Hannah Brautigam, Ph.D.

Neurosciences Icahn School of Medicine at Mount Sinai, New York, NY, United States 
"Hannah Brautigam"
Mean distance: 17.71 (cluster 32)


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Samuel E. Gandy grad student 2013 Mount Sinai School of Medicine
 (Novel early-onset Alzheimer's disease presenilin 1 (PS1) exon 8 mutation with unusual loss of function and allosteric modulation properties.)
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Brautigam H, Moreno CL, Steele JW, et al. (2015) Physiologically generated presenilin 1 lacking exon 8 fails to rescue brain PS1-/- phenotype and forms complexes with wildtype PS1 and nicastrin. Scientific Reports. 5: 17042
Price KA, Varghese M, Sowa A, et al. (2014) Altered synaptic structure in the hippocampus in a mouse model of Alzheimer's disease with soluble amyloid-β oligomers and no plaque pathology. Molecular Neurodegeneration. 9: 41
Steele JW, Brautigam H, Short JA, et al. (2014) Early fear memory defects are associated with altered synaptic plasticity and molecular architecture in the TgCRND8 Alzheimer's disease mouse model. The Journal of Comparative Neurology. 522: 2319-35
Brautigam H, Steele JW, Westaway D, et al. (2012) The isotropic fractionator provides evidence for differential loss of hippocampal neurons in two mouse models of Alzheimer's disease. Molecular Neurodegeneration. 7: 58
Dickstein DL, Brautigam H, Stockton SD, et al. (2010) Changes in dendritic complexity and spine morphology in transgenic mice expressing human wild-type tau. Brain Structure & Function. 214: 161-79
Dickstein DL, Walsh J, Brautigam H, et al. (2010) Role of vascular risk factors and vascular dysfunction in Alzheimer's disease. The Mount Sinai Journal of Medicine, New York. 77: 82-102
Brautigam H, Klingstedt T, Prokop S, et al. (2010) O4-08-06: New Conformation-Sensing Imaging Compounds Distinguish Protein Deposits In Apoe ε3/ε3 Alzheimer's Patients From that in Apoe ε4/ε4 Alzheimer's Patients Alzheimer's & Dementia. 6: e19-e20
Pedrini S, Thomas C, Brautigam H, et al. (2009) Dietary composition modulates brain mass and solubilizable Abeta levels in a mouse model of aggressive Alzheimer's amyloid pathology. Molecular Neurodegeneration. 4: 40
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