We are analyzing https://link.springer.com/article/10.1007/s00401-009-0571-7.

Title:
TARDBP 3′-UTR variant in autopsy-confirmed frontotemporal lobar degeneration with TDP-43 proteinopathy | Acta Neuropathologica
Description:
Pathogenic mutations in the gene encoding TDP-43, TARDBP, have been reported in familial amyotrophic lateral sclerosis (FALS) and, more recently, in families with a heterogeneous clinical phenotype including both ALS and frontotemporal lobar degeneration (FTLD). In our previous study, sequencing analyses identified one variant in the 3′-untranslated region (3′-UTR) of the TARDBP gene in two affected members of one family with bvFTD and ALS and in one unrelated clinically assessed case of FALS. Since that study, brain tissue has become available and provides autopsy confirmation of FTLD-TDP in the proband and ALS in the brother of the bvFTD-ALS family and the neuropathology of those two cases is reported here. The 3′-UTR variant was not found in 982 control subjects (1,964 alleles). To determine the functional significance of this variant, we undertook quantitative gene expression analysis. Allele-specific amplification showed a significant increase of 22% (P < 0.05) in disease-specific allele expression with a twofold increase in total TARDBP mRNA. The segregation of this variant in a family with clinical bvFTD and ALS adds to the spectrum of clinical phenotypes previously associated with TARDBP variants. In summary, TARDBP variants may result in clinically and neuropathologically heterogeneous phenotypes linked by a common molecular pathology called TDP-43 proteinopathy.
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article, google, scholar, pubmed, cas, tdp, frontotemporal, lobar, degeneration, disease, cairns, sclerosis, mutations, amyotrophic, lateral, tardbp, bigio, neurol, usa, acta, gitcho, rademakers, morris, goate, neuropathol, familial, dickson, mackenzie, lee, trojanowski, mutation, baralle, dementia, neumann, van, university, school, medicine, gene, alzheimers, hutton, buratti, baker, department, johnson, pathology, patients, progranulin, genet, neurology,

Topics {✒️}

3′-untranslated region carlos cruchaga & alison month download article/chapter chromosome 9p-linked als-ftd ubiquitin-positive tau-negative inclusions carlos cruchaga disease-specific allele expression allele-specific amplification showed amyotrophic lateral sclerosis barnes-jewish hospital foundation tau-negative inclusions caused frontotemporal lobar degeneration frontotemporal dementia due parkinsonism-dementia complex author information authors full article pdf inclusion body myopathy disease research foundation south-eastern chinese patients disease research center total tardbp mrna important region vcp gene mutations privacy choices/manage cookies check access instant access dna/tissue samples ubiquitin-positive inclusions tardbp 3′-utr variant ayala ym temporal lobar predominance rna binding properties consensus recommendations author correspondence common pathogenic mechanism intrinsically aggregation-prone van deerlin vm frontotemporal dementia nuclear factor tdp-43 washington university school argyrophilic grain disease gene encoding tdp-43 molecular mechanisms responsible related subjects splicing regulator european economic area sequencing analyses identified clinical phenotypes previously c-terminal tail sr proteins promote

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         headline:TARDBP 3′-UTR variant in autopsy-confirmed frontotemporal lobar degeneration with TDP-43 proteinopathy
         description:Pathogenic mutations in the gene encoding TDP-43, TARDBP, have been reported in familial amyotrophic lateral sclerosis (FALS) and, more recently, in families with a heterogeneous clinical phenotype including both ALS and frontotemporal lobar degeneration (FTLD). In our previous study, sequencing analyses identified one variant in the 3′-untranslated region (3′-UTR) of the TARDBP gene in two affected members of one family with bvFTD and ALS and in one unrelated clinically assessed case of FALS. Since that study, brain tissue has become available and provides autopsy confirmation of FTLD-TDP in the proband and ALS in the brother of the bvFTD-ALS family and the neuropathology of those two cases is reported here. The 3′-UTR variant was not found in 982 control subjects (1,964 alleles). To determine the functional significance of this variant, we undertook quantitative gene expression analysis. Allele-specific amplification showed a significant increase of 22% (P < 0.05) in disease-specific allele expression with a twofold increase in total TARDBP mRNA. The segregation of this variant in a family with clinical bvFTD and ALS adds to the spectrum of clinical phenotypes previously associated with TARDBP variants. In summary, TARDBP variants may result in clinically and neuropathologically heterogeneous phenotypes linked by a common molecular pathology called TDP-43 proteinopathy.
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      headline:TARDBP 3′-UTR variant in autopsy-confirmed frontotemporal lobar degeneration with TDP-43 proteinopathy
      description:Pathogenic mutations in the gene encoding TDP-43, TARDBP, have been reported in familial amyotrophic lateral sclerosis (FALS) and, more recently, in families with a heterogeneous clinical phenotype including both ALS and frontotemporal lobar degeneration (FTLD). In our previous study, sequencing analyses identified one variant in the 3′-untranslated region (3′-UTR) of the TARDBP gene in two affected members of one family with bvFTD and ALS and in one unrelated clinically assessed case of FALS. Since that study, brain tissue has become available and provides autopsy confirmation of FTLD-TDP in the proband and ALS in the brother of the bvFTD-ALS family and the neuropathology of those two cases is reported here. The 3′-UTR variant was not found in 982 control subjects (1,964 alleles). To determine the functional significance of this variant, we undertook quantitative gene expression analysis. Allele-specific amplification showed a significant increase of 22% (P < 0.05) in disease-specific allele expression with a twofold increase in total TARDBP mRNA. The segregation of this variant in a family with clinical bvFTD and ALS adds to the spectrum of clinical phenotypes previously associated with TARDBP variants. In summary, TARDBP variants may result in clinically and neuropathologically heterogeneous phenotypes linked by a common molecular pathology called TDP-43 proteinopathy.
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         Motor neuron disease
         Amyotrophic lateral sclerosis
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         TARDBP
         3′-Untranslated region
         Pathology
         Neurosciences
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