William A. Eimer, Ph.D.
Affiliations: | 2013 | Integrated Graduate Program in the Life Sciences | Northwestern University, Evanston, IL |
Area:
Alzheimer'sGoogle:
"William Eimer"Mean distance: 15.83 (cluster 11) | S | N | B | C | P |
Parents
Sign in to add mentor| Robert Vassar | grad student | 2013 | Northwestern | |
| (Intraneuronal Abeta42 Neuron Loss, Dystrophic Neurites, and Heterozygous BACE1 in the 5XFAD Mouse Model of Alzheimer's Disease.) | ||||
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Publications
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| Eimer WA, Vijaya Kumar DK, Navalpur Shanmugam NK, et al. (2018) Alzheimer's Disease-Associated β-Amyloid Is Rapidly Seeded by Herpesviridae to Protect against Brain Infection. Neuron. 99: 56-63.e3 |
| Vijaya Kumar DK, Eimer WA, Tanzi RE, et al. (2016) Alzheimer's disease: the potential therapeutic role of the natural antibiotic amyloid-β peptide. Neurodegenerative Disease Management |
| Kumar DK, Choi SH, Washicosky KJ, et al. (2016) Amyloid-β peptide protects against microbial infection in mouse and worm models of Alzheimer's disease. Science Translational Medicine. 8: 340ra72 |
| Sadleir KR, Eimer WA, Cole SL, et al. (2015) Aβ reduction in BACE1 heterozygous null 5XFAD mice is associated with transgenic APP level. Molecular Neurodegeneration. 10: 1 |
| Sadleir KR, Eimer WA, Kaufman RJ, et al. (2014) Genetic inhibition of phosphorylation of the translation initiation factor eIF2α does not block Aβ-dependent elevation of BACE1 and APP levels or reduce amyloid pathology in a mouse model of Alzheimer's disease. Plos One. 9: e101643 |
| Kandalepas PC, Sadleir KR, Eimer WA, et al. (2013) The Alzheimer's β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques. Acta Neuropathologica. 126: 329-52 |
| Eimer WA, Vassar R. (2013) Neuron loss in the 5XFAD mouse model of Alzheimer's disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation. Molecular Neurodegeneration. 8: 2 |
| Kandalepas PC, Sadleir KR, Eimer WA, et al. (2013) Erratum to: The Alzheimer’s β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques Acta Neuropathologica. 126: 623-623 |
| Youmans KL, Tai LM, Nwabuisi-Heath E, et al. (2012) APOE4-specific changes in Aβ accumulation in a new transgenic mouse model of Alzheimer disease. The Journal of Biological Chemistry. 287: 41774-86 |
| Hitt B, Riordan SM, Kukreja L, et al. (2012) β-Site amyloid precursor protein (APP)-cleaving enzyme 1 (BACE1)-deficient mice exhibit a close homolog of L1 (CHL1) loss-of-function phenotype involving axon guidance defects. The Journal of Biological Chemistry. 287: 38408-25 |