Blood–brain barrier breakdown in Alzheimer disease and other neurodegenerative disorders
Open accessAbstract
The blood–brain barrier (BBB) is a continuous endothelial membrane within brain microvessels that has sealed cell-to-cell contacts and is sheathed by mural vascular cells and perivascular astrocyte end-feet. The BBB protects neurons from factors present in the systemic circulation and maintains the highly regulated CNS internal milieu, which is required for proper synaptic and neuronal functioning. BBB disruption allows influx into the brain of neurotoxic blood-derived debris, cells and microbial pathogens and is associated with inflammatory and immune responses, which can initiate multiple pathways of neurodegeneration. This Review discusses neuroimaging studies in the living human brain and post-mortem tissue as well as biomarker studies demonstrating BBB breakdown in Alzheimer disease, Parkinson disease, Huntington disease, amyotrophic lateral sclerosis, multiple sclerosis, HIV-1-associated dementia and chronic traumatic encephalopathy. The pathogenic mechanisms by which BBB breakdown leads to neuronal injury, synaptic dysfunction, loss of neuronal connectivity and neurodegeneration are described. The importance of a healthy BBB for therapeutic drug delivery and the adverse effects of disease-initiated, pathological BBB breakdown in relation to brain delivery of neuropharmaceuticals are briefly discussed. Finally, future directions, gaps in the field and opportunities to control the course of neurological diseases by targeting the BBB are presented.
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In advanced Alzheimer's disease, widespread leakage and deposition of blood-derived proteins such as fibrinogen, thrombin, and albumin are observed.
“Simultaneously, widespread leakage and deposition of blood-derived proteins such as fibrinogen, thrombin, and albumin are observed [49, 55].”
From Targeted Nanoparticles for Drug Delivery Across the Blood–Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review (2026) · cites this paper as [55]
The 'Postmortem evidence of BBB disruption > Capillary leakages' section reports leakage and accumulation of fibrinogen, thrombin, and albumin in several brain regions of patients with Alzheimer’s disease. It does not specify advanced-stage disease or characterize the leakage as widespread, so those qualifiers are not established by this source. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn late-stage Alzheimer's disease, the blood-brain barrier becomes significantly disrupted due to vascular degeneration, chronic inflammation, and endothelial damage, leading to increased but non-specific permeability.
“As AD progresses to its late stages, the effectiveness of nanoparticle-based therapies often diminishes due to the increased disruption of the BBB [148].”
From Targeted Nanoparticles for Drug Delivery Across the Blood–Brain Barrier in Early and Late Stages of Alzheimer's Disease: A Review (2026) · cites this paper as [162]
The “How BBB breakdown affects drug delivery” section says vascular changes in neurodegeneration persist as disease progresses and hinder delivery of therapeutic agents; it also mentions nanoparticles as a delivery approach (page not available). It does not specifically show that nanoparticle-based therapies become less effective in late-stage Alzheimer’s disease. (LLM, conf=0.86)
Experimental — accuracy not yet measuredStimulating intracellular degradation without restoring BBB efflux may be insufficient to reduce vascular and parenchymal Aβ accumulation.
“Conversely, stimulating intracellular degradation without restoring BBB efflux may be insufficient to reduce vascular and parenchymal A β accumulation [ 58 ].”
From Restores Aβ Clearance by Overcoming PCSK9–LRP1 Dysregulation and TRIB3‐Mediated Autophagy Blockade in Alzheimer's Disease (2026) · cites this paper as [58]
The Postmortem evidence of BBB disruption > Molecular changes section says reduced BBB clearance promotes Aβ accumulation in the brain and that some Aβ-clearance therapies require brain-to-blood transport. It does not assess whether stimulating intracellular degradation without restoring efflux would be insufficient, or establish that conclusion for both vascular and parenchymal Aβ accumulation. Page numbers were not available in our copy. (LLM, conf=0.82)
Experimental — accuracy not yet measuredTJ proteins are affected under multiple pathological conditions or by approaches causing transient disruption, compromising BBB integrity and increasing influx of substances via the paracellular pathway.
“However, the TJ proteins are reported to be affected under multiple pathological conditions or by approaches causing transient disruption, compromising the integrity of BBB and increasing influx of substances via the paracellular pathway [121, 122].”
From Designing and optimizing AAV-mediated gene therapy for neurodegenerative diseases: from bench to bedside (2024) · cites this paper as [122]
The Introduction links tightly sealed endothelial contacts to low paracellular permeability and says BBB breakdown permits blood-derived substances to enter the brain. “BBB breakdown and neurodegeneration” reports loss of tight-junction proteins in neurodegenerative disorders. “How BBB breakdown affects drug delivery” mentions opening the BBB with focused ultrasound, but does not establish that such approaches transiently affect tight-junction proteins or increase influx specifically through the paracellular pathway. Page numbers were not provided in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredAstrocytic processes surround most of the vascular surface and regulate blood-brain barrier permeability by modulating tight junction proteins such as claudin-5 and endothelial proteins such as vimentin.
