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Brett A. Chromy
Researcher at University of California, Davis
Publications - 60
Citations - 8144
Brett A. Chromy is an academic researcher from University of California, Davis. The author has contributed to research in topics: Proteomics & Yersinia pestis. The author has an hindex of 34, co-authored 60 publications receiving 7666 citations. Previous affiliations of Brett A. Chromy include Northwestern University & Lawrence Livermore National Laboratory.
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Journal ArticleDOI
Diffusible, nonfibrillar ligands derived from Aβ1–42 are potent central nervous system neurotoxins
Mary P. Lambert,A. K. Barlow,Brett A. Chromy,C. Edwards,R. Freed,M. Liosatos,Todd E. Morgan,Irina Rozovsky,Barbara L. Trommer,Kirsten L. Viola,Pat Wals,Chuan Zhang,Caleb E. Finch,Grant A. Krafft,William L. Klein +14 more
TL;DR: It is hypothesized that impaired synaptic plasticity and associated memory dysfunction during early stage Alzheimer's disease and severe cellular degeneration and dementia during end stage could be caused by the biphasic impact of Abeta-derived diffusible ligands acting upon particular neural signal transduction pathways.
Journal ArticleDOI
Soluble oligomers of β amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus
Hai Wei Wang,Joseph F. Pasternak,Joseph F. Pasternak,Helen Kuo,Helen Ristic,Mary P. Lambert,Brett A. Chromy,Kirsten L. Viola,William L. Klein,W. Blaine Stine,Grant A. Krafft,Barbara L. Trommer,Barbara L. Trommer +12 more
TL;DR: The data suggest that soluble non-fibrillar amyloid may contribute to the pathogenesis of AD both by impairing LTP/memory formation at the cellular level and by creating 'neuroplasticity imbalance' manifested by unopposed LTD in the setting of impaired capacity for neural repair via reversal of LTD or LTP.
Journal ArticleDOI
Self-assembly of Aβ1-42 into globular neurotoxins
Brett A. Chromy,Richard Nowak,Mary P. Lambert,Kirsten L. Viola,Lei Chang,Pauline T. Velasco,Bryan W. Jones,Sara J. Fernandez,Pascale N. Lacor,Peleg M. Horowitz,Caleb E. Finch,Grant A. Krafft,William L. Klein +12 more
TL;DR: Aβ 1−42 (Aβ1-42) is a self-associating peptide that becomes neurotoxic upon aggregation as discussed by the authors, and its toxicity originally was attributed to the presence of large, readily formed Aβ fibrils.
Journal ArticleDOI
Vaccination with soluble Aβ oligomers generates toxicity-neutralizing antibodies
Mary P. Lambert,Kirsten L. Viola,Brett A. Chromy,Lei Chang,Todd E. Morgan,Jiaxin Yu,Duane L. Venton,Grant A. Krafft,Caleb E. Finch,William L. Klein +9 more
TL;DR: Results support the hypothesis that immunizations of transgenic mice derive therapeutic benefit from the immuno‐neutralization of soluble Aβ‐derived toxins, and suggest analogous immuno-neutralizing of oligomers in humans may be a key in AD vaccines.
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Amyloid-β peptide activates cultured astrocytes: morphological alterations, cytokine induction and nitric oxide release
TL;DR: Treatment of rat cortical astrocyte cultures with aggregated Aβ 1–42 peptide induces activation, as assessed by reactive morphological changes and upregulation of selective glial mRNA and proteins, such as the inflammatory cytokine interleukin-1β.