Temporal memory deficits in Alzheimer's mouse models: rescue by genetic deletion of BACE1

2006 ◽  
Vol 23 (1) ◽  
pp. 251-260 ◽  
Author(s):  
Masuo Ohno ◽  
Lei Chang ◽  
Wilbur Tseng ◽  
Holly Oakley ◽  
Martin Citron ◽  
...  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Vanessa De Castro ◽  
Pascal Girard

AbstractEpisodic memory decline is an early marker of cognitive aging in human. Although controversial in animals and called “episodic-like memory”, several models have been successfully developed, however they rarely focused on ageing. While marmoset is an emerging primate model in aging science, episodic-like memory has never been tested in this species and importantly in aged marmosets. Here, we examined if the recall of the what-when and what-where building blocks of episodic-like memory declines in ageing marmosets. We developed a naturalistic approach using spontaneous exploration of real objects by young and old marmosets in the home cage. We implemented a three-trial task with 1 week inter-trial interval. Two different sets of identical objects were presented in sample trials 1 and 2, respectively. For the test trial, two objects from each set were presented in a former position and two in a new one. We quantified the exploratory behaviour and calculated discrimination indices in a cohort of 20 marmosets. Young animals presented a preserved memory for combined what-where, and what-when components of the experiment, which declined with aging. These findings lead one to expect episodic-like memory deficits in aged marmosets.


2014 ◽  
Vol 17 (12) ◽  
pp. 1736-1743 ◽  
Author(s):  
Yong-Seok Lee ◽  
Dan Ehninger ◽  
Miou Zhou ◽  
Jun-Young Oh ◽  
Minkyung Kang ◽  
...  

2017 ◽  
Vol 13 (7) ◽  
pp. P952
Author(s):  
Delphine Ibghi ◽  
Mati Lopez-Grancha ◽  
Patrick Bernardelli ◽  
Nicolas Moindrot ◽  
Philippe Goniot ◽  
...  

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 803
Author(s):  
Emma C. Tovey Crutchfield ◽  
Sarah E. Garnish ◽  
Joanne M. Hildebrand

Necroptosis is an inflammatory form of lytic programmed cell death that is thought to have evolved to defend against pathogens. Genetic deletion of the terminal effector protein—MLKL—shows no overt phenotype in the C57BL/6 mouse strain under conventional laboratory housing conditions. Small molecules that inhibit necroptosis by targeting the kinase activity of RIPK1, one of the main upstream conduits to MLKL activation, have shown promise in several murine models of non-infectious disease and in phase II human clinical trials. This has triggered in excess of one billion dollars (USD) in investment into the emerging class of necroptosis blocking drugs, and the potential utility of targeting the terminal effector is being closely scrutinised. Here we review murine models of disease, both genetic deletion and mutation, that investigate the role of MLKL. We summarize a series of examples from several broad disease categories including ischemia reperfusion injury, sterile inflammation, pathogen infection and hematological stress. Elucidating MLKL’s contribution to mouse models of disease is an important first step to identify human indications that stand to benefit most from MLKL-targeted drug therapies.


2013 ◽  
Vol 107 ◽  
pp. 26-34 ◽  
Author(s):  
Patrick Leclerc ◽  
Helena Idborg ◽  
Linda Spahiu ◽  
Charlotte Larsson ◽  
Natalia Nekhotiaeva ◽  
...  

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