Tau as a mediator of neurotoxicity associated to cerebral amyloid angiopathy
Open accessAbstract
Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. Currently, there is no clear understanding of the mechanisms underlying the contribution of CAA to neurodegeneration. Despite the fact that CAA is highly associated with accumulation of Aβ, other types of amyloids have been shown to associate with the vasculature. Interestingly, in many cases, vascular amyloidosis is accompanied by significant tau pathology. However, the contribution of tau to neurodegeneration associated to CAA remains to be determined. We used a mouse model of Familial Danish Dementia (FDD), a neurodegenerative disease characterized by the accumulation of Danish amyloid (ADan) in the vasculature, to characterize the contribution of tau to neurodegeneration associated to CAA. We performed histological and biochemical assays to establish tau modifications associated with CAA in conjunction with cell-based and electrophysiological assays to determine the role of tau in the synaptic dysfunction associated with ADan. We demonstrated that ADan aggregates induced hyperphosphorylation and misfolding of tau. Moreover, in a mouse model for CAA, we observed tau oligomers closely associated to astrocytes in the vicinity of vascular amyloid deposits. We finally determined that the absence of tau prevents synaptic dysfunction induced by ADan oligomers. In addition to demonstrating the effect of ADan amyloid on tau misfolding, our results provide compelling evidence of the role of tau in neurodegeneration associated with ADan-CAA and suggest that decreasing tau levels could be a feasible approach for the treatment of CAA.
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The Tg-FDD mouse model accumulates Danish amyloid exclusively in the vasculature.
“The Tg-FDD mouse model accumulates Danish amyloid exclusively in the vasculature.”
From Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease (2026) · cites this paper as [120]
The Results (Fig. 4; page unavailable) confirm ADan amyloid deposits in Tg-FDD cerebral vessels. But the same section reports intracellular ADan oligomers in the cortex, so the paper does not support the word “exclusively.” (LLM, conf=0.88)
Experimental — accuracy not yet measuredTau misfolds and acquires toxic gain-of-function properties in our vascular amyloid model.
“Given that microglia can phagocytose extracellular pathological tau [148, 149], and that tau misfolds and acquires toxic gain-of-function properties in our vascular amyloid model [120], tau ablation likely reduces this pathological burden.”
From Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease (2026) · cites this paper as [120]
The Results (page not available) show increased misfolded tau in Tg-FDD mice, and the Discussion reports that ADan oligomers cause tau-dependent cellular toxicity and synaptic impairment. The paper does not establish that misfolded tau itself acquires a toxic gain of function in the vascular amyloid model; tau dependence does not distinguish that from a role for normal tau. (LLM, conf=0.82)
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Alcohol promotes waste clearance in the CNS via brain vascular reactivity
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Self-citationMicrofluidic Platforms to Unravel Mysteries of Alzheimer’s Disease: How Far Have We Come?
Prasanna, P., Rathee, S., Rahul, V., Mandal, D., Goud, M. S. C., Yadav, P., Hawthorne, S. J., Sharma, A., Gupta, P. K., Ojha, S. K., et al. (2021) · Life · doi:10.3390/life11101022 · Cited by 24 · see citing works
The reduction of astrocytic tau prevents amyloid-β-induced synaptotoxicity
Cisternas, P., Taylor, X., Martínez, P., Maldonado, O., Jury, N., & Lasagna‐Reeves, C. A. (2022) · Brain Communications · doi:10.1093/braincomms/fcac235 · Cited by 14 · see citing works
Self-citationLipid mediated formation of antiparallel aggregates in cerebral amyloid angiopathy
de Oliveira, A. P., Baghel, D., Holcombe, B., Chase, W., Ward, T., Wang, S. J., & Ghosh, A. (2025) · Acta Neuropathologica · doi:10.1007/s00401-025-02911-5 · Cited by 10 · see citing works
Using Neuroimaging to Study Cerebral Amyloid Angiopathy and Its Relationship to Alzheimer’s Disease
Wheeler, K. V., Andrei Irimia, A., & Braskie, M. N. (2024) · Journal of Alzheimer s Disease · doi:10.3233/jad-230553 · Cited by 9 · see citing works
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Self-citationCerebral amyloid angiopathy-related cardiac injury: Focus on cardiac cell death
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A Review on Alzheimer’s disease and mesenchymal stem cell therapy
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Tau Ablation Rewires Brain Cell Programs in Health and Restores Function in Disease
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Self-citationVascular β-amyloid potentially colocalises with phosphorylated tau in cerebral amyloid angiopathy
Tsai, H.-H. C., Lee, B., Liu, C., Chiang, P., Tsai, Y.-C., Tsai, L., & Peng, S. (2025) · Stroke and Vascular Neurology · doi:10.1136/svn-2024-003774
Investigating the physiological function of the amyloid precursor protein in Drosophila melanogaster
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Self-citation
- Authors
- You, Y., Perkins, A., Cisternas, P., Muñoz, B., Taylor, X., You, Y., Garringer, H. J., Oblak, A. L., Atwood, B. K., Vidal, R., & Lasagna-Reeves, C. A.
- Affiliations
- Indiana University Indianapolis (US)
- Indiana University School of Medicine (US)
- ORCID
- Venue
- Acta Neuropathologica Communications
- Published
- 2019-02-26
- Volume
- 7
- Issue
- 1
- Pages
- 26-26
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC6390363
- OpenAlex
- W2915481512
- Cited by
- 33
- References
- 67
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 2 · 2023: 3 · 2022: 5 · 2021: 9 · 2020: 7 · 2019: 2
- FWCI
- 3.94
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- IUScholarWorks (Indiana University) (submittedVersion, cc-by)
- Purdue University Indianapolis (Indiana University) (submittedVersion, cc-by)
- Funders
- National Institute of Neurological Disorders and Stroke (K22NS092688)
- National Institute on Aging (1R01AG059639)
- Alzheimer's Association (AARGD-591887)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Intracerebral and Subarachnoid Hemorrhage Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- cerebral amyloid angiopathy, tau protein, familial Danish dementia, vascular amyloidosis, tau hyperphosphorylation, tau misfolding, tau oligomers, astrocytes, synaptic dysfunction, neurodegeneration, tau-targeted therapy
- MeSH terms
- Amino Acid Sequence, Amyloidosis, Animals, Cataract, Cerebellar Ataxia, Deafness, Dementia, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Cerebral Amyloid Angiopathy, tau Proteins, Mice, Knockout, Mice, HEK293 Cells
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