“Astrocytic processes surround most of the vascular surface, regulating the blood–brain barrier (BBB) permeability [6, 7, 8, 9]—by modulating tight junction proteins such as claudin‐5 [10], or endothelial proteins such vimentin, which is associated with the stability of cerebral vasculature [11]—and integrate neuronal activity with blood flow [1, 2, 3, 4, 5, 12, 13, 14, 15, 16, 17, 18, 19, 20].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [9]
The Introduction (page unavailable) says astrocyte end-feet sheath the endothelial BBB, supporting the claim that astrocytic processes surround the vasculature. It does not establish that they regulate BBB permeability; it describes tight endothelial contacts and limited transcytosis as restricting permeability. The claudin-5 and vimentin mechanisms have separate citations in the citing sentence and are not attributed to this source. (LLM, conf=0.78)
Experimental — accuracy not yet measured
Together with microglia, astrocytes constitute the principal defensive system of the CNS and respond to damage-related stimuli including Aβ and glutamate overload in a process known as astrocyte reactivity.
“Together with microglia, astrocytes constitute the principal defensive system of the CNS [37], responding to numerous damage‐related stimuli [6, 7, 8, 9] including amyloid β peptides (Aβ) and glutamate overload, in a process known as astrocyte reactivity [15, 37, 38, 39, 40].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [9]
The ‘BBB breakdown and neurodegeneration’ section says that accumulated neurotoxic material and reduced blood flow can activate both microglia and astrocytes, leading to inflammation. It does not describe them as the CNS’s principal defensive system or identify Aβ and glutamate overload as triggers of astrocyte reactivity; the ‘BBB molecular architecture’ section discusses Aβ and glutamate clearance at the BBB instead. No page numbers are available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measuredAstrocyte reactivity has frequently been associated with neuroinflammation, unfavorable glial scar formation, glutamate dyshomeostasis, altered coverage of synapses and blood vessels, and BBB breakout.
“Hence, astrocyte reactivity has frequently been associated with neuroinflammation, unfavorable glial scar formation [7, 8, 9, 37, 38, 43, 48, 49], glutamate dyshomeostasis [43, 50, 51], altered coverage of synapses and blood vessels, and BBB breakout [38, 42, 43, 45, 46, 47].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [9]
The Introduction describes astrocyte end-feet covering brain vessels and associates BBB breakdown with inflammatory responses. The ‘BBB breakdown and neurodegeneration’ section says neurotoxic material and reduced blood flow can activate astrocytes, leading to inflammation. These passages support an association among BBB disruption, astrocyte activation and inflammation, but do not establish altered astrocyte coverage of synapses or vessels as a feature of astrocyte reactivity. (LLM, conf=0.82)
Experimental — accuracy not yet measuredWith advancing neurodegenerative disease, BBB integrity becomes compromised.
“With advancing neurodegenerative disease, BBB integrity becomes compromised [63].”
From Evaluation of exploratory fluid biomarkers from a phase 1 senolytic trial in mild Alzheimer's disease (2025) · cites this paper as [63]
Loss of claudins is associated with blood-brain barrier breakdown in human neurodegenerative disorders.
“Loss of claudins is associated with BBB breakdown in human neurodegenerative disorders (155, 569) and acute CNS diseases (692), as well as in animal models of these diseases (420), as discussed below.”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [569]
Increasing evidence supports that early cerebrovascular dysfunction contributes to AD pathophysiology and cognitive impairment.
“In addition to the classic hallmark pathology, A 𝛃 plaques, hyperphosphorylated tau neurofibrillary tangles, and neuron loss, increasing evidence supports that early cerebrovascular dysfunction contributes to AD pathophysiology and cognitive impairment (29, 285, 418, 421, 429, 569, 571, 593, 682, 693).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [569]
FDG-PET reflects mainly the transport activity of the GLUT1 BBB transporter.
“As previously reviewed, FDG-PET reflects mainly the transport activity of GLUT1 BBB transporter (420, 569).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [569]
Focal vascular changes limit CNS distribution of neurotherapeutics in disease-affected regions by disrupting diffusional transport across brain extracellular space and/or by blocking normal interstitial fluid flow dynamics.
“These focal vascular changes limit CNS distribution of neurotherapeutics in disease-affected regions by disrupting diffusional transport across brain ECS and/or by blocking normal ISF flow dynamics (519, 569).”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [569]
FDG-PET and verapamil-PET have been used to test functions of BBB GLUT1 transporter and activity of ABCB1 (P-gp) efflux transporter in AD and PD, respectively.
“Besides FDG-PET and verapamil-PET that have been used to test functions of BBB GLUT1 transporter and activity of ABCB1 (P-gp) efflux transporter in AD and PD (420, 569), respectively”
From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [569]
Drug administration to the brain requires a functionally and structurally healthy BBB; pathological breakdown traps blood-borne medications in enlarged perivascular spaces, preventing them from reaching cerebral cells.
