Clinical, neuroimaging and neuropathological features of a new chromosome 9p-linked FTD-ALS family

Adam L. Boxer(University Memory and Aging Center), Ian R. Mackenzie(Vancouver General Hospital), B. F. Boeve(Mayo Clinic), Matthew Baker(Mayo Clinic in Florida), William W. Seeley(University of California, San Francisco), Richard Crook(Mayo Clinic in Florida), Howard Feldman(University of British Columbia), Ging‐Yuek Robin Hsiung(University of British Columbia), Nicola J. Rutherford(Jacksonville College), Victor Laluz(University Memory and Aging Center), Jennifer Whitwell(Mayo Clinic), Dean Foti(University of British Columbia), Eric McDade(Mayo Clinic), Jesús Molano(Mayo Clinic), Anna Karydas(University of California, San Francisco), Aleksandra Wojtas(Mayo Clinic in Florida), Jill Goldman(Columbia University), Jacob Mirsky(University of California, San Francisco), Pheth Sengdy(University of British Columbia), S. J. DeArmond(University of California, San Francisco), Bruce L. Miller(University of California, San Francisco), R. Rademakers(Jacksonville College)
Journal of Neurology Neurosurgery & Psychiatry
June 20, 2010
Cited by 187

Abstract

BACKGROUND: Frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) is a heritable form of FTD, but the gene(s) responsible for the majority of autosomal dominant FTD-ALS cases have yet to be found. Previous studies have identified a region on chromosome 9p that is associated with FTD and ALS. METHODS: The authors report the clinical, volumetric MRI, neuropathological and genetic features of a new chromosome 9p-linked FTD-ALS family, VSM-20. RESULTS: Ten members of family VSM-20 displayed heterogeneous clinical phenotypes of isolated behavioural-variant FTD (bvFTD), ALS or a combination of the two. Parkinsonism was common, with one individual presenting with a corticobasal syndrome. Analysis of structural MRI scans from five affected family members revealed grey- and white-matter loss that was most prominent in the frontal lobes, with mild parietal and occipital lobe atrophy, but less temporal lobe atrophy than in 10 severity-matched sporadic bvFTD cases. Autopsy in three family members showed a consistent and unique subtype of FTLD-TDP pathology. Genome-wide linkage analysis conclusively linked family VSM-20 to a 28.3 cM region between D9S1808 and D9S251 on chromosome 9p, reducing the published minimal linked region to a 3.7 Mb interval. Genomic sequencing and expression analysis failed to identify mutations in the 10 known and predicted genes within this candidate region, suggesting that next-generation sequencing may be needed to determine the mutational mechanism associated with chromosome 9p-linked FTD-ALS. CONCLUSIONS: Family VSM-20 significantly reduces the region linked to FTD-ALS on chromosome 9p. A distinct pattern of brain atrophy and neuropathological findings may help to identify other families with FTD-ALS caused by this genetic abnormality.


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