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Forest KH, Taketa R, Arora K, et al. The Neuroprotective Beta Amyloid Hexapeptide Core Reverses Deficits in Synaptic Plasticity in the 5xFAD APP/PS1 Mouse Model. Front Mol Neurosci. 2021;14:576038doi: 10.3389/fnmol.2021.576038.
Forest, K. H., Taketa, R., Arora, K., Todorovic, C., & Nichols, R. A. (2021). The Neuroprotective Beta Amyloid Hexapeptide Core Reverses Deficits in Synaptic Plasticity in the 5xFAD APP/PS1 Mouse Model. Frontiers in molecular neuroscience, 14576038. https://doi.org/10.3389/fnmol.2021.576038
Forest, Kelly H, et al. "The Neuroprotective Beta Amyloid Hexapeptide Core Reverses Deficits in Synaptic Plasticity in the 5xFAD APP/PS1 Mouse Model." Frontiers in molecular neuroscience vol. 14 (2021): 576038. doi: https://doi.org/10.3389/fnmol.2021.576038
Forest KH, Taketa R, Arora K, Todorovic C, Nichols RA. The Neuroprotective Beta Amyloid Hexapeptide Core Reverses Deficits in Synaptic Plasticity in the 5xFAD APP/PS1 Mouse Model. Front Mol Neurosci. 2021 Apr 12;14:576038. doi: 10.3389/fnmol.2021.576038. eCollection 2021. PMID: 33912008; PMCID: PMC8075567.
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Front Mol Neurosci. 2021 Apr 12;14:576038. doi: 10.3389/fnmol.2021.576038. eCollection 2021.

The Neuroprotective Beta Amyloid Hexapeptide Core Reverses Deficits in Synaptic Plasticity in the 5xFAD APP/PS1 Mouse Model.

Frontiers in molecular neuroscience

Kelly H Forest, Ruth Taketa, Komal Arora, Cedomir Todorovic, Robert A Nichols

Affiliations

  1. Department of Cell & Molecular Biology, John A. Burns School of Medicine, University of Hawai'i at M?noa, Honolulu, HI, United States.

PMID: 33912008 PMCID: PMC8075567 DOI: 10.3389/fnmol.2021.576038

Abstract

Alzheimer's disease (AD) is the most common cause of dementia in the aging population. Evidence implicates elevated soluble oligomeric Aβ as one of the primary triggers during the prodromic phase leading to AD, effected largely via hyperphosphorylation of the microtubule-associated protein tau. At low, physiological levels (pM-nM), however, oligomeric Aβ has been found to regulate synaptic plasticity as a neuromodulator. Through mutational analysis, we found a core hexapeptide sequence within the N-terminal domain of Aβ (N-Aβcore) accounting for its physiological activity, and subsequently found that the N-Aβcore peptide is neuroprotective. Here, we characterized the neuroprotective potential of the N-Aβcore against dysfunction of synaptic plasticity assessed in

Copyright © 2021 Forest, Taketa, Arora, Todorovic and Nichols.

Keywords: Alzheimer’s disease; beta amyloid (Aβ); hippocampal slice; long-term depression; long-term potentiation; neuroprotection

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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