“to be effective, drug administration to the brain requires a functionally and structurally healthy BBB since its pathological breakdown, which precedes and sustains neurodegeneration, implies perturbations in the endothelial bulk flow transcytosis and in the expression of transporter systems. Consequently, blood-borne medications, including antibodies, proteins, peptides, and small molecules, bec”
From The Emerging Role of PCSK9 in the Pathogenesis of Alzheimer’s Disease: A Possible Target for the Disease Treatment (2024) · cites this paper as [30]
Blood-brain barrier breakdown has been demonstrated to occur in AD in the general population.
“Blood–brain barrier breakdown has been demonstrated to occur in AD in the general population [63], but whether the blood–brain barrier is disrupted in DS or DSAD is currently unknown.”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [63]
BBB disruption is well characterized in other neurodegenerative diseases, including PD, ALS, FTD, and HD.
“BBB disruption is well characterized in other neurodegenerative diseases, including PD, ALS, FTD, and HD.”
From Microbiota–gut–brain axis and its therapeutic applications in neurodegenerative diseases (2024) · cites this paper as [660]
Decreased cerebral blood flow, coupled with increased Aβ levels induced by BBB deterioration can aggravate tau pathology.
“Decreased cerebral blood flow, coupled with increased Aβ levels induced by BBB deterioration can also aggravate tau pathology [628, 629].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [629]
A breakdown of the blood brain barrier has been shown in neurodegenerative diseases.
“Furthermore, a breakdown of the blood brain barrier has been shown in neurodegenerative diseases [81, 82].”
Both patients with AD and AD animal models exhibit neurovascular system impairment including abnormalities in the number, diameter, and density of blood vessels, which lead to decreased brain perfusion and blood-brain barrier disruption.
“Both patients with AD and AD animal models exhibit neurovascular system impairment including abnormalities in the number, diameter, and density of blood vessels, which lead to decreased brain perfusion and blood–brain barrier disruption (10, 39, 40).”
From Single-nucleus transcriptome analysis reveals dysregulation of angiogenic endothelial cells and neuroprotective glia in Alzheimer’s disease (2020) · cites this paper as [39]
The expressions of LRP1 and ABCB1 were reduced during AD, whereas the expression of RAGE is elevated.
“It has been identified that the expressions of the two blood efflux transporters LRP1 and ABCB1 were reduced during AD, whereas the expression of the blood influx transporter RAGE is elevated.21,25”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [21]
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“…to each process of the drug transportation, which have also been accompanied by reviews of latest progress in this fi eld, but most of literature emphasize the BBB breakdown in speci fi c brain disorders, 11 – 14 or give a general review of delivery strategies concentrating on the barrier physiology.”
BackgroundBlood–brain barrier breakdown is an early biomarker of human cognitive dysfunction
Nation, D. A., Sweeney, M. D., Montagne, A., Sagare, A. P., D’Orazio, L. M., Pachicano, M., Sepehrband, F., Nelson, A. R., Buennagel, D. P., Harrington, M. G., et al. (2019) · Nature Medicine · doi:10.1038/s41591-018-0297-y · Cited by 1,728 · see citing works
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“It has been identified that the expressions of the two blood efflux transporters LRP1 and ABCB1 were reduced during AD, whereas the expression of the blood influx transporter RAGE is elevated.(21,25) The perivascular drainage pathway plays a vital role in ISF bulk-flow clearance of Aβ.”
BackgroundPerivascular spaces in the brain: anatomy, physiology and pathology
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Self-citationThe blood-brain barrier in aging and neurodegeneration
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“An increase in BBB permeability is commonly observed via enhanced accumulation of blood-derived proteins in the brains of post-mortem AD patients [101] and supported by the reduction of tight junction proteins [102].”
BackgroundVascular dysfunction—The disregarded partner of Alzheimer's disease
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Clinical applications of stem cell-derived exosomes
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- Authors
- Sweeney, M. D., Sagare, A. P., & Zlokovic, B. V.
- Affiliations
- University of Southern California (US)
- Venue
- Nature Reviews Neurology
- Published
- 2018-01-29
- Volume
- 14
- Issue
- 3
- Pages
- 133-150
- ISSN
- 1759-4758 (ISSN-L)
- 1759-4766
- PMC
- PMC5829048
- OpenAlex
- W2786608785
- Semantic Scholar
- 4d92c092b2819e1ed90219e4dbb45c7fe3d87806
- Cited by
- 3,076
- References
- 257
- Citations by year
- 2026: 419 · 2025: 455 · 2024: 467 · 2023: 402 · 2022: 378 · 2021: 377 · 2020: 313 · 2019: 183 · 2018: 78
- FWCI
- 22.61
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Reviews Neurology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG023084, R01AG039452, F31AG044997, P50AG005142, RF1AG039452, P01AG052350)
- National Institute of Neurological Disorders and Stroke (R01NS100459, R01NS090904, R01NS034467)
- Topics
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Cerebrospinal fluid and hydrocephalus
- Keywords
- blood-brain barrier disruption, neurodegeneration, Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, HIV-associated dementia, chronic traumatic encephalopathy, neuroinflammation, synaptic dysfunction, postmortem brain
- MeSH terms
- Blood-Brain Barrier, Humans, Neurodegenerative Diseases
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