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article, google, scholar, pubmed, lateral, amyotrophic, sclerosis, tdp, cas, tmemb, frontotemporal, disease, degeneration, lobar, neurol, patients, cognitive, risk, impairment, geser, medicine, usa, acta, lee, trojanowski, university, philadelphia, school, privacy, cookies, content, information, research, genotypes, november, ashbridge, van, john, ftldtdp, clinical, pathology, access, alzheimers, motor, neuron, mutations, sporadic, genet, analysis, publish,

Topics {✒️}

major-allele-dominant genetic model ubiquitin-positive tau-negative inclusions month download article/chapter william maul measey-truman frontotemporal lobar degeneration neurodegenerative disease research amyotrophic lateral sclerosis frontotemporal dementia motor neuron disease full article pdf disease-related neurofibrillary chen-plotkin department related subjects privacy choices/manage cookies amyotroph lateral scler frontal lobe impairment tdp-43 a315t mutation brandmeir nj comparing tmem106b genotypes check access instant access multisystem tdp-43 proteinopathies genetic risk factor confer increased risk chen-plotkin van deerlin & john pathological tdp-43 inclusions ftld-tdp ftld-tdp european economic area dana clay-falcone retrospective chart review demonstrated independent effects cell-based models el escorial revisited koller family foundation disease research frontotemporal cognitive human als brain conditions privacy policy histopathological slide review multivariate linear models academic health center article vass neurodegenerative disease cognitive impairment accepting optional cookies ashbridge contributed equally article log main content log

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• Lomen-Hoerth C, Murphy J, Langmore S et al (2003) Are amyotrophic lateral sclerosis patients cognitively normal?

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         headline:Risk genotypes at TMEM106B are associated with cognitive impairment in amyotrophic lateral sclerosis
         description:TMEM106B has recently been identified as a genetic risk factor for frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). Amyotrophic lateral sclerosis (ALS), like FTLD-TDP, is characterized by pathological TDP-43 inclusions. We therefore investigated whether FTLD-TDP-associated risk genotypes at TMEM106B (1) contribute to risk of developing ALS or (2) modify the clinical presentation in ALS. Detailed clinical and pathological information from 61 postmortem ALS patients was collected by database query, retrospective chart review, and histopathological slide review. DNA from these patients, as well as 24 additional ALS patients, was genotyped for three TMEM106B single nucleotide polymorphisms known to confer increased risk of FTLD-TDP. Associations between TMEM106B genotype and ALS were investigated by comparing TMEM106B genotypes in ALS patients (n = 85) and normal controls (n = 553), and associations between TMEM106B genotype and clinical and pathologic features were explored using linear regression. Multivariate linear models were used to evaluate the contributions of TMEM106B genotype and TDP-43 pathology to cognitive performance in ALS as measured by a phonemic verbal fluency test. We found that TMEM106B genotypes did not differ between ALS patients and normal controls. However, protective alleles at TMEM106B were significantly associated with preserved cognition in ALS patients, with the strongest association seen under a major-allele-dominant genetic model. While lower TDP-43 pathology scores and protective alleles at TMEM106B both correlated with better cognitive scores, these factors were not correlated with each other and demonstrated independent effects. These findings implicate the FTLD-TDP risk gene TMEM106B in the development of cognitive impairment in ALS.
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      headline:Risk genotypes at TMEM106B are associated with cognitive impairment in amyotrophic lateral sclerosis
      description:TMEM106B has recently been identified as a genetic risk factor for frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). Amyotrophic lateral sclerosis (ALS), like FTLD-TDP, is characterized by pathological TDP-43 inclusions. We therefore investigated whether FTLD-TDP-associated risk genotypes at TMEM106B (1) contribute to risk of developing ALS or (2) modify the clinical presentation in ALS. Detailed clinical and pathological information from 61 postmortem ALS patients was collected by database query, retrospective chart review, and histopathological slide review. DNA from these patients, as well as 24 additional ALS patients, was genotyped for three TMEM106B single nucleotide polymorphisms known to confer increased risk of FTLD-TDP. Associations between TMEM106B genotype and ALS were investigated by comparing TMEM106B genotypes in ALS patients (n = 85) and normal controls (n = 553), and associations between TMEM106B genotype and clinical and pathologic features were explored using linear regression. Multivariate linear models were used to evaluate the contributions of TMEM106B genotype and TDP-43 pathology to cognitive performance in ALS as measured by a phonemic verbal fluency test. We found that TMEM106B genotypes did not differ between ALS patients and normal controls. However, protective alleles at TMEM106B were significantly associated with preserved cognition in ALS patients, with the strongest association seen under a major-allele-dominant genetic model. While lower TDP-43 pathology scores and protective alleles at TMEM106B both correlated with better cognitive scores, these factors were not correlated with each other and demonstrated independent effects. These findings implicate the FTLD-TDP risk gene TMEM106B in the development of cognitive impairment in ALS.
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            name:University of Pennsylvania School of Medicine
            address:
               name:Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Julia R. Masterman School, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Neurology, Emory University School of Medicine, Atlanta, USA
      name:Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Institute on Aging, University of Pennsylvania School of Medicine, Philadelphia, USA
      name:Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, USA
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