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Updated: Oct 24, 2025
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In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
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Pneumonia initiates a tauopathy.
Ron Balczon1,2, Mike T Lin2,3, Ji Young Lee2,3,4
1Department of Biochemistry and Molecular Biology, University of South Alabama, Mobile, AL, USA.
Summary
Pneumonia triggers toxic amyloid and tau proteins in the blood, leading to cognitive dysfunction by impairing brain function. This tauopathy contributes to memory loss and thinking problems after infection.
Area of Science:
- Neuroscience
- Pathology
- Infectious Diseases
Background:
- Pneumonia frequently causes cognitive dysfunction, but the underlying mechanisms remain unclear.
- Amyloid and tau proteins are implicated in neurodegenerative diseases and cognitive decline.
Purpose of the Study:
- To investigate if pneumonia generates cytotoxic amyloid and tau variants.
- To determine if these variants impair hippocampal function and long-term potentiation (LTP).
- To assess the role of tau in pneumonia-induced cognitive deficits.
Main Methods:
- Detected amyloid and tau species in blood and hippocampus post-pneumonia.
- Introduced blood-borne amyloid and tau into uninfected animals.
- Evaluated LTP in wild-type and tau knockout mice following pneumonia or amyloid/tau administration.
Main Results:
- Cytotoxic amyloid and tau were found in circulation and brain tissue after pneumonia, and in extracorporeal membrane oxygenation (ECMO) circuits of severe cases.
- Infusion of these variants impaired hippocampal processing and LTP in animals.
- Tau knockout mice showed resistance to infection-induced LTP impairment and amyloid/tau variant generation.
Conclusions:
- Pneumonia induces a tauopathy through circulating cytotoxic amyloid and tau variants.
- These variants contribute to cognitive dysfunction by disrupting hippocampal signaling.
- Targeting tau may offer therapeutic strategies for post-pneumonia cognitive deficits.
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