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Published on: January 25, 2018
Enriched odor exposure decrease tau phosphorylation in the rat hippocampus and cortex
Kai Liao1, Dan Liu, Ling-Qiang Zhu
1Department of Pathophysiology, Key Laboratory of Neurological Diseases of Education Committee of China, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, PR China.
Neuroscience Letters
|December 14, 2011
Summary
Long-term exposure to enriched odors significantly reduced tau phosphorylation in rat brains, suggesting a potential therapeutic strategy for Alzheimer's disease (AD). Short-term exposure showed no effect.
Area of Science:
- Neuroscience
- Pathology
- Biochemistry
Background:
- Abnormal tau hyperphosphorylation forms neurofibrillary tangles (NFTs), a key feature of Alzheimer's disease (AD).
- A correlation exists between olfactory dysfunction and AD pathology, but odor's effect on tau phosphorylation is unclear.
Purpose of the Study:
- To investigate the impact of short-term and long-term odor enrichment on tau phosphorylation in rat brains.
- To determine if odor stimulation can alter pathological tau markers relevant to AD.
Main Methods:
- Rats were exposed to enriched odors for short-term and long-term periods.
- Tau phosphorylation levels were measured at multiple sites in the hippocampus and cortex.
Main Results:
- Short-term odor enrichment did not alter tau phosphorylation.
- Long-term odor enrichment significantly reduced tau phosphorylation at key sites (Ser198/199/202, Thr231, Ser396, Ser404) in both hippocampus and cortex.
Conclusions:
- Long-term odor exposure may prevent tau phosphorylation, offering a potential novel therapeutic approach for Alzheimer's disease.
- Odor enrichment could be a viable strategy to mitigate AD-related tau pathology.
