What is the clinical evidence from this study?

Population: Chronic cerebral hypoperfusion (subcortical vascular dementia model). Intervention: Aliskiren or Tempol vs. Untreated control. Primary outcome: Brain damage and working memory deficits.

What question did this study set out to answer?

To investigate the role of the renin-angiotensin system in cognitive decline and brain damage induced by chronic cerebral ischemia.

August 23, 2011HypertensionOpen Access

Attenuation of Brain Damage and Cognitive Impairment by Direct Renin Inhibition in Mice With Chronic Cerebral Hypoperfusion

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Key result

Aliskiren and Tempol ameliorated brain damage and spatial working memory deficits in a mouse model of chronic cerebral hypoperfusion by attenuating oxidative stress.

Why the study?

Does aliskiren or Tempol reduce brain damage and cognitive impairment in a mouse model of chronic cerebral hypoperfusion?

Population

C57BL/6J mice subjected to bilateral common carotid artery stenosis with microcoil

Design

Preclinical

Authors

YDYi‐Fei DongNanchang University KKKeiichiro KataokaKumamoto University KTKensuke ToyamaKurume University

Discussion

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Implication

Supports preclinical renin inhibition testing in hypoperfusion models; hypothesis-generating and should not yet change practice.

Key Points

To investigate the role of the renin-angiotensin system in cognitive decline and brain damage induced by chronic cerebral ischemia.
Induced chronic cerebral hypoperfusion, modeling subcortical vascular dementia, in C57BL/6J mice using bilateral common carotid artery stenosis with microcoils.
Assessed the effects of pre- and post-treatment with the direct renin inhibitor aliskiren or the superoxide scavenger Tempol on brain pathology, oxidative stress markers, and spatial working memory.
Chronic cerebral hypoperfusion elevated brain renin activity and angiotensinogen expression, localized to activated astrocytes and microvessels in white matter.
Aliskiren pretreatment significantly reduced renin activity, p67phox-related NADPH oxidase activity, oxidative stress, glial activation, white matter lesions, and spatial working memory deficits.
Tempol pretreatment mimicked the neuroprotective profile of aliskiren, and post-treatment with either agent successfully prevented cognitive decline.

Structured PICO

Does aliskiren or Tempol reduce brain damage and cognitive impairment in a mouse model of chronic cerebral hypoperfusion?

Population

C57BL/6J mice with chronic cerebral hypoperfusion induced by bilateral common carotid artery stenosis.

Intervention

Aliskiren (a direct renin inhibitor) or Tempol (a superoxide scavenger) administered as pretreatment or posttreatment

Outcome

Brain damage and spatial working memory deficitssurrogate

Direct renin inhibition with aliskiren attenuates brain damage and cognitive impairment in a mouse model of chronic cerebral hypoperfusion by reducing oxidative stress.

Cite This Study

Dong et al. (2011) studied Chronic cerebral hypoperfusion (subcortical vascular dementia model). Aliskiren or Tempol vs. Untreated control was evaluated on Brain damage and working memory deficits. Aliskiren and Tempol ameliorated brain damage and spatial working memory deficits in a mouse model of chronic cerebral hypoperfusion by attenuating oxidative stress.

synapsesocial.com/papers/6a77976f9047b4aa92f6e166 https://doi.org/10.1161/hypertensionaha.111.173534

Topics

Hypertension management

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Attenuation of Brain Damage and Cognitive Impairment by Direct Renin Inhibition in Mice With Chronic Cerebral Hypoperfusion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Topics

Attenuation of Brain Damage and Cognitive Impairment by Direct Renin Inhibition in Mice With Chronic Cerebral Hypoperfusion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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