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No Overt Deficits in Aged Tau-Deficient C57Bl/6.Mapttm1(EGFP)Kit GFP Knockin Mice
Annika van Hummel1, Mian Bi1, Stefania Ippati1
1Dementia Research Unit, Department of Anatomy, School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, NSW, Australia.
Abstract:
Several mouse lines with knockout of the tau-encoding MAPT gene have been reported in the past; they received recent attention due to reports that tau reduction prevented Aβ-induced deficits in mouse models of Alzheimer's disease. However, the effects of long-term depletion of tau in vivo remained controversial. Here, we used the tau-deficient GFP knockin line Mapttm1(EGFP)kit on a pure C57Bl/6 background and subjected a large cohort of males and females to a range of motor, memory and behavior tests and imaging analysis, at the advanced age of over 16 months. Neither heterozygous nor homozygous Mapttm1(EGFP)kit mice presented with deficits or abnormalities compared to wild-type littermates. Differences to reports using other tau knockout models may be due to different genetic backgrounds, respective gene targeting strategies or other confounding factors, such as nutrition. To this end, we report no functional or morphological deficits upon tau reduction or depletion in aged mice.
Insights
Tau gene (MAPT) depletion in mice did not cause functional or morphological deficits. Aged tau knockout mice showed no abnormalities, suggesting genetic background may influence prior findings.
Area of Science:
- Neuroscience
- Genetics
Background:
- The tau-encoding MAPT gene is crucial in neuronal function.
- Previous studies suggested tau reduction may mitigate Alzheimer's disease pathology, but long-term effects remain unclear.
Purpose of the Study:
- To investigate the long-term effects of tau gene (MAPT) depletion in vivo.
- To assess functional and morphological consequences of tau deficiency in aged mice.
Main Methods:
- Utilized the Mapttm1(EGFP)kit tau-deficient GFP knockin mouse line on a C57Bl/6 background.
- Conducted extensive motor, memory, and behavioral tests on aged (over 16 months) male and female mice.
- Performed imaging analysis to evaluate morphological changes.
Main Results:
- Neither heterozygous nor homozygous Mapttm1(EGFP)kit mice exhibited deficits or abnormalities compared to wild-type littermates.
- No functional or morphological deficits were observed in aged mice with tau reduction or depletion.
- Highlighted potential confounding factors like genetic background and nutrition in previous studies.
Conclusions:
- Long-term tau gene (MAPT) depletion does not lead to observable deficits in aged mice.
- Findings suggest that genetic background and experimental conditions are critical when interpreting tau knockout studies.
