Soluble forms of tau are toxic in Alzheimer's disease
Open accessAbstract
Accumulation of neurofibrillary tangles (NFT), intracellular inclusions of fibrillar forms of tau, is a hallmark of Alzheimer Disease. NFT have been considered causative of neuronal death, however, recent evidence challenges this idea. Other species of tau, such as soluble misfolded, hyperphosphorylated, and mislocalized forms, are now being implicated as toxic. Here we review the data supporting soluble tau as toxic to neurons and synapses in the brain and the implications of these data for development of therapeutic strategies for Alzheimer's disease and other tauopathies.
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oTau are neurotoxic and can induce neurodegeneration.
“It has been shown that oTau are neurotoxic and can induce neurodegeneration.58,67,68”
From Microglial APOE3 Christchurch protects neurons from Tau pathology in a human iPSC-based model of Alzheimer’s disease (2024) · cites this paper as [68]
The “Pathological forms of tau” section reports that injected tau oligomers caused synaptic deficits, mitochondrial dysfunction and memory impairments in mice, supporting their neurotoxicity. It also reports cell death from altered or overexpressed tau in vitro, but does not specifically show that tau oligomers induce neuronal death or broader neurodegeneration. (LLM, conf=0.82)
Experimental — accuracy not yet measuredSoluble tau, rather than NFTs, is the pathologic tau species.
“Given the evidence that soluble tau, rather than NFTs, is the pathologic tau species (Santacruz et al., 2005, Yoshiyama et al., 2007, Kopeikina et al., 2012, Lasagna-Reeves et al., 2012, Polydoro et al., 2014, Ghag et al., 2018)”
From Dendritic Spine Remodeling and Synaptic Tau Levels in PS19 Tauopathy Mice (2021) · cites this paper as Kopeikina et al., 2012
The Conclusions and Future directions section favors soluble tau as more toxic to neuronal and synaptic function. But it also says there is evidence that fibrillar tau contributes to dysfunction and that a toxic role for NFTs is not excluded. The claim overstates the paper's position by treating soluble tau as the pathologic species rather than NFTs. (LLM, conf=0.88)
Experimental — accuracy not yet measuredTau tangles alone are not sufficient to cause neuronal death.
“whereas tau tangles alone are not sufficient to cause neuronal death”
From Targeted degradation of aberrant tau in frontotemporal dementia patient-derived neuronal cell models (2019) · cites this paper as Kopeikina et al., 2012
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Self-citationTau Aggregates: Toxic, Inert, or Protective Species?
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de Calignon, A., Spires-Jones, T. L., Pitstick, R., Carlson, G. A., & Hyman, B. T. (2009) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e3181a9fc66 · Cited by 81 · see citing works
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Intracellular calcium signalling in Alzheimer’s disease
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Early Improved and Late Defective Cognition Is Reflected by Dendritic Spines in Tau.P301L Mice
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- [113]de Calignon A Fox LM Pitstick R Carlson GA Bacskai BJ Spires-Jones TL Caspase activation precedes and leads to tangles Nature 2010 464 1201 1204 20357768 PMC3091360
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“Although tau aggregates are hallmarks of AD, several studies have suggested that oligomeric tau in soluble forms may be the most potent neurotoxic form (Wu et al., 2013; Iba et al., 2013, 2015; Stancu et al., 2015; Peeraer et al., 2015; Kopeikina et al., 2012).”
Dendritic Spine Remodeling and Synaptic Tau Levels in PS19 Tauopathy Mice
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- Authors
- Kopeikina, K., Hyman, B., & Spires-Jones, T.
- Affiliations
- Boston University (US)
- Harvard University (US)
- MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts, 02129, USA
- ORCID
- Hyman, Bradley
- Venue
- Translational Neuroscience
- Publisher
- Walter de Gruyter GmbH
- Published
- 2012-08-28
- Volume
- 3
- Issue
- 3
- Pages
- 223-233
- ISSN
- 2081-3856 (ISSN-L)
- 2081-6936
- PMC
- PMC3460520
- OpenAlex
- W2151252981
- Cited by
- 232
- References
- 135
- Citations by year
- 2026: 8 · 2025: 19 · 2024: 16 · 2023: 19 · 2022: 21 · 2021: 25 · 2020: 20 · 2019: 27 · 2018: 15 · 2017: 16 · 2016: 15 · 2015: 10 · 2014: 12 · 2013: 9
- FWCI
- 6.64
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Translational Neuroscience (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Funders
- Alzheimer's Association
- National Institute on Aging (R01AG026249, R00AG033670, R01AG008487, T32AG000277, P50AG005134, K99AG033670, P30AG062421)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- soluble tau, tau toxicity, Alzheimer's disease, tauopathy, neurofibrillary tangles, hyperphosphorylated tau, neuronal cell death, treatment options
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