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Olfactory Assays for Mouse Models of Neurodegenerative Disease
Published on: August 25, 2014
Olfactory dysfunction, central cholinergic integrity and cognitive impairment in Parkinson's disease
Nicolaas I Bohnen1, Martijn L T M Müller, Vikas Kotagal
1Department of Radiology, Division of Nuclear Medicine, University of Michigan, Ann Arbor, MI 48109, USA. nbohnen@umich.edu
Brain : a Journal of Neurology
|April 24, 2010
Summary
Olfactory dysfunction in Parkinson's disease is linked to cholinergic deficits in the brain's limbic regions. This suggests limbic cholinergic denervation, not dopaminergic, is key to smell loss and potential cognitive decline in Parkinson's patients.
Area of Science:
- Neuroscience
- Neurology
- Radiochemistry
Background:
- Olfactory dysfunction is a common, yet poorly understood, non-motor symptom in Parkinson's disease (PD).
- Central cholinergic system deficits are implicated in PD neurodegeneration and affect brain regions involved in odor perception.
- Understanding the neurobiological underpinnings of olfactory dysfunction is crucial for diagnosing and managing PD.
Purpose of the Study:
- To investigate the relationship between olfactory identification performance and forebrain cholinergic denervation in non-demented Parkinson's disease patients.
- To determine whether limbic or neocortical cholinergic deficits, or striatal monoaminergic activity, are the primary drivers of olfactory dysfunction in PD.
Main Methods:
- Fifty-eight non-demented Parkinson's disease patients underwent clinical assessment, olfactory testing (University of Pennsylvania Smell Identification Test), and brain positron emission tomography (PET) scans.
- Acetylcholinesterase activity was measured using [(11)C]methyl-4-piperidinyl propionate PET.
- Parkinson's disease diagnosis was confirmed via [(11)C]dihydrotetrabenazine vesicular monoamine transporter type 2 PET.
Main Results:
- Odour identification scores positively correlated with acetylcholinesterase activity in the hippocampal formation, amygdala, and neocortex.
- Limbic (hippocampal and amygdala) acetylcholinesterase activity was a significant predictor of odour identification performance in multiple regression analysis.
- Striatal monoaminergic activity showed a borderline correlation, while neocortical acetylcholinesterase activity did not significantly predict olfactory function.
Conclusions:
- Cholinergic denervation of the limbic archicortex is a more significant determinant of hyposmia in Parkinson's disease than nigrostriatal dopaminergic denervation.
- Deficits in odour identification may serve as an early indicator of cognitive impairment risk in Parkinson's disease patients.
- Targeting cholinergic pathways may offer therapeutic potential for olfactory and associated cognitive deficits in PD.
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