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| http://dx.doi.org/10.1136/jnnp-2017-315641 | DOI Listing |
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Identification of potential therapeutic targets for Alzheimer's disease from the proteomes of plasma and cerebrospinal fluid in a multicenter Mendelian randomization study.
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First Operating Room, The First Hospital of Jilin University, Changchun, China. Electronic address:
Background: Certain peripheral proteins are believed to be involved in the development of Alzheimer's disease (AD), but the roles of other new protein biomarkers are still unclear. Current treatments aim to manage symptoms, but they are not effective in stopping the progression of the disease. New drug targets are needed to prevent Alzheimer's disease.
View Article and Find Full Text PDFTMEM106B C-terminal fragments aggregate and drive neurodegenerative proteinopathy in transgenic Caenorhabditis elegans.
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December 2024
Geriatrics Research Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, Washington, USA.
Introduction: Genetic variation in the lysosomal and transmembrane protein 106B (TMEM106B) modifies risk for several neurodegenerative disorders, especially frontotemporal lobar degeneration (FTLD). The C-terminal (CT) domain of TMEM106B occurs as fibrillar protein deposits in the brains of dementia patients.
Methods: To determine the TMEM CT aggregation propensity and neurodegenerative potential, we generated transgenic Caenorhabditis elegans expressing the human TMEM CT fragment aggregating in FTLD cases.
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Department of Neurology and Alzheimer Centre, Erasmus MC University Medical Centre (Erasmus MC), Dr. Molenwaterplein 40, 3015 CE, Rotterdam, The Netherlands.
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View Article and Find Full Text PDFGene-Specific Effects on Brain Volume and Cognition of in Frontotemporal Lobar Degeneration.
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From the VIB Center for Molecular Neurology (M.V., R.R., V.B., S.W.); Department of Biomedical Sciences (M.V., M.V.B., S.W., R.R.), University of Antwerp, Belgium; Department of Neurology (E.M.R., M.F.M.), David Geffen School of Medicine, University of California, Los Angeles; Department of Neurology (N.C.-L., V.K.R., T.K., K.K., B.F.B.); Department of Psychiatry and Psychology (N.C.-L., J.A.F., D.S.K., L.K.F.), Mayo Clinic, Rochester, MN; Department of Epidemiology and Biostatistics (J.K.), University of California, San Francisco; Department of Quantitative Health Sciences (C.M., D.E.B.), Mayo Clinic, Rochester, MN; Department of Neurology (A.M.S., A.A.W.), Memory and Aging Center, University of California, San Francisco; Weill Institute for Neurosciences, San Francisco, California; Institute for Precision Health (D.H.G.), Departments of Neurology, Psychiatry and Human Genetics at David Geffen School of Medicine, UCLA; Department of Neuroscience (T.G., L.P., M.B., N.R.G.-R.), Mayo Clinic, Jacksonville, FL; Alzheimer's Disease and Other Cognitive Disorders Unit (S.B.-É.), Neurology Service, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Fundació Clínic per a la Recerca Biomèdica, Uni; Department of Neurology (B.A., B.C.D.), Case Western Reserve University, Cleveland, OH; Department of Neurology (S.B.), University of Michigan, Ann Arbor; Department of Neurology (A.C.B.), University of North Carolina, Chapel Hill; Department of Neurology (D.C.), Indiana University, Indianapolis; Department of Neurology (R.R.D.), Vanderbilt University, Nashville, TN; Department of Neurology (K.D.-R.), University of Washington, Seattle, WA; Department of Neurosciences (D.G., G.C.L., I.L.), University of California, San Diego, La Jolla; Departments of Neurology and Psychiatry (N.G.), Washington University School of Medicine, Washington University, St. Louis, MO; Department of Psychiatry and Behavioral Sciences (I.M.G.), Northwestern Feinberg School of Medicine, Chicago, IL; Taub Institute for Research on Alzheimer's Disease and the Aging Brain (L.S.H.), College of Physicians and Surgeons; Department of Neurology (L.S.H.), Columbia University, New York; Division of Neurology (G.-Y.R.H.), University of British Columbia, Vancouver, Canada; Department of Psychiatry and Human Behavior (E.D.H.), Alpert Medical School of Brown University, Providence, RI; Department of Neurology and Penn Frontotemporal Degeneration Center (D.J.I.), Perelman School of Medicine, University of Pennsylvania, Philadelphia; National Institute of Neurological Disorders and Stroke (J.Y.K., A.S.), National Institutes of Health, Bethesda, MD; Department of Neurology (J.C.M., B.P.), Houston Methodist, TX; Department of Psychiatry and Behavioral Sciences (C.U.O.), Johns Hopkins University, Baltimore, MD; Department of Neurology (P.S.P.), University of Colorado, Aurora; Cleveland Clinic Lou Ruvo Center for Brain Health (A.R., D.W.), Las Vegas, NV; Department of Neurology (E.D.R.), University of Alabama at Birmingham; Glenn Biggs Institute for Alzheimer's & Neurodegenerative Diseases (A.C.S.), UT Health San Antonio; Tanz Centre for Research in Neurodegenerative Diseases (M.C.T.), Division of Neurology, University of Toronto, Ontario, Canada; Department of Neurology (H.W.H., A.L.B., H.J.R.), Memory and Aging Center, University of California, San Francisco; Weill Institute for Neurosciences, San Francisco, CA; and Department of Neuroscience (R.R.), Mayo Clinic, Jacksonville, FL.
Article Synopsis
- The study investigates the role of the genetic variant rs1990622 as a potential modifier of disease risk in frontotemporal lobar degeneration (FTLD), particularly among those with pathogenic variants.
- Researchers enrolled participants from the ALLFTD study, analyzing the impact of rs1990622 on gray matter volume and cognitive function across various genetic groups related to FTD.
- Results indicate that carriers of the minor allele of rs1990622 show increased gray matter volume and better cognitive performance, especially in the thalamus and among presymptomatic individuals.
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