Mild Cognitive Impairment in Parkinson’s Disease
Prospective studies conducted during the last decade have shown that the majority of patients with Parkinson’s disease (PD) develop dementia. In addition, using a variety of definitions and methods, more recent research suggests that approximately a quarter of PD patients without dementia have mild...
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Veröffentlicht in: | Current neurology and neuroscience reports 2011-08, Vol.11 (4), p.371-378 |
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description | Prospective studies conducted during the last decade have shown that the majority of patients with Parkinson’s disease (PD) develop dementia. In addition, using a variety of definitions and methods, more recent research suggests that approximately a quarter of PD patients without dementia have mild cognitive impairment (PD-MCI). Furthermore, several studies have shown that approximately 20% have MCI even at time of diagnosis of PD. The typical cognitive deficits include visuospatial, attentional, and executive deficits, but memory deficits have also been shown. The etiology of PD-MCI is not known, but it is likely that mechanisms known to contribute to dementia in PD (ie, limbic and cortical Lewy bodies, amyloid plaques, and cholinergic deficits) play a role, in addition to dysfunction of dopaminergic frontostriatal circuits. PD-MCI predicts a shorter time to dementia, and preliminary evidence suggests that this is particularly true for posterior cognitive deficits. There are currently no systematic clinical trials in PD-MCI. |
doi_str_mv | 10.1007/s11910-011-0203-1 |
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In addition, using a variety of definitions and methods, more recent research suggests that approximately a quarter of PD patients without dementia have mild cognitive impairment (PD-MCI). Furthermore, several studies have shown that approximately 20% have MCI even at time of diagnosis of PD. The typical cognitive deficits include visuospatial, attentional, and executive deficits, but memory deficits have also been shown. The etiology of PD-MCI is not known, but it is likely that mechanisms known to contribute to dementia in PD (ie, limbic and cortical Lewy bodies, amyloid plaques, and cholinergic deficits) play a role, in addition to dysfunction of dopaminergic frontostriatal circuits. PD-MCI predicts a shorter time to dementia, and preliminary evidence suggests that this is particularly true for posterior cognitive deficits. 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In addition, using a variety of definitions and methods, more recent research suggests that approximately a quarter of PD patients without dementia have mild cognitive impairment (PD-MCI). Furthermore, several studies have shown that approximately 20% have MCI even at time of diagnosis of PD. The typical cognitive deficits include visuospatial, attentional, and executive deficits, but memory deficits have also been shown. The etiology of PD-MCI is not known, but it is likely that mechanisms known to contribute to dementia in PD (ie, limbic and cortical Lewy bodies, amyloid plaques, and cholinergic deficits) play a role, in addition to dysfunction of dopaminergic frontostriatal circuits. PD-MCI predicts a shorter time to dementia, and preliminary evidence suggests that this is particularly true for posterior cognitive deficits. There are currently no systematic clinical trials in PD-MCI.</description><subject>Cerebrospinal Fluid - chemistry</subject><subject>Clinical Trials as Topic</subject><subject>Cognition Disorders - epidemiology</subject><subject>Cognition Disorders - etiology</subject><subject>Cognition Disorders - pathology</subject><subject>Cognition Disorders - physiopathology</subject><subject>Humans</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurology</subject><subject>Neuropsychological Tests</subject><subject>Neurosciences</subject><subject>Neurotransmitter Agents - deficiency</subject><subject>Parkinson Disease - complications</subject><subject>Parkinson Disease - epidemiology</subject><subject>Parkinson Disease - pathology</subject><subject>Parkinson Disease - physiopathology</subject><subject>Parkinson's disease</subject><issn>1528-4042</issn><issn>1534-6293</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kM1O3DAQx60KVD4foJcq6oWTy4xjJ_ax2vIlLYJDe7bsZHZl2CSLvSnixmv09fokeLVbkJA4eWT_PPOfH2NfEL4jQH2aEA0CB0QOAkqOn9g-qlLySphyZ10LzSVIsccOUrqDDEFtPrM9gVLXdQn7TFyHRVtMhnkfVuEPFVfd0oXYUb8qQl_cungf-jT0_57_puJnSOQSHbHdmVskOt6eh-z3-dmvySWf3lxcTX5MeSNBr7huUVbonVBa1K2nGZBrvQINoqxb6XOuhrDUDTWqAq-kb70GZyrZGKkUlIeMb_qmR1qO3i5j6Fx8soMLdnt1nyuySkojMfMnG34Zh4eR0sp2ITW0WLiehjFZXSupDYoqk9_ekXfDGPu8TIakgWzVZAg3UBOHlCLNXgMg2LV-u9Fvs3671m_XEb5uG4--o_b1x3_fGRDbnfJTP6f4Nvnjri-4E47n</recordid><startdate>20110801</startdate><enddate>20110801</enddate><creator>Aarsland, Dag</creator><creator>Brønnick, Kolbjørn</creator><creator>Fladby, Tormod</creator><general>Current Science Inc</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope></search><sort><creationdate>20110801</creationdate><title>Mild Cognitive Impairment in Parkinson’s Disease</title><author>Aarsland, Dag ; 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In addition, using a variety of definitions and methods, more recent research suggests that approximately a quarter of PD patients without dementia have mild cognitive impairment (PD-MCI). Furthermore, several studies have shown that approximately 20% have MCI even at time of diagnosis of PD. The typical cognitive deficits include visuospatial, attentional, and executive deficits, but memory deficits have also been shown. The etiology of PD-MCI is not known, but it is likely that mechanisms known to contribute to dementia in PD (ie, limbic and cortical Lewy bodies, amyloid plaques, and cholinergic deficits) play a role, in addition to dysfunction of dopaminergic frontostriatal circuits. PD-MCI predicts a shorter time to dementia, and preliminary evidence suggests that this is particularly true for posterior cognitive deficits. 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subjects | Cerebrospinal Fluid - chemistry Clinical Trials as Topic Cognition Disorders - epidemiology Cognition Disorders - etiology Cognition Disorders - pathology Cognition Disorders - physiopathology Humans Medicine Medicine & Public Health Neurology Neuropsychological Tests Neurosciences Neurotransmitter Agents - deficiency Parkinson Disease - complications Parkinson Disease - epidemiology Parkinson Disease - pathology Parkinson Disease - physiopathology Parkinson's disease |
title | Mild Cognitive Impairment in Parkinson’s Disease |
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