S. Fromholt

发表

Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology

D. Borchelt, B. Giasson, Jada Lewis, 2018, Molecular neurodegeneration.

Changes in proteome solubility indicate widespread proteostatic disruption in mouse models of neurodegenerative disease

D. Borchelt, B. Giasson, Jada Lewis, 2018, Acta Neuropathologica.

Collusion of α-Synuclein and Aβ aggravating co-morbidities in a novel prion-type mouse model

D. Borchelt, B. Giasson, Cara J. Riffe, 2021, Molecular Neurodegeneration.

Reduction of low-density lipoprotein receptor-related protein (LRP1) in hippocampal neurons does not proportionately reduce, or otherwise alter, amyloid deposition in APPswe/PS1dE9 transgenic mice

D. Borchelt, Guilian M. Xu, S. Fromholt, 2012, Alzheimer's Research & Therapy.

Distinct conformers of transmissible misfolded SOD1 distinguish human SOD1-FALS from other forms of familial and sporadic ALS

Jacob I. Ayers, D. Borchelt, J. Glass, 2016, Acta Neuropathologica.

Direct and indirect mechanisms for wild-type SOD1 to enhance the toxicity of mutant SOD1 in bigenic transgenic mice.

D. Borchelt, Guilian M. Xu, S. Fromholt, 2015, Human molecular genetics.

Immunoglobulin G-class mouse monoclonal antibodies to major brain gangliosides.

Hiromi Ito, M. Kiso, R. Schnaar, 2002, Analytical biochemistry.

Systematic synthesis and MAG-binding activity of novel sulfated GM1b analogues as mimics of Chol-1 (alpha-series) gangliosides: highly active ligands for neural siglecs.

Hiromi Ito, M. Kiso, R. Schnaar, 2003, Carbohydrate research.

Substantially elevating the levels of αB‐crystallin in spinal motor neurons of mutant SOD1 mice does not significantly delay paralysis or attenuate mutant protein aggregation

D. Borchelt, Zoe B Siemienski, Keith W Crosby, 2015, Journal of neurochemistry.

Generation of a new transgenic mouse model for assessment of tau gene silencing therapies

D. Borchelt, Jada Lewis, S. Fromholt, 2016, Alzheimer's Research & Therapy.

High‐Affinity Anti‐Ganglioside IgG Antibodies Raised in Complex Ganglioside Knockout Mice

R. Schnaar, J. Griffin, James E. K. Hildreth, 2000, Journal of neurochemistry.

Experimental transmissibility of mutant SOD1 motor neuron disease

Jacob I. Ayers, D. Borchelt, Guilian M. Xu, 2014, Acta Neuropathologica.

Anti-Ganglioside Antibodies Bind with Enhanced Affinity to Gangliosides Containing Very Long Chain Fatty Acids

H. Moser, A. Moser, R. Schnaar, 2002, Neurochemical Research.

Distinctive features of the D101N and D101G variants of superoxide dismutase 1; two mutations that produce rapidly progressing motor neuron disease

Jacob I. Ayers, D. Borchelt, J. Valentine, 2014, Journal of neurochemistry.

Analysis of spinal and muscle pathology in transgenic mice overexpressing wild-type and ALS-linked mutant MATR3

D. Borchelt, Jada Lewis, Zoe B Siemienski, 2018, Acta Neuropathologica Communications.

Retraction Note: Transgenic mice overexpressing the ALS-linked protein Matrin 3 develop a profound muscle phenotype

D. Borchelt, M. Swanson, L. Notterpek, 2017, Acta Neuropathologica Communications.

Transgenic mice overexpressing the ALS-linked protein Matrin 3 develop a profound muscle phenotype

D. Borchelt, M. Swanson, L. Notterpek, 2016, Acta Neuropathologica Communications.

Prion-like propagation of mutant SOD1 misfolding and motor neuron disease spread along neuroanatomical pathways

Jacob I. Ayers, D. Borchelt, S. Fromholt, 2015, Acta Neuropathologica.

Modeling the Competition between Misfolded Aβ Conformers That Produce Distinct Types of Amyloid Pathology in Alzheimer’s Disease

D. Borchelt, Guilian M. Xu, S. Fromholt, 2022, Biomolecules.

Gangliosides are functional nerve cell ligands for myelin-associated glycoprotein (MAG), an inhibitor of nerve regeneration

M. Schachner, R. Schnaar, J. Dang, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Experimental mutagenesis of huntingtin to map cleavage sites: different outcomes in cell and mouse models.

