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Updated: Jun 7, 2026

In Vitro Assays to Assess Blood-brain Barrier Mesh-like Vessel Formation and Disruption
Published on: June 20, 2017
Aging and cerebrovascular dysfunction: contribution of hypertension, cerebral amyloid angiopathy, and immunotherapy
Vitaly Vasilevko1, Giselle F Passos, Daniel Quiring
1Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, California, USA.
Insights
Age-related cerebrovascular dysfunction contributes to stroke and cognitive decline. New strategies are needed to improve blood-brain barrier function and reduce cerebral amyloid angiopathy, a key risk factor.
Area of Science:
- Neuroscience
- Cerebrovascular Biology
- Neurodegenerative Diseases
Background:
- Age-related cerebrovascular dysfunction is implicated in stroke, hemorrhages, and cognitive decline.
- This dysfunction plays a secondary role in neurodegenerative diseases like Alzheimer's disease.
- Cerebral amyloid angiopathy (CAA) and amyloid beta (Aβ) accumulation are linked to blood-brain barrier (BBB) lesions and stroke.
Purpose of the Study:
- To highlight the critical need for novel therapeutic strategies targeting cerebrovascular dysfunction.
- To emphasize the importance of improving blood-brain barrier (BBB) function.
- To address the challenge of limiting beta-amyloidosis in the cerebral vasculature, particularly in the context of CAA.
Main Methods:
- Review of existing literature on age-related cerebrovascular dysfunction.
- Analysis of the role of amyloid beta (Aβ) in cerebrovascular pathologies.
- Examination of clinical trial data for anti-amyloid immunotherapies and associated adverse events.
Main Results:
- Cerebrovascular dysfunction is a significant contributor to various neurological conditions, including stroke and cognitive impairment.
- Amyloid beta (Aβ) accumulation in cerebral vasculature is a risk factor for intracerebral hemorrhage (ICH) and linked to BBB dysfunction.
- Current anti-Aβ therapies show promise in clearing amyloid but are associated with CAA-related complications, indicating a need for safer approaches.
Conclusions:
- Effective management of hypertension and atherosclerosis can reduce ICH incidence but does not address CAA.
- There are currently no approved therapies specifically for attenuating cerebral amyloid angiopathy (CAA).
- Developing new strategies to enhance BBB integrity and mitigate cerebral β-amyloidosis is crucial for preventing cerebrovascular and neurodegenerative diseases.
Abstract:
Age-related cerebrovascular dysfunction contributes to ischemic stroke, intracerebral hemorrhages (ICHs), microbleeds, cerebral amyloid angiopathy (CAA), and cognitive decline. Importantly, there is increasing recognition that this dysfunction plays a critical secondary role in many neurodegenerative diseases, including Alzheimer's disease (AD). Atherosclerosis, hypertension, and CAA are the most common causes of blood-brain barrier (BBB) lesions. The accumulation of amyloid beta (Aβ) in the cerebrovascular system is a significant risk factor for ICH and has been linked to endothelial transport failure and blockage of perivascular drainage. Moreover, recent anti-Aβ immunotherapy clinical trials demonstrated efficient clearance of parenchymal amyloid deposits but have been plagued by CAA-associated adverse events. Although management of hypertension and atherosclerosis can reduce the incidence of ICH, there are currently no approved therapies for attenuating CAA. Thus, there is a critical need for new strategies that improve BBB function and limit the development of β-amyloidosis in the cerebral vasculature.
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