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Tau-induced pathology in epilepsy and dementia: notions from patients and animal models.
Open accessAbstract
Patients with dementia present epilepsy more frequently than the general population. Seizures are more common in patients with Alzheimer’s disease (AD), dementia with Lewy bodies (LBD), frontotemporal dementia (FTD) and progressive supranuclear palsy (PSP) than in other dementias. Missense mutations in the microtubule associated protein tau (MAPT) gene have been found to cause familial FTD and PSP, while the P301S mutation in MAPT has been associated with early-onset fast progressive dementia and the presence of seizures. Brains of patients with AD, LBD, FTD and PSP show hyperphosphorylated tau aggregates, amyloid-β plaques and neuropil threads. Increasing evidence suggests the existence of overlapping mechanisms related to the generation of network hyperexcitability and cognitive decline. Neuronal overexpression of tau with various mutations found in FTD with parkinsonism-linked to chromosome 17 (FTDP-17) in mice produces epileptic activity. On the other hand, the use of certain antiepileptic drugs in animal models with AD prevents cognitive impairment. Further efforts should be made to search for plausible common targets for both conditions. Moreover, attempts should also be made to evaluate the use of drugs targeting tau and amyloid-β as suitable pharmacological interventions in epileptic disorders. The diagnosis of dementia and epilepsy in early stages of those diseases may be helpful for the initiation of treatments that could prevent the generation of epileptic activity and cognitive deterioration.
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“However, the possibility of seizures and hyperexcitability in primary tauopathies should not be ruled out, as they occur more frequently in these diseases than in the general population (Beagle et al., 2017; Sanchez et al., 2018).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Sanchez et al., 2018
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“Given that neurodegenerative conditions characterized by hyperphosphorylated tau aggregations exhibit increased rates of epilepsy, epilepsies are being re-conceptualized within a tauopathy context (Xi et al., 2011; Sanchez et al., 2018; Ali et al., 2019).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Sanchez et al., 2018
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“Furthermore, tau pathology is repeatedly found in human epilepsy (Sanchez et al., 2018).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Sanchez et al., 2018
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“While individuals with dementia have higher rates of epilepsy, seizures are experienced more frequently in tauopathy-associated dementias like AD than in other dementias (Sanchez et al., 2018).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Sanchez et al., 2018
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“seizures are experienced more frequently in tauopathy-associated dementias like AD than in other dementias (Sanchez et al., 2018).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Sanchez et al., 2018
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Metadata
- Authors
- Sánchez, M., García-Cabrero, A., Sánchez-Elexpuru, G., Burgos, D., & Serratosa, J.
- Affiliations
- Centre for Biomedical Network Research on Rare Diseases (ES)
- Consejo Superior de Investigaciones Científicas (ES)
- Laboratory of Neurology, IIS (Instituto Investigación Sanitaria/Health Research Institute)-Jiménez Díaz Foundation, UAM (Universidad Autonoma de Madrid/Autonomous University of Madrid) and Biomedical Research Network Center on Rare Diseases (CIBERER), 28045 Madrid, Spain
- Corresponding author
- Sánchez, Marina
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2018-04-05
- Volume
- 19
- Issue
- 4
- Pages
- 1092
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC5979593
- OpenAlex
- W2795704013
- Cited by
- 68
- References
- 217
- Citations by year
- 2026: 8 · 2025: 5 · 2024: 7 · 2023: 9 · 2022: 7 · 2021: 14 · 2020: 10 · 2019: 5 · 2018: 3
- FWCI
- 1.05
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (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, cc-by-sa)
- Funders
- Carlos III Institute of Health (PI13/00865)
- Biomedical Research Network Center on Rare Diseases, CIBERER
- NINDS, NIH (P01NS097197)
- Spanish Ministry of Economy (SAF2014-59594-R)
- Conchita Rábago Foundation
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Epilepsy research and treatment
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- tau pathology, epilepsy, dementia, Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia, progressive supranuclear palsy, MAPT mutations, amyloid plaques, neuropil threads, network hyperexcitability, cognitive decline, FTDP-17, antiepileptic drugs, animal models, early diagnosis
- MeSH terms
- Animals, Brain, Dementia, Epilepsy, Humans, tau Proteins
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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