ArticleActa neuropathologica communications2015
Tau depletion prevents progressive blood-brain barrier damage in a mouse model of tauopathy.
Article in Acta neuropathologica communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 116 papers.
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Who cites it
116 citing papers in PubMed, 192 citations in OpenAlex.
- Review
- A Small-Molecule DEPTAC Rescues Cognitive Deficits by Targeted Dephosphorylation of Pathological Tau.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Tau Oligomers Induce Brain Endothelial Cell Hyperpermeability and Increase NLRP3 Inflammasome Signaling and MMP-9 Activity.Microcirculation (New York, N.Y. : 1994) · 2026Article
- Hippocampus-targeted BDNF gene therapy to rescue cognitive impairments of Alzheimer's disease in multiple mouse models.Genes & diseases · 2026Article
- Interleukin-6, CD8Frontiers in aging neuroscience · 2026Review
- Mechanistic insights into the synaptic damage-repair and regeneration processes in neurodegenerative Alzheimer's disease: phytochemicals as neuroprotective agents.Frontiers in synaptic neuroscience · 2026Review
- Single-cell Spatial Transcriptional Profiling Uncovers Heterogeneous Cellular Responses to Pathogenic Tau in a Mouse Model of Neurodegeneration.bioRxiv : the preprint server for biology · 2025Article
- Advances of therapeutic strategies for Alzheimer's disease.Journal of neurology · 2025Review
- Emerging roles for innate and adaptive immunity in tauopathies.Cell reports · 2025Review
- Microbial Metabolomes in Alzheimer's Disease: From Pathogenesis to Therapeutic Potential.Current issues in molecular biology · 2025Review
- The intersection of circadian rhythms and the blood-brain barrier with drug efficacy and delivery in neurological disorders.Advanced drug delivery reviews · 2025Review
- From Acute Injury to Chronic Neurodegeneration: Molecular Mechanisms Linking Secondary Brain Injury to Long-Term Pathology.International journal of molecular sciences · 2025Review
- Fibrinogen-tau Aggregates Exacerbate Tau Pathology and Memory Deficits in Alzheimer's Disease Model Mice.Neuroscience bulletin · 2025Article
- Tau depletion diminishes vascular amyloid-related deficits in a mouse model of cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Blood-brain barrier disruption: a pervasive driver and mechanistic link between traumatic brain injury and Alzheimer's disease.Translational neurodegeneration · 2025Review
- Fibrillar tau alters cerebral endothelial cell metabolism, vascular inflammatory activation, and barrier function in vitro and in vivo.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Cross-sectional and longitudinal relationships among blood-brain barrier disruption, Alzheimer's disease biomarkers, and cognition in cognitively normal older adults.Neurobiology of aging · 2025Article
- Increased frontocortical microvascular raspberry density in frontotemporal lobar degeneration compared to Lewy body disease and control cases: a neuropathological study.Free neuropathology · 2025Article
- Structure and function of the blood-brain barrier in perioperative neurocognitive disorders.Frontiers in neuroscience · 2025Review
56 more citing papers are in PubMed but not listed here.
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11 authors at 2 institutions in 1 country.
Funding
Abstract
introductionThe blood-brain barrier (BBB) is damaged in tauopathies, including progressive supranuclear palsy (PSP) and Alzheimer's disease (AD), which is thought to contribute to pathogenesis later in the disease course. In AD, BBB dysfunction has been associated with amyloid beta (Aß) pathology, but the role of tau in this process is not well characterized. Since increased BBB permeability is found in tauopathies without Aß pathology, like PSP, we suspected that tau accumulation alone could not only be sufficient, but even more important than Aß for BBB damage.
resultsLongitudinal evaluation of brain tissue from the tetracycline-regulatable rTg4510 tau transgenic mouse model showed progressive IgG, T cell and red blood cell infiltration. The Evans blue (EB) dye that is excluded from the brain when the BBB is intact also permeated the brains of rTg4510 mice following peripheral administration, indicative of a bonafide BBB defect, but this was only evident later in life. Thus, despite the marked brain atrophy and inflammation that occurs earlier in this model, BBB integrity is maintained. Interestingly, BBB dysfunction emerged at the same time that perivascular tau emerged around major hippocampal blood vessels. However, when tau expression was suppressed using doxycycline, BBB integrity was preserved, suggesting that the BBB can be stabilized in a tauopathic brain by reducing tau levels.
conclusionsFor the first time, these data demonstrate that tau alone can initiate breakdown of the BBB, but the BBB is remarkably resilient, maintaining its integrity in the face of marked brain atrophy, neuroinflammation and toxic tau accumulation. Moreover, the BBB can recover integrity when tau levels are reduced. Thus, late stage interventions targeting tau may slow the vascular contributions to cognitive impairment and dementia that occur in tauopathies.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.