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Hippocampal BDNF expression in a tau transgenic mouse model.
Sylvie Burnouf1, Karim Belarbi, Laetitia Troquier
1Max-Planck Institute für Biologie des Alterns/Max-Planck Institute for Biology of Ageing, Köln, Germany. sylvie.burnouf@age.mpg.de
Current Alzheimer Research
|January 26, 2012
Summary
This study investigated the impact of Tau pathology on Brain-Derived Neurotrophic Factor (BDNF) levels in Alzheimer's disease (AD). Findings suggest amyloid pathology, not Tau, is linked to reduced BDNF in AD brains.
Area of Science:
- Neuroscience
- Molecular Biology
- Neurodegenerative Diseases
Background:
- Alzheimer's disease (AD) involves amyloid plaques and neurofibrillary tangles (NFTs) from hyperphosphorylated Tau.
- Brain-Derived Neurotrophic Factor (BDNF) is crucial for memory and synaptic plasticity, with reduced levels observed in AD.
- Amyloid peptides are implicated in BDNF decrease, but Tau's role remains unclear.
Purpose of the Study:
- To investigate the relationship between Tau pathology and BDNF expression in a mouse model of AD.
- To determine if Tau pathology contributes to the reduction of BDNF observed in Alzheimer's disease.
Main Methods:
- Utilized the THY-Tau22 transgenic mouse strain exhibiting Tau pathology and memory deficits.
- Employed quantitative PCR, Western blot, and ELISA to assess BDNF mRNA and protein levels.
- Correlated Tau pathology progression with changes in BDNF expression.
Main Results:
- Tau pathology in the THY-Tau22 model was not associated with decreased BDNF mRNA levels.
- Tau pathology did not lead to a reduction in BDNF protein levels.
- These findings indicate Tau pathology does not directly down-regulate BDNF.
Conclusions:
- The observed reduction of BDNF in Alzheimer's disease brains may be primarily linked to amyloid pathology.
- Tau pathology does not appear to be the direct cause of BDNF dysregulation in this AD model.
- Further research should focus on the interplay between amyloid pathology and BDNF homeostasis in AD.
