scholarly journals Characterization of the Retinal Changes of the 3xTg-AD Mouse Model of Alzheimer’s Disease

2019 ◽  
pp. 1816-1821
Author(s):  
Hugo Ferreira ◽  
João Martins ◽  
Ana Nunes ◽  
Paula I. Moreira ◽  
Miguel Castelo-Branco ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

Characterization of the 3xTg-AD mouse model of Alzheimer's disease: Part 2. Behavioral and cognitive changes

2010 ◽  
Vol 1348 ◽  
pp. 149-155 ◽  
Author(s):  
Roxanne Sterniczuk ◽  
Michael C. Antle ◽  
Frank M. LaFerla ◽  
Richard H. Dyck
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Changes ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

Characterization of the 3xTg-AD mouse model of Alzheimer's disease: Part 1. Circadian changes

2010 ◽  
Vol 1348 ◽  
pp. 139-148 ◽  
Author(s):  
Roxanne Sterniczuk ◽  
Richard H. Dyck ◽  
Frank M. LaFerla ◽  
Michael C. Antle
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Circadian Changes ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

scholarly journals Characterization of the retinal changes of the 3×Tg-AD mouse model of Alzheimer’s disease

2020 ◽  
Vol 10 (4) ◽  
pp. 875-883 ◽  
Author(s):  
Hugo Ferreira ◽  
João Martins ◽  
Ana Nunes ◽  
Paula I. Moreira ◽  
Miguel Castelo-Branco ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model

Characterization of a 3xTg-AD mouse model of Alzheimer's disease with the senescence accelerated mouse prone 8 (SAMP8) background

Synapse ◽  
2018 ◽  
Vol 72 (4) ◽  
pp. e22025 ◽  
Author(s):  
Jessica Virgili ◽  
Meryem Lebbadi ◽  
Cyntia Tremblay ◽  
Isabelle St-Amour ◽  
Caroline Pierrisnard ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Model Of Alzheimer’S Disease ◽  
Ad Mouse Model ◽  
Senescence Accelerated Mouse

Characterization of retinal changes in a mouse model of Alzheimer’s disease using multi-contrast optical coherence tomography (Conference Presentation)

2020 ◽  
Author(s):  
Bernhard Baumann ◽  
Danielle J. Harper ◽  
Antonia Lichtenegger ◽  
Johanna Gesperger ◽  
Tanja Himmel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Optical Coherence Tomography ◽  
Mouse Model ◽  
Optical Coherence ◽  
Model Of Alzheimer’S Disease

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.

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