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Updated: Jul 26, 2025
Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
Published on: April 23, 2021
Cerebral venous congestion alters brain metabolite profiles, impairing cognitive function
Huimin Wei1, Huimin Jiang2, Yifan Zhou2
1Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, School of Biological Science and Medical Engineering, Beihang University, Beijing, China.
Insights
Cerebral venous congestion impairs cognition by affecting synaptic function, linked to N-acetyl-L-cysteine (NAC) deficiency. Supplementing NAC may help treat vascular cognitive impairment (VCI).
Area of Science:
- Neuroscience
- Neurology
- Pathophysiology
Background:
- Vascular cognitive impairment (VCI) is a major cause of dementia, with cerebral venous congestion emerging as a key factor.
- While arterial ischemia's role in cognitive decline is known, the mechanisms of venous congestion are less understood.
- This research investigates the neuropathophysiological basis of cognitive impairment due to cerebral venous congestion.
Purpose of the Study:
- To elucidate the role of cerebral venous congestion in cognitive-behavioral deterioration.
- To explore the electrophysiological mechanisms underlying VCI caused by venous congestion.
- To identify potential therapeutic targets for VCI.
Main Methods:
- Cerebral venous congestion rat models were used to assess cognitive function and synaptic plasticity.
- Untargeted metabolomics identified biochemical changes in affected rats.
- N-acetyl-L-cysteine (NAC) supplementation was tested for its therapeutic effects.
- Patient cohorts with cerebral venous congestion were analyzed for NAC levels and cognitive scores.
Main Results:
- Rats with cerebral venous congestion showed reduced long-term potentiation (LTP) and impaired spatial memory.
- A deficiency in N-acetyl-L-cysteine (NAC) was observed in these rats.
- NAC supplementation improved synaptic function, restored LTP, and mitigated cognitive deficits.
- In patients, decreased NAC levels correlated with cognitive decline.
Conclusions:
- Cerebral venous congestion contributes to cognitive impairment through specific neuropathophysiological alterations.
- N-acetyl-L-cysteine (NAC) deficiency is implicated in VCI pathogenesis.
- NAC shows therapeutic potential for preventing and treating vascular cognitive impairment.
Abstract:
Vascular cognitive impairment (VCI) represents the second most common cause of dementia after Alzheimer's disease, and pathological changes in cerebral vascular structure and function are pivotal causes of VCI. Cognitive impairment caused by arterial ischemia has been extensively studied the whole time; the influence of cerebral venous congestion on cognitive impairment draws doctors' attention in recent clinical practice, but the underlying neuropathophysiological alterations are not completely understood. This study elucidated the specific pathogenetic role of cerebral venous congestion in cognitive-behavioral deterioration and possible electrophysiological mechanisms. Using cerebral venous congestion rat models, we found these rats exhibited decreased long-term potentiation (LTP) in the hippocampal dentate gyrus and impaired spatial learning and memory. Based on untargeted metabolomics, N-acetyl-L-cysteine (NAC) deficiency was detected in cerebral venous congestion rats; supplementation with NAC appeared to ameliorate synaptic deficits, rescue impaired LTP, and mitigate cognitive impairment. In a cohort of cerebral venous congestion patients, NAC levels were decreased; NAC concentration was negatively correlated with subjective cognitive decline (SCD) score but positively correlated with mini-mental state examination (MMSE) score. These findings provide a new perspective on cognitive impairment and support further exploration of NAC as a therapeutic target for the prevention and treatment of VCI.
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