We are analyzing https://link.springer.com/article/10.1007/s00415-010-5815-x.

Title:
Familial frontotemporal dementia with amyotrophic lateral sclerosis and a shared haplotype on chromosome 9p | Journal of Neurology
Description:
Families with autosomal dominant frontotemporal dementia and amyotrophic lateral sclerosis (FTD/ALS) have previously been linked to a locus on chromosome 9p21. We describe the clinical phenotype and pathology of a large family with autosomal dominant FTD/ALS with nine affected members originating from Gwent in South Wales, UK. We also further refine the locus on chromosome 9p21 using a haplotype sharing approach and assess heterogeneity in 9p21 linked families. Within this family, affected individuals present with either FTD or ALS or both diseases simultaneously. In addition there was marked phenotypic variation including ataxia, Parkinsonism, psychosis and visuo-spatial cognitive deficits. The pathological features of the three cases described were consistent with type 2 FTD pathology, as previously reported in similar families. However, we also report distinctive cerebellar and glial pathology and a significant proportion of TDP-43 negative inclusions. No mutations in known genes for FTD or ALS were found. We identified a large 4.8-megabase haplotype on chromosome 9p21, which was shared by all affected family members. This haplotype overlaps and limits the previously reported FTD/ALS linkage region on chromosome 9p21. Sequencing of this region did not identify any evidence of a pathogenic exonic mutation. This suggests that the pathogenic change affects non-coding DNA and that the disease is caused by variation in gene or protein expression.
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article, pubmed, google, scholar, frontotemporal, amyotrophic, lateral, dementia, sclerosis, chromosome, cas, disease, neurology, familial, neurol, research, morris, pathology, family, lobar, cardiff, privacy, cookies, content, journal, haplotype, huw, families, tdp, access, motor, neuron, degeneration, university, data, publish, search, williams, ftdals, locus, wales, ftd, variation, mutations, linkage, miller, mackenzie, hospital, national, health,

Topics {✒️}

month download article/chapter chromosome 9p-linked ftd-als family chromosome 9p-linked als-ftd chromosome 9p confers susceptibility population-based linkage analyses visuo-spatial cognitive deficits motor neuron disease autosomal dominant ftd/als chromosome 9p-linked families amyotrophic lateral sclerosis full article pdf privacy choices/manage cookies frontotemporal lobar degeneration familial frontotemporal dementia cairns nj related subjects intramural research program medical research council type 2 ftd pathology european economic area affected individuals present pathogenic exonic mutation c9orf72-mediated als white cl 3rd st george-hyslop cardiovascular risk factors project z01 ag000951-06 electronic supplementary material conditions privacy policy van doorn pa rna processing protein de bakker pi de deyn pp report distinctive cerebellar article journal affected members originating haplotype sharing approach van swieten jc frontotemporal atrophy 9p21 linked families neurol neurosurg psychiatry accepting optional cookies de rijik mc jennifer stott pathogenic change affects article log de vos kj affected family members brown rh jr journal finder publish

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Is amyotrophic lateral sclerosis/frontotemporal dementia an autophagy disease?

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         description:Families with autosomal dominant frontotemporal dementia and amyotrophic lateral sclerosis (FTD/ALS) have previously been linked to a locus on chromosome 9p21. We describe the clinical phenotype and pathology of a large family with autosomal dominant FTD/ALS with nine affected members originating from Gwent in South Wales, UK. We also further refine the locus on chromosome 9p21 using a haplotype sharing approach and assess heterogeneity in 9p21 linked families. Within this family, affected individuals present with either FTD or ALS or both diseases simultaneously. In addition there was marked phenotypic variation including ataxia, Parkinsonism, psychosis and visuo-spatial cognitive deficits. The pathological features of the three cases described were consistent with type 2 FTD pathology, as previously reported in similar families. However, we also report distinctive cerebellar and glial pathology and a significant proportion of TDP-43 negative inclusions. No mutations in known genes for FTD or ALS were found. We identified a large 4.8-megabase haplotype on chromosome 9p21, which was shared by all affected family members. This haplotype overlaps and limits the previously reported FTD/ALS linkage region on chromosome 9p21. Sequencing of this region did not identify any evidence of a pathogenic exonic mutation. This suggests that the pathogenic change affects non-coding DNA and that the disease is caused by variation in gene or protein expression.
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      description:Families with autosomal dominant frontotemporal dementia and amyotrophic lateral sclerosis (FTD/ALS) have previously been linked to a locus on chromosome 9p21. We describe the clinical phenotype and pathology of a large family with autosomal dominant FTD/ALS with nine affected members originating from Gwent in South Wales, UK. We also further refine the locus on chromosome 9p21 using a haplotype sharing approach and assess heterogeneity in 9p21 linked families. Within this family, affected individuals present with either FTD or ALS or both diseases simultaneously. In addition there was marked phenotypic variation including ataxia, Parkinsonism, psychosis and visuo-spatial cognitive deficits. The pathological features of the three cases described were consistent with type 2 FTD pathology, as previously reported in similar families. However, we also report distinctive cerebellar and glial pathology and a significant proportion of TDP-43 negative inclusions. No mutations in known genes for FTD or ALS were found. We identified a large 4.8-megabase haplotype on chromosome 9p21, which was shared by all affected family members. This haplotype overlaps and limits the previously reported FTD/ALS linkage region on chromosome 9p21. Sequencing of this region did not identify any evidence of a pathogenic exonic mutation. This suggests that the pathogenic change affects non-coding DNA and that the disease is caused by variation in gene or protein expression.
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