D. Borchelt, Andrew T. N. Tebbenkamp, L. Tessarollo, 2014, Journal of Huntington's disease.

Murine Aβ over-production produces diffuse and compact Alzheimer-type amyloid deposits

D. Borchelt, T. Golde, Guilian M. Xu, 2015, Acta neuropathologica communications.

TAPPing into the potential of inducible tau/APP transgenic mice

D. Borchelt, Jada Lewis, Guilian M. Xu, 2022, Neuropathology and applied neurobiology.

Analysis of spinal and muscle pathology in transgenic mice overexpressing wild-type and ALS-linked mutant MATR3

D. Borchelt, Jada Lewis, S. Fromholt, 2018, Acta neuropathologica communications.

Reversible Pathologic and Cognitive Phenotypes in an Inducible Model of Alzheimer-Amyloidosis

D. Borchelt, A. Savonenko, T. Golde, 2013, The Journal of Neuroscience.

Widespread and efficient transduction of spinal cord and brain following neonatal AAV injection and potential disease modifying effect in ALS mice.

Jacob I. Ayers, D. Borchelt, T. Golde, 2015, Molecular therapy : the journal of the American Society of Gene Therapy.

Soluble brain homogenates from diverse human and mouse sources preferentially seed diffuse Aβ plaque pathology when injected into newborn mouse hosts.

Hunter S. Futch, D. Borchelt, T. Golde, 2021, Free neuropathology.

Transgenic mice expressing caspase-6-derived N-terminal fragments of mutant huntingtin develop neurologic abnormalities with predominant cytoplasmic inclusion pathology composed largely of a smaller proteolytic derivative.

D. Borchelt, Andrew T. N. Tebbenkamp, R. Mandel, 2011, Human molecular genetics.

Membrane redistribution of gangliosides and glycosylphosphatidylinositol-anchored proteins in brain tissue sections under conditions of lipid raft isolation.

R. Schnaar, L. Nimrichter, G. Lauc, 2005, Biochimica et biophysica acta.

Myelin-associated glycoprotein and complementary axonal ligands, gangliosides, mediate axon stability in the CNS and PNS: Neuropathology and behavioral deficits in single- and double-null mice

T. Crawford, R. Schnaar, J. Griffin, 2005, Experimental Neurology.

Transgenic mice overexpressing the ALS-linked protein Matrin 3 develop a profound muscle phenotype

D. Borchelt, M. Swanson, L. Notterpek, 2016, Acta neuropathologica communications.

Reduction of low-density lipoprotein receptor-related protein (LRP1) in hippocampal neurons does not proportionately reduce, or otherwise alter, amyloid deposition in APPswe/PS1dE9 transgenic mice

D. Borchelt, S. Fromholt, Guilian Xu, 2012, Alzheimer's Research & Therapy.

Membrane redistribution of gangliosides and glycosylphosphatidylinositol-anchored proteins under conditions of lipid raft isolation

R. Schnaar, L. Nimrichter, G. Lauc, 2005 .

Retraction Note: Transgenic mice overexpressing the ALS-linked protein Matrin 3 develop a profound muscle phenotype

D. Borchelt, M. Swanson, L. Notterpek, 2016, Acta neuropathologica communications.

Differential induction of mutant SOD1 misfolding and aggregation by tau and α-synuclein pathology

D. Borchelt, B. Giasson, Jada Lewis, 2018, Molecular neurodegeneration.

Relationship between mutant Cu/Zn superoxide dismutase 1 maturation and inclusion formation in cell models

Jacob I. Ayers, D. Borchelt, J. Valentine, 2017, Journal of neurochemistry.

Generation of a new transgenic mouse model for assessment of tau gene silencing therapies

D. Borchelt, Jada Lewis, S. Fromholt, 2016, Alzheimer's Research & Therapy.

The role of Trp‐82 in the folding of intestinal fatty acid binding protein

Paula M Dalessio, Susan E Fromholt, Ira J Ropson, 2005, Proteins.

Diversity in Aβ deposit morphology and secondary proteome insolubility across models of Alzheimer-type amyloidosis

D. Borchelt, T. Golde, Paramita Chakrabarty, 2020, Acta Neuropathologica Communications.

Multiple Factors Influence the Incubation Period of ALS Prion-like Transmission in SOD1 Transgenic Mice

Jacob I. Ayers, D. Borchelt, S. Fromholt, 2023, Viruses.

Gangliosides are functional nerve cell ligands for myelin-associated glycoprotein (MAG), an inhibitor of nerve regeneration

M. Schachner, R. Schnaar, J. Dang, 2002, Proceedings of the National Academy of Sciences of the United States of America.

Changes in proteome solubility indicate widespread proteostatic disruption in mouse models of neurodegenerative disease

D. Borchelt, B. Giasson, Jada Lewis, 2018, Acta Neuropathologica.