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Updated: Oct 24, 2025
In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
Published on: January 2, 2015
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.
Abstract:
Pneumonia causes short- and long-term cognitive dysfunction in a high proportion of patients, although the mechanism(s) responsible for this effect are unknown. Here, we tested the hypothesis that pneumonia-elicited cytotoxic amyloid and tau variants: (1) are present in the circulation during infection; (2) lead to impairment of long-term potentiation; and, (3) inhibit long-term potentiation dependent upon tau. Cytotoxic amyloid and tau species were recovered from the blood and the hippocampus following pneumonia, and they were present in the extracorporeal membrane oxygenation oxygenators of patients with pneumonia, especially in those who died. Introduction of immunopurified blood-borne amyloid and tau into either the airways or the blood of uninfected animals acutely and chronically impaired hippocampal information processing. In contrast, the infection did not impair long-term potentiation in tau knockout mice and the amyloid- and tau-dependent disruption in hippocampal signaling was less severe in tau knockout mice. Moreover, the infection did not elicit cytotoxic amyloid and tau variants in tau knockout mice. Therefore, pneumonia initiates a tauopathy that contributes to cognitive dysfunction.
Insights
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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