MovDisordV3, Main, Exploration, bibRecord, 000398

The Neurobiological Basis of Cognitive Impairment in Parkinson'S Disease

Identifieur interne : 000398 ( Main/Exploration ); précédent : 000397; suivant : 000399

The Neurobiological Basis of Cognitive Impairment in Parkinson'S Disease

Auteurs : Glenda M. Halliday [Australie] ; James B. Leverenz [États-Unis] ; Jay S. Schneider [États-Unis] ; Charles H. Adler [États-Unis]

Source :

Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2014.

RBID : PMC:4049032

English descriptors

KwdEn :
- Animals, Brain (pathology), Cognition (physiology), Cognition Disorders (metabolism), Dopamine (metabolism), Humans, Parkinson Disease (metabolism), Risk Factors.
MESH :
- chemical , metabolism : Dopamine.
- metabolism : Cognition Disorders, Parkinson Disease.
- pathology : Brain.
- physiology : Cognition.
- Animals, Humans, Risk Factors.

Abstract

The recent formalization of clinical criteria for PD with dementia (PD-D) codifies many studies on this topic, including those assessing biological correlates. These studies show that the emergence of PD-D occurs on the background of severe dopamine deficits with the main pathological drivers of cognitive decline being a synergistic effect between α -synuclein and Alzheimer's disease pathology. The presence of these pathologies correlates with a marked loss of limbic and cortically projecting dopamine, noradrenaline, serotonin and acetylcholine neurons, although the exact timing of these relationships remains to be determined. Genetic factors, such as triplications in the α-synuclein gene, lead to a clear increased risk of PD-D, while others, such as parkin mutations, are associated with a reduced risk of PD-D. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD-MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low dose MPTP treatment in primates recapitulates PD-MCI over time, enhancing the current biological concept of PD-MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems. Data from other animal models support multiple transmitter involvement in cognitive impairment in PD. While dopamine dysfunction has been highlighted because of its obvious role in PD, the role of the other neurotransmitter systems, neurodegenerative pathologies and genetic factors in PD-MCI remain to be fully elucidated.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4049032

DOI: 10.1002/mds.25857
PubMed: 24757112
PubMed Central: 4049032

Affiliations:

Le document en format XML

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<front><div type="abstract" xml:lang="en"><p id="P1">The recent formalization of clinical criteria for PD with dementia (PD-D) codifies many studies on this topic, including those assessing biological correlates. These studies show that the emergence of PD-D occurs on the background of severe dopamine deficits with the main pathological drivers of cognitive decline being a synergistic effect between α -synuclein and Alzheimer's disease pathology. The presence of these pathologies correlates with a marked loss of limbic and cortically projecting dopamine, noradrenaline, serotonin and acetylcholine neurons, although the exact timing of these relationships remains to be determined. Genetic factors, such as triplications in the <italic>α-synuclein</italic>
 gene, lead to a clear increased risk of PD-D, while others, such as <italic>parkin</italic>
 mutations, are associated with a reduced risk of PD-D. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD-MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low dose MPTP treatment in primates recapitulates PD-MCI over time, enhancing the current biological concept of PD-MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems. Data from other animal models support multiple transmitter involvement in cognitive impairment in PD. While dopamine dysfunction has been highlighted because of its obvious role in PD, the role of the other neurotransmitter systems, neurodegenerative pathologies and genetic factors in PD-MCI remain to be fully elucidated.</p>
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Movement Disorders (revue)

The Neurobiological Basis of Cognitive Impairment in Parkinson'S Disease

The Neurobiological Basis of Cognitive Impairment in Parkinson'S Disease

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

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Pour générer des pages wiki

	Movement Disorders (revue)
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