Tau induces blood vessel abnormalities and angiogenesis-related gene expression in P301L transgenic mice and human Alzheimer’s disease
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Significance: This work provides evidence that the protein tau induces changes in blood vessels distinct from the effects of amyloid beta on vasculature and indicates a previously unknown pathway by which pathological tau may accelerate cognitive decline in Alzheimer’s disease.
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Reduced vascular diameters have been documented in aged individuals and Alzheimer's disease (AD).
“reduced vascular diameters and increased capillary densities [123] have been documented in aged individuals and AD [124]”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [123]
The Results section reports reduced blood-vessel diameters in aged Tg4510 mice compared with controls. The Discussion describes collapsed capillaries in human AD, but does not establish reduced vascular diameters in aged individuals or people with AD. The claim extends a mouse finding to humans. (LLM, conf=0.87)
Experimental — accuracy not yet measuredIncreased capillary densities have been documented in aged individuals and Alzheimer's disease (AD).
“reduced vascular diameters and increased capillary densities [123] have been documented in aged individuals and AD [124]”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [123]
The Results (Time Course of Blood Vessel Density Changes) document increased vessel density in 15-month-old tau-transgenic mice, not aged people. The Discussion says studies of capillary density in human AD are conflicting and suggests any increase may be transient, so the source does not establish increased capillary density in aged individuals with AD. (LLM, conf=0.87)
Experimental — accuracy not yet measuredBoth Aβ deposits and tau pathology aggravate vascular damage.
“Chronic inflammation‐induced disruption of the BBB is an early biomarker of human cognitive dysfunction and often leads to dementia, 113 and both Aβ deposits and tau pathology aggravate vascular damage. 114 , 115”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [114]
Accumulation of Aβ and tau are causally linked to pericyte dysfunction, which contributes to reduced cerebral blood flow in early AD.
“It has been argued that the accumulation of Aβ and tau are causally linked to pericyte dysfunction, which contributes to reduced cerebral blood flow in early AD. 114 , 118”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [114]
Increased expression of angiogenic genes in endothelial cells is associated with the blood vessel abnormalities observed in mouse models of neurodegeneration.
“Notably, increased expression of angiogenic genes in endothelial cells is associated with the blood vessel abnormalities observed in mouse models of neurodegeneration (40).”
From Single-nucleus transcriptome analysis reveals dysregulation of angiogenic endothelial cells and neuroprotective glia in Alzheimer’s disease (2020) · cites this paper as [40]
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 [40]
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Tau as a mediator of neurotoxicity associated to cerebral amyloid angiopathy
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Henao‐Restrepo, J., López‐Murillo, C., Valderrama‐Carmona, P., Orozco‐Santa, N., Gomez, J., Gutiérrez‐Vargas, J., Moraga, R., Toledo, J., Littau, J. L., Härtel, S., et al. (2023) · Brain Pathology · doi:10.1111/bpa.13119 · Cited by 11 · see citing works
- Authors
- Bennett, R. E., Robbins, A. B., Hu, M., Cao, X., Betensky, R. A., Clark, T., Das, S., & Hyman, B. T.
- Affiliations
- Harvard University (US)
- Corresponding author
- Hyman, Bradley T.
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2018-01-22
- Volume
- 115
- Issue
- 6
- Pages
- E1289-E1298
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC5819390
- OpenAlex
- W2784733460
- Cited by
- 299
- References
- 58
- Citations by year
- 2026: 10 · 2025: 38 · 2024: 42 · 2023: 41 · 2022: 42 · 2021: 51 · 2020: 40 · 2019: 28 · 2018: 7
- FWCI
- 21.51
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion, cc-by-nc-nd)
- PubMed Central (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Funders
- HHS | NIH | National Institute on Aging (T32 AG000222, AG026249, AG005134)
- BrightFocus Foundation (A2016404F)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Barrier Structure and Function Studies
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tau protein, Alzheimer's disease, angiogenesis, cerebral microvasculature, endothelial cells, CD31, gene expression, transgenic mice, temporal lobe, limbic system, neurodegeneration
- MeSH terms
- Aging, Alzheimer Disease, Animals, Brain, Cells, Cultured, Cerebrovascular Circulation, Humans, Mice, Transgenic, Neurons, Amyloid beta-Peptides, tau Proteins, Angiogenesis Inducing Agents, Mice
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