Abstract
BACKGROUND: Hyperphosphorylation of the neuronal tau protein contributes to Alzheimer's disease (AD) by promoting tau pathology and neuronal and cognitive deficits. In contrast, we have previously shown that site-specific tau phosphorylation can inhibit toxic signals induced by amyloid-β (Aβ) in mouse models. The post-synaptic mitogen-activated protein (MAP) kinase p38γ mediates this site-specific phosphorylation on tau at Threonine-205 (T205).
| Original language | English |
|---|---|
| Pages (from-to) | e054596 |
| Number of pages | 1 |
| Journal | Alzheimer's & dementia : the journal of the Alzheimer's Association |
| Volume | 17 |
| Issue number | S3 |
| DOIs | |
| Publication status | Published - Dec 2021 |
| Externally published | Yes |
| Event | Alzheimer's Association International Conference 2021 - Denver, United States Duration: 26 Jul 2021 → 30 Jul 2021 |
Keywords
- Hyperphosphorylation
- Tau protein
- MAP kinase
- p38 MAP kinase
- memory deficits
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