Limiting RyR2 open time prevents Alzheimer's disease‐related deficits in the 3xTG‐AD mouse model

2021 ◽  
Author(s):  
Yajing Liu ◽  
Jinjing Yao ◽  
Zhenpeng Song ◽  
Wenting Guo ◽  
Bo Sun ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Open Time ◽  
Ad Mouse Model

REST/NRSF-induced changes of ChAT protein expression in the neocortex and hippocampus of the 3xTg-AD mouse model for Alzheimer's disease

Life Sciences ◽  
2014 ◽  
Vol 116 (2) ◽  
pp. 83-89 ◽  
Author(s):  
E. Orta-Salazar ◽  
A. Aguilar-Vázquez ◽  
H. Martínez-Coria ◽  
S. Luquín-De Anda ◽  
M. Rivera-Cervantes ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Protein Expression ◽  
Induced Changes ◽  
Ad Mouse Model

scholarly journals Altered slow (<1 Hz) and fast (beta and gamma) neocortical oscillations in the 3xTg-AD mouse model of Alzheimer's disease under anesthesia

2019 ◽  
Vol 79 ◽  
pp. 142-151 ◽  
Author(s):  
Patricia Castano-Prat ◽  
Lorena Perez-Mendez ◽  
Maria Perez-Zabalza ◽  
Coral Sanfeliu ◽  
Lydia Giménez-Llort ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

scholarly journals Sex Differences in Healthspan Predict Lifespan in the 3xTg-AD Mouse Model of Alzheimer’s Disease

2018 ◽  
Vol 10 ◽  
Author(s):  
Alice E. Kane ◽  
Sooyoun Shin ◽  
Aimee A. Wong ◽  
Emre Fertan ◽  
Natalia S. Faustova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sex Differences ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

scholarly journals Enhanced caffeine-induced Ca2+ release in the 3xTg-AD mouse model of Alzheimer's disease

2005 ◽  
Vol 94 (6) ◽  
pp. 1711-1718 ◽  
Author(s):  
Ian F. Smith ◽  
Brian Hitt ◽  
Kim N. Green ◽  
Salvatore Oddo ◽  
Frank M. LaFerla
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

scholarly journals Microglial analysis in whole‐mount retina of Alzheimer's disease 3xTg‐AD mouse model

2019 ◽  
Vol 97 (S263) ◽  
Author(s):  
Ana I. Ramírez ◽  
Elena Salobrar‐García ◽  
Ana C. Rodrigues‐Neves ◽  
Rosa Hoz ◽  
Juan J. Salazar ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Whole Mount ◽  
Ad Mouse Model

scholarly journals Neurovascular coupling preserved in a chronic mouse model of Alzheimer’s disease: Methodology is critical

2018 ◽  
Author(s):  
Paul S Sharp ◽  
Kam Ameen-Ali ◽  
Luke Boorman ◽  
Sam Harris ◽  
Stephen Wharton ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Animal Models ◽  
Mouse Model ◽  
Neurovascular Coupling ◽  
Hemodynamic Responses ◽  
Experimental Procedure ◽  
Model Of Alzheimer’S Disease ◽  
Disease Condition ◽  
Ad Mouse Model

