scholarly journals Towards spatial frequency domain optical imaging of neurovascular coupling in a mouse model of Alzheimer's disease

2012 ◽  
Author(s):  
Alexander J. Lin ◽  
Soren D. Konecky ◽  
Tyler B. Rice ◽  
Kim N. Green ◽  
Bernard Choi ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Spatial Frequency ◽  
Optical Imaging ◽  
Frequency Domain ◽  
Neurovascular Coupling ◽  
Model Of Alzheimer’S Disease ◽  
Spatial Frequency Domain

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

2019 ◽  
Vol 40 (11) ◽  
pp. 2289-2303 ◽  
Author(s):  
Paul S Sharp ◽  
Kamar E Ameen-Ali ◽  
Luke Boorman ◽  
Sam Harris ◽  
Stephen Wharton ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cerebral Blood Volume ◽  
Neurovascular Coupling ◽  
Repeated Measurements ◽  
Hemodynamic Responses ◽  
Experimental Procedure ◽  
Cranial Window ◽  
Model Of Alzheimer’S Disease

Impaired neurovascular coupling has been suggested as an early pathogenic factor in Alzheimer’s disease (AD), which could serve as an early biomarker of cerebral pathology. We have established an anaesthetic regime to allow repeated measurements of neurovascular function over three months in the J20 mouse model of AD (J20-AD) and wild-type (WT) controls. Animals were 9–12 months old at the start of the experiment. Mice were chronically prepared with a cranial window through which 2-Dimensional optical imaging spectroscopy (2D-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 2D-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.

P4-063: NEUROVASCULAR COUPLING DEFICITS ARISE PRIOR TO COGNITIVE DYSFUNCTION IN A MOUSE MODEL OF ALZHEIMER'S DISEASE

2006 ◽  
Vol 14 (7S_Part_27) ◽  
pp. P1456-P1457
Author(s):  
Candice E. Van Skike ◽  
Stacy A. Hussong ◽  
Angela B. Olson ◽  
Stephen F. Hernandez ◽  
Andy Banh ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Cognitive Dysfunction ◽  
Neurovascular Coupling ◽  
Model Of Alzheimer’S Disease

Optical Imaging of Synaptic Disruption in a Mouse Model of Alzheimer's Disease

2004 ◽  
Vol 10 (S02) ◽  
pp. 166-167
Author(s):  
Julia Tsai ◽  
Jaime Grutzendler ◽  
Wen Biao Gan
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Optical Imaging ◽  
Model Of Alzheimer’S Disease

Extended abstract of a paper presented at Microscopy and Microanalysis 2004 in Savannah, Georgia, USA, August 1–5, 2004.

scholarly journals Enhanced Cerebral Blood Volume under Normobaric Hyperoxia in the J20-hAPP Mouse Model of Alzheimer’s Disease

2019 ◽  
Author(s):  
Osman Shabir ◽  
Paul Sharp ◽  
Monica A Rebollar ◽  
Luke Boorman ◽  
Clare Howarth ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Blood Volume ◽  
Neural Activity ◽  
Cerebral Blood Volume ◽  
Neurovascular Coupling ◽  
Cranial Window ◽  
Model Of Alzheimer’S Disease ◽  
The Brain

AbstractEarly impairments to neurovascular coupling have been proposed to be a key pathogenic factor in the onset and progression of Alzheimer’s disease (AD). Studies have shown impaired neurovascular function in several mouse models of AD, including the J20-hAPP mouse. In this study, we aimed to investigate early neurovascular changes using wild-type (WT) controls and J20-hAPP mice at 6-9 months of age, by measuring cerebral haemodynamics and neural activity to physiological sensory stimulations. A thinned cranial window was prepared to allow access to cortical vasculature and imaged using 2D-optical imaging spectroscopy (2D-OIS). After chronic imaging sessions where the skull was intact, a terminal acute imaging session was performed where an electrode was inserted into the brain to record simultaneous neural activity. We found that cerebral haemodynamic changes were significantly enhanced in J20-hAPP mice compared with controls in response to physiological stimulations, potentially due to the significantly higher neural activity (hyperexcitability) seen in the J20-hAPP mice. Thus, neurovascular coupling remained preserved under a chronic imaging preparation. Further, under hyperoxia, the baseline blood volume and saturation of all vascular compartments in the brains of J20-hAPP mice were substantially enhanced compared to WT controls, but this effect disappeared under normoxic conditions. This study highlights novel findings not previously seen in the J20-hAPP mouse model, and may point towards a potential therapeutic strategy by driving an increased baseline blood flow to the brain, thereby potentially enhancing the clearance of beta-amyloid.

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