Olfactory dysfunction, central cholinergic integrity and cognitive impairment in Parkinsons disease
Identifieur interne : 000449 ( Main/Exploration ); précédent : 000448; suivant : 000450Olfactory dysfunction, central cholinergic integrity and cognitive impairment in Parkinsons disease
Auteurs : Nicolaas I. Bohnen [États-Unis] ; Martijn L. T. M. Mller [États-Unis] ; Vikas Kotagal [États-Unis] ; Robert A. Koeppe [États-Unis] ; Michael A. Kilbourn [États-Unis] ; Roger L. Albin [États-Unis] ; Kirk A. Frey [États-Unis]Source :
- Brain [ 0006-8950 ] ; 2010-06.
Abstract
Olfactory dysfunction is common in subjects with Parkinsons disease. The pathophysiology of such dysfunction, however, remains poorly understood. Neurodegeneration within central regions involved in odour perception may contribute to olfactory dysfunction in Parkinsons disease. Central cholinergic deficits occur in Parkinsons disease and cholinergic neurons innervate regions, such as the limbic archicortex, involved in odour perception. We investigated the relationship between performance on an odour identification task and forebrain cholinergic denervation in Parkinsons disease subjects without dementia. Fifty-eight patients with Parkinsons disease (mean Hoehn and Yahr stage 2.5 0.5) without dementia (mean Mini-Mental State Examination, 29.0 1.4) underwent a clinical assessment, [11C]methyl-4-piperidinyl propionate acetylcholinesterase brain positron emission tomography and olfactory testing with the University of Pennsylvania Smell Identification Test. The diagnosis of Parkinsons disease was confirmed by [11C]dihydrotetrabenazine vesicular monoamine transporter type 2 positron emission tomography. We found that odour identification test scores correlated positively with acetylcholinesterase activity in the hippocampal formation (r 0.56, P < 0.0001), amygdala (r 0.50, P < 0.0001) and neocortex (r 0.46, P 0.0003). Striatal monoaminergic activity correlated positively with odour identification scores (r 0.30, P < 0.05). Multiple regression analysis including limbic (hippocampal and amygdala) and neocortical acetylcholinesterase activity as well as striatal monoaminergic activity, using odour identification scores as the dependent variable, demonstrated a significant regressor effect for limbic acetylcholinesterase activity (F 10.1, P < 0.0001), borderline for striatal monoaminergic activity (F 1.6, P 0.13), but not significant for cortical acetylcholinesterase activity (F 0.3, P 0.75). Odour identification scores correlated positively with scores on cognitive measures of episodic verbal learning (r 0.30, P < 0.05). These findings indicate that cholinergic denervation of the limbic archicortex is a more robust determinant of hyposmia than nigrostriatal dopaminergic denervation in subjects with moderately severe Parkinson's disease. Greater deficits in odour identification may identify patients with Parkinson's disease at risk for clinically significant cognitive impairment.
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DOI: 10.1093/brain/awq079
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The pathophysiology of such dysfunction, however, remains poorly understood. Neurodegeneration within central regions involved in odour perception may contribute to olfactory dysfunction in Parkinsons disease. Central cholinergic deficits occur in Parkinsons disease and cholinergic neurons innervate regions, such as the limbic archicortex, involved in odour perception. We investigated the relationship between performance on an odour identification task and forebrain cholinergic denervation in Parkinsons disease subjects without dementia. Fifty-eight patients with Parkinsons disease (mean Hoehn and Yahr stage 2.5 0.5) without dementia (mean Mini-Mental State Examination, 29.0 1.4) underwent a clinical assessment, [11C]methyl-4-piperidinyl propionate acetylcholinesterase brain positron emission tomography and olfactory testing with the University of Pennsylvania Smell Identification Test. The diagnosis of Parkinsons disease was confirmed by [11C]dihydrotetrabenazine vesicular monoamine transporter type 2 positron emission tomography. We found that odour identification test scores correlated positively with acetylcholinesterase activity in the hippocampal formation (r 0.56, P < 0.0001), amygdala (r 0.50, P < 0.0001) and neocortex (r 0.46, P 0.0003). Striatal monoaminergic activity correlated positively with odour identification scores (r 0.30, P < 0.05). Multiple regression analysis including limbic (hippocampal and amygdala) and neocortical acetylcholinesterase activity as well as striatal monoaminergic activity, using odour identification scores as the dependent variable, demonstrated a significant regressor effect for limbic acetylcholinesterase activity (F 10.1, P < 0.0001), borderline for striatal monoaminergic activity (F 1.6, P 0.13), but not significant for cortical acetylcholinesterase activity (F 0.3, P 0.75). Odour identification scores correlated positively with scores on cognitive measures of episodic verbal learning (r 0.30, P < 0.05). These findings indicate that cholinergic denervation of the limbic archicortex is a more robust determinant of hyposmia than nigrostriatal dopaminergic denervation in subjects with moderately severe Parkinson's disease. Greater deficits in odour identification may identify patients with Parkinson's disease at risk for clinically significant cognitive impairment.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Michigan</li></region></list><tree><country name="États-Unis"><region name="Michigan"><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I." last="Bohnen">Nicolaas I. Bohnen</name></region><name sortKey="Albin, Roger L" sort="Albin, Roger L" uniqKey="Albin R" first="Roger L." last="Albin">Roger L. Albin</name><name sortKey="Albin, Roger L" sort="Albin, Roger L" uniqKey="Albin R" first="Roger L." last="Albin">Roger L. Albin</name><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I." last="Bohnen">Nicolaas I. Bohnen</name><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I." last="Bohnen">Nicolaas I. Bohnen</name><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I." last="Bohnen">Nicolaas I. Bohnen</name><name sortKey="Frey, Kirk A" sort="Frey, Kirk A" uniqKey="Frey K" first="Kirk A." last="Frey">Kirk A. Frey</name><name sortKey="Frey, Kirk A" sort="Frey, Kirk A" uniqKey="Frey K" first="Kirk A." last="Frey">Kirk A. Frey</name><name sortKey="Kilbourn, Michael A" sort="Kilbourn, Michael A" uniqKey="Kilbourn M" first="Michael A." last="Kilbourn">Michael A. Kilbourn</name><name sortKey="Koeppe, Robert A" sort="Koeppe, Robert A" uniqKey="Koeppe R" first="Robert A." last="Koeppe">Robert A. Koeppe</name><name sortKey="Kotagal, Vikas" sort="Kotagal, Vikas" uniqKey="Kotagal V" first="Vikas" last="Kotagal">Vikas Kotagal</name><name sortKey="Mller, Martijn L T M" sort="Mller, Martijn L T M" uniqKey="Mller M" first="Martijn L. T. M." last="Mller">Martijn L. T. M. Mller</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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