scholarly journals mGlu5 receptors and cellular prion protein mediate amyloid-β-facilitated synaptic long-term depression in vivo

2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Neng-Wei Hu ◽  
Andrew J. Nicoll ◽  
Dainan Zhang ◽  
Alexandra J. Mably ◽  
Tiernan O’Malley ◽  
...  
Keyword(s):  
Prion Protein ◽  
Amyloid Β ◽  
Cellular Prion Protein ◽  
Long Term Depression ◽  
Mglu5 Receptors

scholarly journals Cellular prion protein null mice display normal AMPA receptor mediated long term depression

Prion ◽  
2008 ◽  
Vol 2 (2) ◽  
pp. 48-50 ◽  
Author(s):  
Houman Khosravani ◽  
Yunfeng Zhang ◽  
Gerald W. Zamponi
Keyword(s):  
Prion Protein ◽  
Ampa Receptor ◽  
Cellular Prion Protein ◽  
Long Term Depression

Soluble tau aggregates inhibit synaptic long-term depression and amyloid β-facilitated LTD in vivo

2019 ◽  
Vol 127 ◽  
pp. 582-590 ◽  
Author(s):  
Tomas Ondrejcak ◽  
Neng-Wei Hu ◽  
Yingjie Qi ◽  
Igor Klyubin ◽  
Grant T. Corbett ◽  
...  
Keyword(s):  
Amyloid Β ◽  
Long Term Depression

scholarly journals Synthetic amyloid-β oligomers impair long-term memory independently of cellular prion protein

2010 ◽  
Vol 107 (5) ◽  
pp. 2295-2300 ◽  
Author(s):  
Claudia Balducci ◽  
Marten Beeg ◽  
Matteo Stravalaci ◽  
Antonio Bastone ◽  
Alessandra Sclip ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Prion Protein ◽  
Amyloid Β ◽  
Cellular Prion Protein ◽  
Long Term Memory ◽  
Ample Evidence ◽  
Knock Out ◽  
Intracerebroventricular Injections ◽  
Knock Out Mice

Inability to form new memories is an early clinical sign of Alzheimer’s disease (AD). There is ample evidence that the amyloid-β (Aβ) peptide plays a key role in the pathogenesis of this disorder. Soluble, bio-derived oligomers of Aβ are proposed as the key mediators of synaptic and cognitive dysfunction, but more tractable models of Aβ−mediated cognitive impairment are needed. Here we report that, in mice, acute intracerebroventricular injections of synthetic Aβ1–42 oligomers impaired consolidation of the long-term recognition memory, whereas mature Aβ1–42 fibrils and freshly dissolved peptide did not. The deficit induced by oligomers was reversible and was prevented by an anti-Aβ antibody. It has been suggested that the cellular prion protein (PrPC) mediates the impairment of synaptic plasticity induced by Aβ. We confirmed that Aβ1–42 oligomers interact with PrPC, with nanomolar affinity. However, PrP-expressing and PrP knock-out mice were equally susceptible to this impairment. These data suggest that Aβ1–42 oligomers are responsible for cognitive impairment in AD and that PrPC is not required.

scholarly journals Prion protein and prion disease at a glance

2021 ◽  
Vol 134 (17) ◽  
Author(s):  
Caihong Zhu ◽  
Adriano Aguzzi
Keyword(s):  
Prion Protein ◽  
Prion Disease ◽  
Neurodegenerative Disorders ◽  
Prion Diseases ◽  
Amyloid Β ◽  
Cellular Prion Protein ◽  
Future Studies ◽  
Associated Proteins ◽  
Main Component ◽  
Conformational Conversion

ABSTRACT Prion diseases are neurodegenerative disorders caused by conformational conversion of the cellular prion protein (PrPC) into scrapie prion protein (PrPSc). As the main component of prion, PrPSc acts as an infectious template that recruits and converts normal cellular PrPC into its pathogenic, misfolded isoform. Intriguingly, the phenomenon of prionoid, or prion-like, spread has also been observed in many other disease-associated proteins, such as amyloid β (Aβ), tau and α-synuclein. This Cell Science at a Glance and the accompanying poster highlight recently described physiological roles of prion protein and the advanced understanding of pathogenesis of prion disease they have afforded. Importantly, prion protein may also be involved in the pathogenesis of other neurodegenerative disorders such as Alzheimer's and Parkinson's disease. Therapeutic studies of prion disease have also exploited novel strategies to combat these devastating diseases. Future studies on prion protein and prion disease will deepen our understanding of the pathogenesis of a broad spectrum of neurodegenerative conditions.

Long-term depression in the sensorimotor cortex induced by repeated delivery of 10 Hz trains in vivo

Neuroscience ◽  
2006 ◽  
Vol 140 (1) ◽  
pp. 13-20 ◽  
Author(s):  
C.M. Werk ◽  
H.S. Klein ◽  
C.E. Nesbitt ◽  
C.A. Chapman
Keyword(s):  
Sensorimotor Cortex ◽  
Long Term Depression

scholarly journals Impact of the Cellular Prion Protein on Amyloid-β and 3PO-Tau Processing

2013 ◽  
Vol 38 (3) ◽  
pp. 551-565 ◽  
Author(s):  
Matthias Schmitz ◽  
Katharina Wulf ◽  
Sandra C. Signore ◽  
Walter J. Schulz-Schaeffer ◽  
Pawel Kermer ◽  
...  
Keyword(s):  
Prion Protein ◽  
Amyloid Β ◽  
Cellular Prion Protein
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