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Neuritin can normalize neural deficits of Alzheimer's disease SCIE SCOPUS

Title
Neuritin can normalize neural deficits of Alzheimer's disease
Authors
An, KJung, JHJeong, AYKim, HGJung, SYLee, KKim, HJKim, SJJeong, TYSon, YKim, HSKim, JH
Date Issued
2014-11
Publisher
Nature Pub. Group
Abstract
Reductions in hippocampal neurite complexity and synaptic plasticity are believed to contribute to the progressive impairment in episodic memory and the mild cognitive decline that occur particularly in the early stages of Alzheimer's disease (AD). Despite the functional and therapeutic importance for patients with AD, intervention to rescue or normalize dendritic elaboration and synaptic plasticity is scarcely provided. Here we show that overexpression of neuritin, an activity-dependent protein, promoted neurite outgrowth and maturation of synapses in parallel with enhanced basal synaptic transmission in cultured hippocampal neurons. Importantly, exogenous application of recombinant neuritin fully restored dendritic complexity as well as spine density in hippocampal neurons prepared from Tg2576 mice, whereas it did not affect neurite branching of neurons from their wild-type littermates. We also showed that soluble recombinant neuritin, when chronically infused into the brains of Tg2576 mice, normalized synaptic plasticity in acute hippocampal slices, leading to intact long-term potentiation. By revealing the protective actions of soluble neuritin against AD-related neural defects, we provide a potential therapeutic approach for patients with AD.
Keywords
TERM SYNAPTIC PLASTICITY; AMYLOID-BETA PROTEIN; DENDRITIC SPINES; MOUSE MODEL; A-BETA; VISUAL-CORTEX; IN-VIVO; ANTIDEPRESSANT ACTIONS; CASPASE-3 ACTIVATION; PYRAMIDAL NEURONS
URI
https://oasis.postech.ac.kr/handle/2014.oak/9867
DOI
10.1038/CDDIS.2014.478
ISSN
2041-4889
Article Type
Article
Citation
Cell death and disease, vol. 5, page. E1523, 2014-11
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김정훈KIM, JOUNG HUN
Dept of Life Sciences
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