Looking beyond the standard version of the Morris water task in the assessment of mouse models of cognitive deficits

Hippocampus ◽  
2018 ◽  
Vol 29 (1) ◽  
pp. 3-14 ◽  
Author(s):  
Jogender Mehla ◽  
Scott H. Deibel ◽  
Jamshid Faraji ◽  
Takashi Saito ◽  
Takaomi C Saido ◽  
...  
2020 ◽  
Vol 134 ◽  
pp. 104681 ◽  
Author(s):  
Joanna Sikora ◽  
Brigitte L. Kieffer ◽  
Pierre Paoletti ◽  
Abdel-Mouttalib Ouagazzal

2017 ◽  
Vol 27 (2) ◽  
pp. 180-191 ◽  
Author(s):  
Roger Prades ◽  
Eva Munarriz-Cuezva ◽  
Leyre Urigüen ◽  
Itziar Gil-Pisa ◽  
Lídia Gómez ◽  
...  

2013 ◽  
Vol 33 (11) ◽  
pp. 1666-1684 ◽  
Author(s):  
Diewertje I Bink ◽  
Katja Ritz ◽  
Eleonora Aronica ◽  
Louise van der Weerd ◽  
Mat JAP Daemen

Recent clinical data indicates that hemodynamic changes caused by cardiovascular diseases such as atherosclerosis, heart failure, and hypertension affect cognition. Yet, the underlying mechanisms of the resulting vascular cognitive impairment (VCI) are poorly understood. One reason for the lack of mechanistic insights in VCI is that research in dementia primarily focused on Alzheimer's disease models. To fill in this gap, we critically reviewed the published data and various models of VCI. Typical findings in VCI include reduced cerebral perfusion, blood–brain barrier alterations, white matter lesions, and cognitive deficits, which have also been reported in different cardiovascular mouse models. However, the tests performed are incomplete and differ between models, hampering a direct comparison between models and studies. Nevertheless, from the currently available data we conclude that a few existing surgical animal models show the key features of vascular cognitive decline, with the bilateral common carotid artery stenosis hypoperfusion mouse model as the most promising model. The transverse aortic constriction and myocardial infarction models may be good alternatives, but these models are as yet less characterized regarding the possible cerebral changes. Mixed models could be used to study the combined effects of different cardiovascular diseases on the deterioration of cognition during aging.


2019 ◽  
Author(s):  
Pishan Chang ◽  
Daniel Bush ◽  
Stephanie Schorge ◽  
Mark Good ◽  
Tara Canonica ◽  
...  

SummaryAltered neural dynamics in medial prefrontal cortex (mPFC) and hippocampus may contribute to cognitive impairments in the complex chromosomal disorder, Down Syndrome (DS). Here, we demonstrate non-overlapping behavioural differences associated with distinct abnormalities in hippocampal and mPFC electrophysiology during a canonical spatial memory task in three partially trisomic mouse models of DS (Dp1Tyb, Dp10Yey, Dp17Yey) that together cover all regions of homology with human chromosome 21 (Hsa21). Dp1Tyb mice showed slower decision-making (unrelated to the gene dose of DYRK1A, which has been implicated in DS cognitive dysfunction) and altered theta dynamics (reduced frequency, increased hippocampal-mPFC coherence, increased modulation of hippocampal high gamma); Dp10Yey mice showed impaired alternation performance and reduced theta modulation of hippocampal low gamma; while Dp17Yey mice were no different from wildtype mice. These results link specific hippocampal and mPFC circuit dysfunctions to cognitive deficits in DS models and, importantly, map them to discrete regions of Hsa21.


2021 ◽  
pp. 1-17
Author(s):  
Jesse Britz ◽  
Emmanuel Ojo ◽  
Asmita Dhukhwa ◽  
Takashi Saito ◽  
Takaomi C. Saido ◽  
...  

Background: Circadian disruption has long been recognized as a symptom of Alzheimer’s disease (AD); however, emerging data suggests that circadian dysfunction occurs early on in disease development, potentially preceding any noticeable cognitive deficits. Objective: This study compares the onset of AD in male and female wild type (C57BL6/J), transgenic (AβPP/PS1), and knock-in (APPNL - F/NL - F) AD mouse models from the period of plaque initiation (6 months) through 12 months. Methods: Rhythmic daily activity patterns, glucose sensitivity, cognitive function (Morris water maze, MWM), and AD pathology (plaques formation) were assessed. A comparison was made across sexes. Results: Sex-dependent hyperactivity in AβPP/PS1 mice was observed. In comparison to C57BL/6J animals, 6-month-old male AβPP/PS1 demonstrated nighttime hyperactivity, as did 12-month-old females. Female AβPP/PS1 animals performed significantly worse on a MWM task than AβPP/PS1 males at 12 months and trended toward increased plaque pathology. APPNL - F/NL - F 12-month-old males performed significantly worse on the MWM task compared to 12-month-old females. Significantly greater plaque pathology occurred in AβPP/PS1 animals as compared to APPNL - F/NL - F animals. Female AβPP/PS1 animals performed significantly worse than APPNL - F/NL - F animals in spatial learning and memory tasks, though this was reversed in males. Conclusion: Taken together, this study provides novel insights into baseline sex differences, as well as characterizes baseline diurnal activity variations, in the AβPP/PS1 and APPNL - F/NL - F AD mouse models.


2013 ◽  
Vol 58 (2) ◽  
pp. 278-288 ◽  
Author(s):  
Rafael De la Torre ◽  
Susana De Sola ◽  
Meritxell Pons ◽  
Arnaud Duchon ◽  
María Martínez de Lagran ◽  
...  

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