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Updated: Nov 21, 2025
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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
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Tau Protein and Frontotemporal Dementias
Michel Goedert1, Maria Grazia Spillantini2, Benjamin Falcon3
1MRC Laboratory of Molecular Biology, Cambridge, UK. mg@mrc-lmb.cam.ac.uk.
Advances in Experimental Medicine and Biology
|January 12, 2021
Summary
Tau protein dysfunction causes neurodegeneration and dementia in frontotemporal dementias (FTDs). Specific tau protein folds are linked to distinct FTDs, including Pick's disease and chronic traumatic encephalopathy.
Area of Science:
- Neuroscience
- Genetics
- Pathology
Background:
- Filamentous tau protein inclusions characterize frontotemporal dementias (FTDs).
- Mutations in the MAPT (tau) gene account for about 5% of FTD cases.
- Tau protein dysfunction is sufficient to cause neurodegeneration and dementia.
Purpose of the Study:
- To investigate the structural characteristics of tau filaments in various frontotemporal dementias.
- To determine if specific tau protein folds are associated with distinct FTD subtypes.
Main Methods:
- Electron cryo-microscopy was used to determine the structure of tau filaments.
- Analysis included tau filaments from cases of Pick's disease, corticobasal degeneration, and chronic traumatic encephalopathy.
Main Results:
- Specific tau protein folds were identified in Pick's disease and corticobasal degeneration.
- These tau folds showed no inter-individual variation within each disease.
- Similar findings were observed in chronic traumatic encephalopathy.
Conclusions:
- Tau protein structure is disease-specific in frontotemporal dementias.
- Distinct tau folds may serve as pathological hallmarks for different FTD subtypes.
- Understanding tau pathology is crucial for FTD research and potential therapeutic strategies.
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