1999) Tau pathology in a family with dementia and a P301L mutation in tau. J Neuropathol Exp Neurol58: 333-345. Bird TD, Nochlin D, Poorkaj P et al. (1999) A clinical pathological comparison of three families with frontotemporal dementia and identical mutations in the tau gene (P301L). Brain 122: 741-756.
Brain Pathol 8: 387-402. Poorkaj P, Bird TO, Wijsman E et aI. (1998) Tau is a candidate gene for chromosome 17 frontotemporal dementia. Ann Neurol 43: 815-825. Hutton M, Lendon CL, Rizzu P et al. (1998) Association of missense and 5'-splice-site mutations in tau with the inherited dementia FTDP-17. Nature 393: 702-705. Spillantini MG, Murrell JR. Goedert M et al. (1998) Mutation in the tau gene in familial multiple system tauopathy with presenile dementia. Proc Natl Acad Sci USA 95: 7737-7741. Goedert M, Wischik CM, Crowther RA et al.
ArGs consist of aggregates of9 to 18 nm filaments 14,18,23 and of bundles of 25 nm smooth tubules 24 ,25, Paired helical filaments of AD or twisted ribbons reported in some FTDP-17 families 5 are not a component of ArGs. 2 Coiled bodies Coiled bodies are conspicuous curvaceous whip-like often branched oligodendroglial inclusions which are in close vicinity to the cell nucleus (Figure Id). By electron microscopy, they consist of straight 10-13 nm filaments or tubular structures23 ,24. g. PSP, CBD, PiD, AD and FTDP-17), and are therefore considered as a non-specific finding 26 ,27.
Neuropathology and Genetics of Dementia by Martin N. Rossor (auth.), Markus Tolnay, Alphonse Probst (eds.)