Neurochemistry and the non-motor aspects of PD
Parkinson disease (PD) is a systemic disease with variegated non-motor deficits and neurological symptoms, including impaired olfaction, autonomic failure, cognitive impairment and psychiatric symptoms, in addition to the classical motor symptoms. Many non-motor symptoms appear before or in parallel...
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| Format: | Article |
| Language: | English |
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Elsevier
2012-06-01
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| Series: | Neurobiology of Disease |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0969996111003512 |
| _version_ | 1818352694265380864 |
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| author | I. Ferrer I. López-Gonzalez M. Carmona E. Dalfó A. Pujol A. Martínez |
| author_facet | I. Ferrer I. López-Gonzalez M. Carmona E. Dalfó A. Pujol A. Martínez |
| author_sort | I. Ferrer |
| collection | DOAJ |
| description | Parkinson disease (PD) is a systemic disease with variegated non-motor deficits and neurological symptoms, including impaired olfaction, autonomic failure, cognitive impairment and psychiatric symptoms, in addition to the classical motor symptoms. Many non-motor symptoms appear before or in parallel with motor deficits and then worsen with disease progression. Although there is a relationship, albeit not causal, between motor symptoms and the presence of Lewy bodies (LBs) and neurites filled with abnormal α-synuclein, other neurological alterations are independent of the amount of α-synuclein inclusions in neurons and neurites, thereby indicating that different mechanisms probably converge in the degenerative process. This may apply to complex alterations interfering with olfactory and autonomic nervous system functions, emotions, sleep regulation, and behavioral, cognitive and mental performance. Involvement of the cerebral cortex leading to impaired behavior and cognition is related to several convergent altered factors including: a. dopaminergic, noradrenergic, serotoninergic and cholinergic cortical innervation; b. synapses; c. cortical metabolism; d. mitochondrial function and energy production; e. oxidative damage; f. transcription; g. protein expression; h. lipid composition; and i. ubiquitin–proteasome system and autophagy, among others. This complex situation indicates that multiple subcellular failure in selected cell populations is difficult to reconcile with a reductionistic scenario of a single causative cascade of events leading to non-motor symptoms in PD. Furthermore, these alterations may appear at early stages of the disease and may precede the appearance of substantial irreversible cell loss by years. These observations have important implications in the design of therapeutic approaches geared to prevention and treatment of PD. |
| first_indexed | 2024-12-13T18:57:42Z |
| format | Article |
| id | doaj.art-956a179f10724764a76596c4e650619f |
| institution | Directory Open Access Journal |
| issn | 1095-953X |
| language | English |
| last_indexed | 2024-12-13T18:57:42Z |
| publishDate | 2012-06-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Neurobiology of Disease |
| spelling | doaj.art-956a179f10724764a76596c4e650619f2022-12-21T23:34:45ZengElsevierNeurobiology of Disease1095-953X2012-06-01463508526Neurochemistry and the non-motor aspects of PDI. Ferrer0I. López-Gonzalez1M. Carmona2E. Dalfó3A. Pujol4A. Martínez5Institute of Neuropathology, Service of Pathology, University Hospital of Bellvitge, Spain; Faculty of Medicine, University of Barcelona, Spain; Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Spain; Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Spain; Corresponding author at: Institut de Neuropatologia, Servei Anatomia Patològica, IDIBELL-Hospital Universitari de Bellvitge, carrer Feixa Llarga sn, 08908 Hospitalet de Llobregat, Spain. Fax: +34 932607503.Institute of Neuropathology, Service of Pathology, University Hospital of Bellvitge, SpainInstitute of Neuropathology, Service of Pathology, University Hospital of Bellvitge, SpainInstitute of Neuropathology, Service of Pathology, University Hospital of Bellvitge, Spain; Neurometabolic Diseases Laboratory, Spain; Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Spain; Center for Biomedical Research on Rare Diseases (CIBERER), SpainInstitute of Neuropathology, Service of Pathology, University Hospital of Bellvitge, Spain; Neurometabolic Diseases Laboratory, Spain; Bellvitge Biomedical Research Institute (IDIBELL), Hospitalet de Llobregat, Spain; Center for Biomedical Research on Rare Diseases (CIBERER), Spain; Catalan Institution of Research and Advanced Studies (ICREA), Barcelona, Catalonia, SpainInstitute of Neuropathology, Service of Pathology, University Hospital of Bellvitge, SpainParkinson disease (PD) is a systemic disease with variegated non-motor deficits and neurological symptoms, including impaired olfaction, autonomic failure, cognitive impairment and psychiatric symptoms, in addition to the classical motor symptoms. Many non-motor symptoms appear before or in parallel with motor deficits and then worsen with disease progression. Although there is a relationship, albeit not causal, between motor symptoms and the presence of Lewy bodies (LBs) and neurites filled with abnormal α-synuclein, other neurological alterations are independent of the amount of α-synuclein inclusions in neurons and neurites, thereby indicating that different mechanisms probably converge in the degenerative process. This may apply to complex alterations interfering with olfactory and autonomic nervous system functions, emotions, sleep regulation, and behavioral, cognitive and mental performance. Involvement of the cerebral cortex leading to impaired behavior and cognition is related to several convergent altered factors including: a. dopaminergic, noradrenergic, serotoninergic and cholinergic cortical innervation; b. synapses; c. cortical metabolism; d. mitochondrial function and energy production; e. oxidative damage; f. transcription; g. protein expression; h. lipid composition; and i. ubiquitin–proteasome system and autophagy, among others. This complex situation indicates that multiple subcellular failure in selected cell populations is difficult to reconcile with a reductionistic scenario of a single causative cascade of events leading to non-motor symptoms in PD. Furthermore, these alterations may appear at early stages of the disease and may precede the appearance of substantial irreversible cell loss by years. These observations have important implications in the design of therapeutic approaches geared to prevention and treatment of PD.http://www.sciencedirect.com/science/article/pii/S0969996111003512Parkinson diseaseAmygdalaOlfactionAutonomic nervous systemSleep disordersDementia |
| spellingShingle | I. Ferrer I. López-Gonzalez M. Carmona E. Dalfó A. Pujol A. Martínez Neurochemistry and the non-motor aspects of PD Neurobiology of Disease Parkinson disease Amygdala Olfaction Autonomic nervous system Sleep disorders Dementia |
| title | Neurochemistry and the non-motor aspects of PD |
| title_full | Neurochemistry and the non-motor aspects of PD |
| title_fullStr | Neurochemistry and the non-motor aspects of PD |
| title_full_unstemmed | Neurochemistry and the non-motor aspects of PD |
| title_short | Neurochemistry and the non-motor aspects of PD |
| title_sort | neurochemistry and the non motor aspects of pd |
| topic | Parkinson disease Amygdala Olfaction Autonomic nervous system Sleep disorders Dementia |
| url | http://www.sciencedirect.com/science/article/pii/S0969996111003512 |
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