Early Locus Coeruleus noradrenergic axon loss drives olfactory dysfunction in Alzheimer's disease
Overview
Paper Summary
This study found that in a mouse model of Alzheimer's disease, early loss of noradrenergic axons in the olfactory bulb leads to decreased sense of smell. This axon loss is driven by microglia, the brain's immune cells, which recognize and eliminate the axons. Early LC axon degeneration and increased microglial activity were also observed in post-mortem human olfactory bulbs, as well as increased TSPO signals in prodromal AD patients suggesting similar mechanisms may be at play in humans.
Explain Like I'm Five
In a mouse model of Alzheimer's, loss of specific brain connections in the olfactory bulb (the smell center) leads to a reduced sense of smell. This may explain why many Alzheimer's patients experience a diminished sense of smell early on.
Possible Conflicts of Interest
None identified.
Identified Limitations
Rating Explanation
This study combines detailed animal studies with human post-mortem tissue analysis and PET imaging to provide strong evidence for a specific neuronal mechanism underlying early olfactory dysfunction in Alzheimer's. While mainly conducted in mice, the translational components lend credibility to the findings and highlight potential early biomarkers for the disease. Despite some mechanistic details needing further investigation and the limited sample size in the human component, the research is well-executed and provides valuable insights.
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