Age-related murine hippocampal CA1 laminae oxidative stress measured in vivo by QUEnch-assiSTed (QUEST) MRI: impact of isoflurane anesthesia

Berkowitz, Bruce A.; Podolsky, Robert H.; Childers, Karen Lins; Gow, Alexander; Schneider, Brandy L.; Lloyd, Scott C; Bosse, Kelly E.; Conti, Alana C.; Roberts, Robin; Berri, Ali M; Graffice, Emma; Sinan, Kenan; Eliwat, Waleed; Shen, Yimin

doi:10.1007/s11357-020-00162-8

Cited by 9 publications

(8 citation statements)

References 87 publications

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“…Animal exposure to anesthesia, such as isoflurane employed in our study, is another limiting factor. Repeated exposure to isoflurane, while generally considered a safe anesthetic option, has been reported to cause anxiety, motor deficits, altered white matter integrity (Bajwa et al, 2019), and oxidative stress (Berkowitz et al, 2020). The qualitative micelle pharmacokinetic characterization performed in Figure 2 illustrates the tradeoff between effective vascular detection and complete micelle washout between imaging sessions.…”

Section: Discussionmentioning

confidence: 99%

Detection of Cerebrovascular Loss in the Normal Aging C57BL/6 Mouse Brain Using in vivo Contrast-Enhanced Magnetic Resonance Angiography

Hill

Hoang

Chiriboga

et al. 2020

Front. Aging Neurosci.

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Microvascular rarefaction, or the decrease in vascular density, has been described in the cerebrovasculature of aging humans, rats, and, more recently, mice in the presence and absence of age-dependent diseases. Given the wide use of mice in modeling age-dependent human diseases of the cerebrovasculature, visualization, and quantification of the global murine cerebrovasculature is necessary for establishing the baseline changes that occur with aging. To provide in vivo whole-brain imaging of the cerebrovasculature in aging C57BL/6 mice longitudinally, contrast-enhanced magnetic resonance angiography (CE-MRA) was employed using a house-made gadoliniumbearing micellar blood pool agent. Enhancement in the vascular space permitted quantification of the detectable, or apparent, cerebral blood volume (aCBV), which was analyzed over 2 years of aging and compared to histological analysis of the cerebrovascular density. A significant loss in the aCBV was detected by CE-MRA over the aging period. Histological analysis via vessel-probing immunohistochemistry confirmed a significant loss in the cerebrovascular density over the same 2-year aging period, validating the CE-MRA findings. While these techniques use widely different methods of assessment and spatial resolutions, their comparable findings in detected vascular loss corroborate the growing body of literature describing vascular rarefaction aging. These findings suggest that such age-dependent changes can contribute to cerebrovascular and neurodegenerative diseases, which are modeled using wild-type and transgenic laboratory rodents.

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Section: Discussionmentioning

confidence: 99%

Detection of Cerebrovascular Loss in the Normal Aging C57BL/6 Mouse Brain Using in vivo Contrast-Enhanced Magnetic Resonance Angiography

Hill

Hoang

Chiriboga

et al. 2020

Front. Aging Neurosci.

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“…Oxidative stress is non-invasively evaluated in retinal laminae using QUEnch-assiSTed (QUEST) magnetic resonance imaging (MRI), in subretinal space using QUEST optical coherence tomography (OCT), and in cone-based vision with QUEST optokinetic tracking (OKT) [ 20 , 24 , 28 , 29 ]. QUEST MRI accurately evaluates panretinal, layer-specific, paramagnetic free radical-generated contrast as a decrease in 1/T1 with anti-oxidants [ 29 , 30 ]. QUEST MRI oxidative stress measurements have been validated in animal models against several ex vivo assays [ 29 ].…”

