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Updated: Apr 15, 2026
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Published on: July 8, 2025
Chronic cerebral hypoperfusion induces vascular plasticity and hemodynamics but also neuronal degeneration and
Zhen Jing1, Changzheng Shi2, Lihui Zhu3
1Department of Neurology, The First Affiliated Hospital, Jinan University, Guangzhou, China.
Insights
Chronic cerebral hypoperfusion (CCH) impairs cognition. While the brain attempts to compensate for reduced cerebral blood flow (CBF), this mechanism is insufficient to prevent neuronal damage and cognitive decline.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Pathology
Background:
- Chronic cerebral hypoperfusion (CCH) is linked to cognitive impairment.
- The brain's compensatory mechanisms for reduced cerebral blood flow (CBF) remain incompletely understood.
- Investigating dynamic changes in CBF, angiogenesis, and cellular pathology is crucial for understanding CCH.
Purpose of the Study:
- To investigate dynamic changes in CBF, angiogenesis, and cellular pathology in response to CCH.
- To assess cognitive impairment in rats following bilateral common carotid artery occlusion (BCCAO).
- To elucidate the brain's compensatory mechanisms against CCH.
Main Methods:
- Bilateral common carotid artery occlusion (BCCAO) model in rats.
- Magnetic resonance imaging (MRI) for CBF measurement.
- Immunochemistry for cellular pathology assessment.
- Morris water maze for cognitive function evaluation.
Main Results:
- CCH significantly reduced CBF in the cortex, striatum, and cerebellum.
- Microvessel density initially declined but increased by 6 weeks post-BCCAO.
- Neuronal degeneration was observed, with a notable increase in glial cells at 4 weeks.
- Cognitive impairment correlated directly with the duration of ischemia.
Conclusions:
- CCH triggers a compensatory response to maintain brain perfusion.
- This compensation is limited and cannot fully prevent neuronal loss and cognitive deficits.
- Understanding these mechanisms is vital for developing therapeutic strategies for CCH-induced cognitive impairment.
Abstract:
Chronic cerebral hypoperfusion (CCH) induces cognitive impairment, but the compensative mechanism of cerebral blood flow (CBF) is not fully understood. The present study mainly investigated dynamic changes in CBF, angiogenesis, and cellular pathology in the cortex, the striatum, and the cerebellum, and also studied cognitive impairment of rats induced by bilateral common carotid artery occlusion (BCCAO). Magnetic resonance imaging (MRI) techniques, immunochemistry, and Morris water maze were employed to the study. The CBF of the cortex, striatum, and cerebellum dramatically decreased after right common carotid artery occlusion (RCCAO), and remained lower level at 2 weeks after BCCAO. It returned to the sham level from 3 to 6 weeks companied by the dilation of vertebral arteries after BCCAO. The number of microvessels declined at 2, 3, and 4 weeks but increased at 6 weeks after BCCAO. Neuronal degeneration occurred in the cortex and striatum from 2 to 6 weeks, but the number of glial cells dramatically increased at 4 weeks after BCCAO. Cognitive impairment of ischemic rats was directly related to ischemic duration. Our results suggest that CCH induces a compensative mechanism attempting to maintain optimal CBF to the brain. However, this limited compensation cannot prevent neuronal loss and cognitive impairment after permanent ischemia.
