Related Experiment Video
Updated: Jul 31, 2025

Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Transmission of Alzheimer's Disease-Associated Microbiota Dysbiosis and its Impact on Cognitive Function: Evidence
Yiying Zhang1, Yuan Shen2, Ning Liufu1
1Massachusetts General Hospital.
Abstract:
Spouses of Alzheimer's disease (AD) patients are at higher risk of developing AD dementia, but the reasons and underlying mechanism are unknown. One potential factor is gut microbiota dysbiosis, which has been associated with AD. However, it remains unclear whether the gut microbiota dysbiosis can be transmitted to non-AD individuals and contribute to the development of AD pathogenesis and cognitive impairment. The present study found that co-housing wild-type mice with AD transgenic mice or giving them AD transgenic mice feces caused AD-associated gut microbiota dysbiosis, Tau phosphorylation, and cognitive impairment. Gavage with Lactobacillus and Bifidobacterium restored these changes. The oral and gut microbiota of AD patient partners resembled that of AD patients but differed from healthy controls, indicating the transmission of oral and gut microbiota and its impact on cognitive function. The underlying mechanism of these findings includes that the butyric acid-mediated acetylation of GSK3β at lysine 15 regulated its phosphorylation at serine 9, consequently impacting Tau phosphorylation. These results provide insight into a potential link between gut microbiota dysbiosis and AD and underscore the need for further research in this area.
Insights
Spouses of Alzheimer's disease (AD) patients may develop AD dementia due to transmissible gut microbiota dysbiosis. Probiotic treatment with Lactobacillus and Bifidobacterium reversed these AD-like changes in mice.
Area of Science:
- Microbiology
- Neuroscience
- Gastroenterology
Background:
- Spouses of Alzheimer's disease (AD) patients exhibit increased AD dementia risk, with unknown mechanisms.
- Gut microbiota dysbiosis is linked to AD, but its transmissibility and role in non-AD individuals are unclear.
Approach:
- Wild-type mice co-housed with AD transgenic mice or gavaged with AD feces developed AD-associated gut dysbiosis, Tau phosphorylation, and cognitive deficits.
- Probiotic administration of Lactobacillus and Bifidobacterium ameliorated these AD-like pathological and cognitive changes.
- Analysis of oral and gut microbiota in AD patient partners revealed similarities to AD patients, distinct from healthy controls.
Key Points:
- Gut microbiota dysbiosis is transmissible from AD patients to non-AD individuals via co-housing or fecal transfer.
- Transmitted dysbiosis induces AD-like pathology, including Tau phosphorylation and cognitive impairment.
- Specific bacterial interventions (Lactobacillus, Bifidobacterium) can restore gut microbiota balance and mitigate AD-related effects.
Conclusions:
- Gut microbiota dysbiosis can be transmitted and contribute to Alzheimer's disease pathogenesis and cognitive decline.
- Butyric acid-mediated GSK3β acetylation is a key molecular mechanism linking gut microbiota to Tau phosphorylation.
- Findings highlight the gut microbiome as a potential therapeutic target for Alzheimer's disease prevention and treatment.
Related Concept Videos
Alzheimer's Disease: Overview
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ...
Role of Neurotransmitters in Memory
Glutamate and Synaptic Plasticity
Glutamate, the brain's main excitatory neurotransmitter, is...
Alzheimer's Disease: Treatment
Fungal Phylum Microsporidia
Dementia
The progression of dementia is generally gradual....

