Functional brain imaging of cognitive dysfunction in Parkinson's disease
Identifieur interne : 000042 ( Main/Exploration ); précédent : 000041; suivant : 000043Functional brain imaging of cognitive dysfunction in Parkinson's disease
Auteurs : Shigeki Hirano [Japon] ; Hitoshi Shinotoh [Japon] ; David Eidelberg [États-Unis]Source :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2012-10.
Abstract
Multiple factors are involved in the development of cognitive impairment in Parkinson's disease (PD) and related disorders. Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.
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DOI: 10.1136/jnnp-2011-301818
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Notably, several underlying factors, such as monoaminergic dysfunction, Lewy body pathology, Alzheimer disease-like pathology and cerebrovascular disease are implied in the PD pathophysiology of cognitive impairment. The mesocortical dopaminergic system is associated with executive functions which are frequently affected in PD and are influenced by local levodopa concentration, dopamine metabolism and baseline performance status. The ventral striatum and frontal cortex are associated with impulse control disorders reported in PD patients treated with dopamine replacement therapy. Cholinergic impairment in PD plays a cardinal role in the development of dementia. Acetylcholinesterase positron emission tomography demonstrates that posterior brain areas are related to cognitive decline in PD patients. Amyloid radiotracer illustrates that patients with PD with severe cognitive impairment were prone to accompanied cortical amyloid deposition. Metabolism/perfusion change associated with cognitive impairment in PD, so-called PD related cognitive pattern, is characterised by reduced frontoparietal activity and is an effective way to differentiate and monitor cognitive function of individual PD patients. Cognitive impairment in PD cannot be explained by a single mechanism and is entangled by multiple factors. Imaging studies can unravel each pathological domain, further shed light on the interrelation between different pathomechanisms, not only in PD but also in other dementia related disorders, and thereby integrate its interpretation to apply to therapeutics in individual patients.</div></front></TEI><affiliations><list><country><li>Japon</li><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="Japon"><noRegion><name sortKey="Hirano, Shigeki" sort="Hirano, Shigeki" uniqKey="Hirano S" first="Shigeki" last="Hirano">Shigeki Hirano</name></noRegion><name sortKey="Hirano, Shigeki" sort="Hirano, Shigeki" uniqKey="Hirano S" first="Shigeki" last="Hirano">Shigeki Hirano</name><name sortKey="Hirano, Shigeki" sort="Hirano, Shigeki" uniqKey="Hirano S" first="Shigeki" last="Hirano">Shigeki Hirano</name><name sortKey="Shinotoh, Hitoshi" sort="Shinotoh, Hitoshi" uniqKey="Shinotoh H" first="Hitoshi" last="Shinotoh">Hitoshi Shinotoh</name><name sortKey="Shinotoh, Hitoshi" sort="Shinotoh, Hitoshi" uniqKey="Shinotoh H" first="Hitoshi" last="Shinotoh">Hitoshi Shinotoh</name></country><country name="États-Unis"><region name="État de New York"><name sortKey="Eidelberg, David" sort="Eidelberg, David" uniqKey="Eidelberg D" first="David" last="Eidelberg">David Eidelberg</name></region><name sortKey="Eidelberg, David" sort="Eidelberg, David" uniqKey="Eidelberg D" first="David" last="Eidelberg">David Eidelberg</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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