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Arlene M. Manelli

Researcher at NorthShore University HealthSystem

Publications -  21
Citations -  3330

Arlene M. Manelli is an academic researcher from NorthShore University HealthSystem. The author has contributed to research in topics: Apolipoprotein E & Amyloid precursor protein. The author has an hindex of 18, co-authored 20 publications receiving 3172 citations. Previous affiliations of Arlene M. Manelli include University of Illinois at Chicago.

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Oligomeric and Fibrillar Species of Amyloid-β Peptides Differentially Affect Neuronal Viability

TL;DR: Data demonstrate that protocols developed to produce oligomeric and fibrillar Aβ-(1–42) are useful in distinguishing the structural and functional differences between A β-(1-42) and Aβ-1–40 and genetic mutations of Aβ.
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Isoform-specific binding of apolipoprotein E to beta-amyloid.

TL;DR: Apolipoprotein E (apoE), particularly the e4 allele, is genetically linked to the incidence of Alzheimer's disease, and the presence of an approximately 45-kDa complex with both A beta and apoE immunoreactivity is revealed.
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Differential effects of oligomeric and fibrillar amyloid-β1–42 on astrocyte-mediated inflammation

TL;DR: The results suggest that oligomers induced a profound, early inflammatory response, whereas fibrillar Abeta showed less increase of pro-inflammatory molecules, consistent with a more chronic form of inflammation.
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Intraneuronal Aβ detection in 5xFAD mice by a new Aβ-specific antibody

TL;DR: Both intraneuronal Aβ accumulation and extracellular A β deposition was demonstrated in 5xFAD mice and 3xTg mice with MOAB-2, an antibody that will help differentiate intracellular Aβ from APP, however, further investigation is required to determine whether a molecular mechanism links the presence of intraneuonal A β with neurotoxicity.
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Serine mutations in transmembrane V of the dopamine D1 receptor affect ligand interactions and receptor activation

TL;DR: The results suggest that serines present in transmembrane V of the D1 receptor affect ligand interactions and receptor signal transduction, but not entirely in the manner that would be predicted from the model proposed for the beta-adrenergic receptor.