Related Experiment Video
Updated: Nov 21, 2025
Stereotaxic Infusion of Oligomeric Amyloid-beta into the Mouse Hippocampus
Published on: June 17, 2015
Learning Deficits Accompanied by Microglial Proliferation After the Long-Term Post-Injection of Alzheimer's Disease
Tetsuo Hayashi1, Shotaro Shimonaka2,3, Montasir Elahi1,2
1Department of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Background:
Human tauopathy brain injections into the mouse brain induce the development of tau aggregates, which spread to functionally connected brain regions; however, the features of this neurotoxicity remain unclear. One reason may be short observational periods because previous studies mostly used mutated-tau transgenic mice and needed to complete the study before these mice developed neurofibrillary tangles.
Objective:
To examine whether long-term incubation of Alzheimer's disease (AD) brain in the mouse brain cause functional decline.
Methods:
We herein used Tg601 mice, which overexpress wild-type human tau, and non-transgenic littermates (NTg) and injected an insoluble fraction of the AD brain into the unilateral hippocampus.
Results:
After a long-term (17-19 months) post-injection, mice exhibited learning deficits detected by the Barnes maze test. Aggregated tau pathology in the bilateral hippocampus was more prominent in Tg601 mice than in NTg mice. No significant changes were observed in the number of Neu-N positive cells or astrocytes in the hippocampus, whereas that of Iba-I-positive microglia increased after the AD brain injection.
Conclusion:
These results potentially implicate tau propagation in functional decline and indicate that long-term changes in non-mutated tau mice may reflect human pathological conditions.
Insights
Long-term brain injections of Alzheimer's disease (AD) brain tissue into mice caused learning deficits and increased tau pathology. This suggests tau propagation contributes to neurodegeneration and functional decline in tauopathies.
Area of Science:
- Neuroscience
- Pathology
- Neurodegenerative Diseases
Background:
- Human tauopathy can induce tau aggregate formation and spread in mouse brains, but neurotoxicity features remain unclear.
- Previous studies were limited by short observation periods and the use of mutated-tau transgenic mice.
Purpose of the Study:
- To investigate if long-term incubation of Alzheimer's disease (AD) brain tissue in mice leads to functional decline.
Main Methods:
- Tg601 mice (overexpressing wild-type human tau) and non-transgenic (NTg) littermates received unilateral hippocampal injections of an insoluble AD brain fraction.
- Mice were observed for 17-19 months post-injection.
Main Results:
- Mice exhibited learning deficits in the Barnes maze test.
- Aggregated tau pathology was more pronounced in the hippocampus of Tg601 mice compared to NTg mice.
- Microglial activation (Iba-1 positive cells) increased post-injection, while neuronal and astrocyte counts remained unchanged.
Conclusions:
- Tau propagation may contribute to functional decline in tauopathies.
- Long-term changes in non-mutated tau mice could model human pathological conditions.
More Related Videos
08:01Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
08:27Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
Published on: July 29, 2018