AbstractNeurovascular coupling is the process by which neural activity causes localised changes in cerebral blood flow. Impaired neurovascular coupling has been suggested as an early pathogenic factor in Alzheimer’s disease (AD), and if so, could serve as an early biomarker of cerebral pathology. We have established an anaesthetic regime in which evoked hemodynamic responses are comparable to those in awake mice. This protocol was adapted to allow repeated measurements of neurovascular function over three months in the hAPP-J20 mouse model of AD (J20-AD) and wild-type (WT) controls. Animals were 9-12 months old at the start of the experiment, which is when deficits due to the disease condition would be expected. Mice were chronically prepared with a cranial window through which optical imaging spectroscopy (OIS) was used to generate functional maps of the cerebral blood volume and saturation changes evoked by whisker stimulation and vascular reactivity challenges. Unexpectedly, the hemodynamic responses were largely preserved in the J20-AD group. This result failed to confirm previous investigations using the J20-AD model. However, a final acute electrophysiology and OIS experiment was performed to measure both neural and hemodynamic responses concurrently. In this experiment, previously reported deficits in neurovascular coupling in the J20-AD model were observed. This suggests that J20-AD mice may be more susceptible to the physiologically stressing conditions of an acute experimental procedure compared to WT animals. These results therefore highlight the importance of experimental procedure when determining the characteristics of animal models of human disease.Significance StatementUsing a chronic anaesthetised preparation, we measured hemodynamic responses evoked by sensory stimulation and respiratory gases in the J20-AD mouse model of Alzheimer’s Disease over a period of 3 months. We showed that neurovascular responses were preserved compared to age matched wildtype controls. These results failed to confirm previous investigations reporting a marked reduction of neurovascular coupling in the J20-AD mouse model. However, when our procedure involved acute surgical procedures, previously reported neurovascular deficits were observed. The effects of acute electrode implantation were caused by disturbances to baseline physiology rather than a consequence of the disease condition. These results highlight the importance of experimental procedure when determining the characteristics of animal models of human disease.

scholarly journals Bacteria isolated from the stools of Alzheimer’s disease patients exacerbate cognitive impairment in 3xTg AD mouse model

2020 ◽  
Vol 16 (S2) ◽  
Author(s):  
Moira Marizzoni ◽  
Benjamin Tournier ◽  
Arthur Pauis ◽  
Philippe Millet ◽  
Peppino Mirabelli ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Ad Mouse Model

scholarly journals Ganoderic Acid A Promotes Amyloid-β Clearance (In Vitro) and Ameliorates Cognitive Deficiency in Alzheimer’s Disease (Mouse Model) Through Autophagy Induced by Activating Axl

2021 ◽  
Vol 22 (11) ◽  
pp. 5559
Author(s):  
Li-Feng-Rong Qi ◽  
Shuai Liu ◽  
Yu-Ci Liu ◽  
Ping Li ◽  
Xiaojun Xu
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Β ◽  
Microglial Cells ◽  
Confocal Laser ◽  
Ganoderic Acid ◽  
Aβ Clearance ◽  
Cognitive Deficiency ◽  
Ad Mouse Model

Alzheimer’s disease (AD) is thought to be caused by amyloid-β (Aβ) accumulation in the central nervous system due to deficient clearance. The aim of the present study was to investigate the effect of ganoderic acid A (GAA) on Aβ clearance in microglia and its anti-AD activity. Aβ degradation in BV2 microglial cells was determined using an intracellular Aβ clearance assay. GAA stimulated autophagosome formation via the Axl receptor tyrosine kinase (Axl)/RAC/CDC42-activated kinase 1 (Pak1) pathway was determined by Western blot analyses, and fluorescence-labeled Aβ42 was localized in lysosomes in confocal laser microscopy images. The in vivo anti-AD activity of GAA was evaluated by object recognition and Morris water maze (MWM) tests in an AD mouse model following intracerebroventricular injection of aggregated Aβ42. The autophagy level in the hippocampus was assayed by immunohistochemical assessment against microtubule-associated proteins 1A/1B light-chain 3B (LC3B). Intracellular Aβ42 levels were significantly reduced by GAA treatment in microglial cells. Additionally, GAA activated autophagy according to increased LC3B-II levels, with this increased autophagy stimulated by upregulating Axl and Pak1 phosphorylation. The effect of eliminating Aβ by GAA through autophagy was reversed by R428, an Axl inhibitor, or IPA-3, a Pak1 inhibitor. Consistent with the cell-based assay, GAA ameliorated cognitive deficiency and reduced Aβ42 levels in an AD mouse model. Furthermore, LC3B expression in the hippocampus was up-regulated by GAA treatment, with these GAA-specific effects abolished by R428. GAA promoted Aβ clearance by enhancing autophagy via the Axl/Pak1 signaling pathway in microglial cells and ameliorated cognitive deficiency in an AD mouse model.

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