JNK Plays a Key Role in Tau Hyperphosphorylation in Alzheimer's Disease Models
Open accessAbstract
Alzheimer's disease (AD) is a major clinical concern, and the search for new molecules to combat disease progression remains important. One of the major hallmarks in AD pathogenesis is the hyperphosphorylation of tau and subsequent formation of neurofibrillary tangles. Several kinases are involved in this process. Amongst them, c-Jun N-terminal kinases (JNKs) are activated in AD brains and are also associated with the development of amyloid plaques. This study was designed to investigate the contribution of JNK in tau hyperphosphorylation and whether it may represent a potential therapeutic target for the fight against AD. The specific inhibition of JNK by the cell permeable peptide D-JNKI-1 led to a reduction of p-tau at S202/T205 and S422, two established target sites of JNK, in rat neuronal cultures and in human fibroblasts cultures. Similarly, D-JNKI-1 reduced p-tau at S202/T205 in an in vivo model of AD (TgCRND8 mice). Our findings support the fundamental role of JNK in the regulation of tau hyperphosphorylation and subsequently in AD pathogenesis.
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Induction of the NF-kB pathway by TNF-α stimulates the release of COX-2 and activation of JNK, which has been shown to phosphorylate tau.
“Additionally, induction of the NF-kB pathway by TNF-α stimulates the release of the proinflammatory enzyme cyclooxygenase 2 (COX-2) [140], as well as activation of c-Jun N-terminal kinase (JNK) which has been shown to phosphorylate tau [143].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [143]
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References 66 · Cited by 145
- Authors
- Ploia, C., Antoniou, X., Sclip, A., Grande, V., Cardinetti, D., Colombo, A., Canu, N., Benussi, L., Ghidoni, R., Forloni, G., & Borsello, T.
- Affiliations
- Mario Negri Institute for Pharmacological Research (IT)
- University of Rome Tor Vergata (IT)
- Centro San Giovanni di Dio Fatebenefratelli (IT)
- Corresponding author
- Borsello, Tiziana
- ORCID
- Venue
- Journal of Alzheimer's Disease
- Publisher
- SAGE Publications
- Published
- 2011-09-09
- Volume
- 26
- Issue
- 2
- Pages
- 315-329
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- OpenAlex
- W2170531576
- Cited by
- 145
- References
- 66
- Citations by year
- 2026: 5 · 2025: 10 · 2024: 15 · 2023: 5 · 2022: 10 · 2021: 16 · 2020: 9 · 2019: 17 · 2018: 7 · 2017: 11 · 2016: 5 · 2015: 13 · 2014: 9 · 2013: 9 · 2012: 3
- FWCI
- 4.80
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- other-oa
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- Cineca Institutional Research Information System (Tor Vergata University) (submittedVersion, other-oa)
- DZNE Pub (submittedVersion)
- Funders
- Fondazione Cariplo
- 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
- c-Jun N-terminal kinase, JNK
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Animals, Cells, Cultured, Cerebral Cortex, Female, Humans, Male, Middle Aged, Neurons, Phosphorylation, Neurofibrillary Tangles, tau Proteins, Mitogen-Activated Protein Kinases, JNK Mitogen-Activated Protein Kinases, Rats
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