Hyperphosphorylated tau is implicated in acquired epilepsy and neuropsychiatric comorbidities.
Open accessAbstract
Epilepsy is a common group of neurological diseases. Acquired epilepsy can be caused by brain insults, such as trauma, infection or tumour, and followed by a latent period from several months to years before the emergence of recurrent spontaneous seizures. More than 50% of epilepsy cases will develop chronic neurodegenerative, neurocognitive and neuropsychiatric comorbidities. It is important to understand the mechanisms by which a brain insult results in acquired epilepsy and comorbidities in order to identify targets for novel therapeutic interventions that may mitigate these outcomes. Recent studies have implicated the hyperphosphorylated tubulin-associated protein (tau) in rodent models of epilepsy and Alzheimer's disease, and in experimental and clinical studies of traumatic brain injury. This potentially represents a novel target to mitigate epilepsy and associated neurocognitive and psychiatric disorders post-brain injury. This article reviews the potential role of tau-based mechanisms in the pathophysiology of acquired epilepsy and its neurocognitive and neuropsychiatric comorbidities, and the potential to target these for novel disease-modifying treatments.
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Tau hyperphosphorylation is consistently present in the initial and long-term secondary mechanisms initiated by traumatic brain injury.
“Tau hyperphosphorylation is also consistently present in the initial and long-term secondary mechanisms initiated by traumatic brain injury (TBI) (Petraglia et al., 2014; Zheng et al., 2014; Rubenstein et al., 2015; Ali et al., 2019; Tan et al., 2020), a leading cause of morbidity and mortality worldwide (Hay et al., 2016).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Zheng et al., 2014
The “PP2A Linkage to TBI” section reports increased phosphorylated tau from 10 minutes to 12 hours after injury in a compression-injury model. “Hyperphosphorylated Tau in TBI” links hyperphosphorylated tau to severe TBI and to chronic changes after repeated concussions. These passages support early and later associations, but not the stronger claim that tau hyperphosphorylation is consistently present throughout the initial and long-term secondary mechanisms of TBI. (LLM, conf=0.86)
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Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms
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- Authors
- Zheng, P., Shultz, S. R., Hovens, C. M., Velakoulis, D., Jones, N. C., & O’Brien, T. J.
- Affiliations
- The Royal Melbourne Hospital (AU)
- Corresponding author
- Zheng, Ping
- Venue
- Molecular Neurobiology
- Published
- 2013-12-10
- Volume
- 49
- Issue
- 3
- Pages
- 1532-1539
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- OpenAlex
- W1996444571
- Cited by
- 48
- References
- 9
- Citations by year
- 2026: 1 · 2024: 3 · 2023: 2 · 2022: 5 · 2021: 6 · 2020: 8 · 2019: 6 · 2018: 4 · 2017: 4 · 2016: 4 · 2015: 3 · 2014: 2
- FWCI
- 0.41
- Type
- journal article
- Language
- en
- Open access
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Minerva Access (University of Melbourne) (submittedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
- Keywords
- hyperphosphorylated tau, acquired epilepsy, neuropsychiatric comorbidity, traumatic brain injury, epilepsy pathophysiology, disease-modifying therapy, tau-targeted therapy, Alzheimer's disease
- MeSH terms
- Animals, Mental Disorders, Epilepsy, Humans, Phosphorylation, Comorbidity, tau Proteins
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