Section: Introductionmentioning

confidence: 99%

Sildenafil-evoked photoreceptor oxidative stress in vivo is unrelated to impaired visual performance in mice

et al. 2021

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Purpose The phosphodiesterase inhibitor sildenafil is a promising treatment for neurodegenerative disease, but it can cause oxidative stress in photoreceptors ex vivo and degrade visual performance in humans. Here, we test the hypotheses that in wildtype mice sildenafil causes i) wide-spread photoreceptor oxidative stress in vivo that is linked with ii) impaired vision. Methods In dark or light-adapted C57BL/6 mice ± sildenafil treatment, the presence of oxidative stress was evaluated in retina laminae in vivo by QUEnch-assiSTed (QUEST) magnetic resonance imaging, in the subretinal space in vivo by QUEST optical coherence tomography, and in freshly excised retina by a dichlorofluorescein assay. Visual performance indices were also evaluated by QUEST optokinetic tracking. Results In light-adapted mice, 1 hr post-sildenafil administration, oxidative stress was most evident in the superior peripheral outer retina on both in vivo and ex vivo examinations; little evidence was noted for central retina oxidative stress in vivo and ex vivo. In dark-adapted mice 1 hr after sildenafil, no evidence for outer retina oxidative stress was found in vivo. Evidence for sildenafil-induced central retina rod cGMP accumulation was suggested as a panretinally thinner, dark-like subretinal space thickness in light-adapted mice at 1 hr but not 5 hr post-sildenafil. Cone-based visual performance was impaired by 5 hr post-sildenafil and not corrected with anti-oxidants; vision was normal at 1 hr and 24 hr post-sildenafil. Conclusions The sildenafil-induced spatiotemporal pattern of oxidative stress in photoreceptors dominated by rods was unrelated to impairment of cone-based visual performance in wildtype mice.

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“…Thanks to the advances in molecular biology, our knowledge of aging and cognitive decline constantly increases. Many signalling pathways involved in the regulation of aging and lifespan have been identified, and recent studies have demonstrated the involvement of these signalling pathways in age-related cognitive decline [37,38]. These pathways may represent important targets to develop novel and effective disease-modifying drugs to treat, delay, or prevent age-related neurodegenerative diseases.…”

Section: The Role Of Aging and Oxidative Stress In Chronic Neurodegenmentioning

confidence: 99%

Common Protective Strategies in Neurodegenerative Disease: Focusing on Risk Factors to Target the Cellular Redox System

Hrelia

Sita

Ziche

et al. 2020

Oxidative Medicine and Cellular Longevity

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Neurodegenerative disease is an umbrella term for different conditions which primarily affect the neurons in the human brain. In the last century, significant research has been focused on mechanisms and risk factors relevant to the multifaceted etiopathogenesis of neurodegenerative diseases. Currently, neurodegenerative diseases are incurable, and the treatments available only control the symptoms or delay the progression of the disease. This review is aimed at characterizing the complex network of molecular mechanisms underpinning acute and chronic neurodegeneration, focusing on the disturbance in redox homeostasis, as a common mechanism behind five pivotal risk factors: aging, oxidative stress, inflammation, glycation, and vascular injury. Considering the complex multifactorial nature of neurodegenerative diseases, a preventive strategy able to simultaneously target multiple risk factors and disease mechanisms at an early stage is most likely to be effective to slow/halt the progression of neurodegenerative diseases.

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Age-related murine hippocampal CA1 laminae oxidative stress measured in vivo by QUEnch-assiSTed (QUEST) MRI: impact of isoflurane anesthesia

Cited by 9 publications

References 87 publications

Detection of Cerebrovascular Loss in the Normal Aging C57BL/6 Mouse Brain Using in vivo Contrast-Enhanced Magnetic Resonance Angiography

Detection of Cerebrovascular Loss in the Normal Aging C57BL/6 Mouse Brain Using in vivo Contrast-Enhanced Magnetic Resonance Angiography

Sildenafil-evoked photoreceptor oxidative stress in vivo is unrelated to impaired visual performance in mice

Common Protective Strategies in Neurodegenerative Disease: Focusing on Risk Factors to Target the Cellular Redox System

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