scholarly journals RAPGEF2 mediates oligomeric Aβ‐induced synaptic loss and cognitive dysfunction in the 3xTg‐AD mouse model of Alzheimer’s disease

2021 ◽  
Author(s):  
You‐Na Jang ◽  
HoChung Jang ◽  
Gyu Hyun Kim ◽  
Jeong‐Eun Noh ◽  
Keun‐A Chang ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Dysfunction ◽  
Synaptic Loss ◽  
Model Of Alzheimer’S Disease ◽  
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 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 Impaired Spatial Reorientation in the 3xTg-AD Mouse Model of Alzheimer’s Disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Alina C. Stimmell ◽  
David Baglietto-Vargas ◽  
Shawn C. Moseley ◽  
Valérie Lapointe ◽  
Lauren M. Thompson ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Spatial Reorientation ◽  
Ad Mouse Model

P1-414: GLUCOSE SUPPRESSES AKINESIA EPISODES AND REDUCES AMYLOID PATHOLOGY IN THE 3XTG-AD MOUSE MODEL OF ALZHEIMER'S DISEASE

2014 ◽  
Vol 10 ◽  
pp. P465-P465
Author(s):  
Dany Arsenault ◽  
Milene Vandal ◽  
Caroline Pierrisnard ◽  
Cyntia Tremblay ◽  
Isabelle St-Amour ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Amyloid Pathology ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

scholarly journals Reduced nitric oxide bioavailability mediates cerebroarterial dysfunction independent of cerebral amyloid angiopathy in a mouse model of Alzheimer’s disease

2017 ◽  
Vol 312 (2) ◽  
pp. H232-H238 ◽  
Author(s):  
Mario Merlini ◽  
Yi Shi ◽  
Stephan Keller ◽  
Gianluigi Savarese ◽  
Alexander Akhmedov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Model Of Alzheimer’S Disease ◽  
No Bioavailability ◽  
Cerebral Amyloid ◽  
Ad Mouse Model

In Alzheimer’s disease (AD), cerebral arteries, in contrast to cerebral microvessels, show both cerebral amyloid angiopathy (CAA) -dependent and -independent vessel wall pathology. However, it remains unclear whether CAA-independent vessel wall pathology affects arterial function, thereby chronically reducing cerebral perfusion, and, if so, which mechanisms mediate this effect. To this end, we assessed the ex vivo vascular function of the basilar artery and a similar-sized peripheral artery (femoral artery) in the Swedish-Arctic (SweArc) transgenic AD mouse model at different disease stages. Furthermore, we used quantitative immunohistochemistry to analyze CAA, endothelial morphology, and molecular pathways pertinent to vascular relaxation. We found that endothelium-dependent, but not smooth muscle-dependent, vasorelaxation was significantly impaired in basilar and femoral arteries of 15-mo-old SweArc mice compared with that of age-matched wild-type and 6-mo-old SweArc mice. This impairment was accompanied by significantly reduced levels of cyclic GMP, indicating a reduced nitric oxide (NO) bioavailability. However, no age- and genotype-related differences in oxidative stress as measured by lipid peroxidation were observed. Although parenchymal capillaries, arterioles, and arteries showed abundant CAA in the 15-mo-old SweArc mice, no CAA or changes in endothelial morphology were detected histologically in the basilar and femoral artery. Thus our results suggest that, in this AD mouse model, dysfunction of large intracranial, extracerebral arteries important for brain perfusion is mediated by reduced NO bioavailability rather than by CAA. This finding supports the growing body of evidence highlighting the therapeutic importance of targeting the cerebrovasculature in AD. NEW & NOTEWORTHY We show that vasorelaxation of the basilar artery, a large intracranial, extracerebral artery important for cerebral perfusion, is impaired independent of cerebral amyloid angiopathy in a transgenic mouse model of Alzheimer’s disease. Interestingly, this dysfunction is specifically endothelium related and is mediated by impaired nitric oxide–cyclic GMP bioavailability. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/cerebroarterial-dysfunction-in-swedish-arctic-ad-mice/ .

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