The role of brain vasculature in neurodegenerative disorders
Open accessAbstract
Adequate supply of blood and structural and functional integrity of blood vessels are key to normal brain functioning. On the other hand, cerebral blood flow shortfalls and blood-brain barrier dysfunction are early findings in neurodegenerative disorders in humans and animal models. Here we first examine molecular definition of cerebral blood vessels, as well as pathways regulating cerebral blood flow and blood-brain barrier integrity. Then we examine the role of cerebral blood flow and blood-brain barrier in the pathogenesis of Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. We focus on Alzheimer's disease as a platform of our analysis because more is known about neurovascular dysfunction in this disease than in other neurodegenerative disorders. Finally, we propose a hypothetical model of Alzheimer's disease biomarkers to include brain vasculature as a factor contributing to the disease onset and progression, and we suggest a common pathway linking brain vascular contributions to neurodegeneration in multiple neurodegenerative disorders.
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Binding of AGEs and amyloid beta to RAGE causes additional oxidative stress that contributes to neuronal death and vascular dementia in Alzheimer disease.
“AGE and Aβ binding to RAGE leads to further oxidative stress that contributes to neuronal death and vascular dementia in AD45–48.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [48]
The Alzheimer’s disease blood–brain barrier sections (page unavailable) identify RAGE as an Aβ influx transporter and report increased RAGE-mediated Aβ influx in AD models. They do not state that AGE and Aβ binding to RAGE causes oxidative stress leading to neuronal death and vascular dementia. (LLM, conf=0.84)
Experimental — accuracy not yet measuredGlycation may slow the conversion of amyloid beta into fibrils, keeping it longer in toxic oligomeric forms.
“Glycation may slow the conversion of Aβ to fibrils, keeping them longer in the toxic oligomeric forms48.”
From Oxidative stress, dysfunctional glucose metabolism and Alzheimer disease (2019) · cites this paper as [48]
The Blood-brain barrier in Alzheimer’s disease sections discuss Aβ transport and accumulation, including a receptor for advanced glycation endproducts, but do not address glycation of Aβ itself. Searches for slowed fibril formation and prolonged toxic oligomeric forms found no passage supporting that mechanism; page numbers were not available in our copy. (LLM, conf=0.74)
Experimental — accuracy not yet measuredExisting cerebrovascular-function-modulating therapeutics eventually failed to alleviate cognitive deficits in AD patients and AD model mice.
“However, these efforts eventually failed to alleviate the cognitive deficits in AD patients and AD model mice,[ 7 , 8 ]”
From Multifunctional Nanostructure RAP‐RL Rescues Alzheimer's Cognitive Deficits through Remodeling the Neurovascular Unit (2021) · cites this paper as [7]
The ‘Cerebral blood flow in Alzheimer’s disease > Animal studies’ section says that counteracting Aβ effects after vascular deposition did not reverse neurovascular dysfunction in an APP mouse model. It does not report whether cerebrovascular-function-modulating therapeutics failed to alleviate cognitive deficits in those mice or in AD patients; searches for treatment failures and cognitive outcomes found no such passage in our copy. (LLM, conf=0.74)
Experimental — accuracy not yet measuredBBB dysfunction is an early and independent contributor to AD pathogenesis, involving pericyte loss, tight-junction breakdown, and increased vascular permeability.
“BBB dysfunction is now recognized as an early and independent contributor to AD pathogenesis, involving pericyte loss, tight-junction breakdown, and increased vascular permeability (Montagne et al., 2017; Sweeney et al., 2018).”
From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Sweeney et al., 2018
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Cerebral capillary blood flow upsurge during REM sleep is mediated by A2a receptors
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“To keep the brain supplied with glucose, lipids, and other building blocks for normal function, a high degree of blood perfusion is necessary, and dysfunction in brain vasculature may play a role in cognitive decline and disease [55].”
BackgroundGJ-4 alleviates Aβ25-35-induced memory dysfunction in mice through protecting the neurovascular unit
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Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease
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- Authors
- Sweeney, M. D., Kisler, K., Montagne, A., Toga, A. W., & Zlokovic, B. V.
- Affiliations
- University of Southern California (US)
- Venue
- Nature Neuroscience
- Published
- 2018-09-24
- Volume
- 21
- Issue
- 10
- Pages
- 1318-1331
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- PMC
- PMC6198802
- OpenAlex
- W2890224686
- Cited by
- 998
- References
- 151
- Citations by year
- 2026: 113 · 2025: 154 · 2024: 152 · 2023: 137 · 2022: 117 · 2021: 142 · 2020: 116 · 2019: 64 · 2018: 3
- FWCI
- 7.68
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Fondation Leducq
- National Institutes of Health
- National Institute on Aging (R01AG023084, R01AG039452, P50AG005142, RF1AG039452, P01AG052350)
- National Institute of Neurological Disorders and Stroke (R01NS100459, R01NS090904, R01NS034467)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- cerebral vasculature, neurodegenerative diseases, cerebral blood flow, blood-brain barrier dysfunction, neurovascular dysfunction, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, Alzheimer's disease biomarkers, vascular integrity
- MeSH terms
- Animals, Blood Vessels, Brain, Humans, Neurodegenerative Diseases
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