Parkinson's Disease, Proteins, and Prions: Milestones
Identifieur interne : 000574 ( PascalFrancis/Corpus ); précédent : 000573; suivant : 000575Parkinson's Disease, Proteins, and Prions: Milestones
Auteurs : C. Warren Olanow ; K. McnaughtSource :
- Movement disorders [ 0885-3185 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD.
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NO : | PASCAL 11-0264654 INIST |
---|---|
ET : | Parkinson's Disease, Proteins, and Prions: Milestones |
AU : | OLANOW (C. Warren); MCNAUGHT (K.) |
AF : | Department of Neurology and Neuroscience, Mount Sinai School of Medicine/New York, New York/Etats-Unis (1 aut.); National Tourette Syndrome Association/Bayside, New York/Etats-Unis (2 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2011; Vol. 26; No. 6; Pp. 1056-1071; Bibl. 187 ref. |
LA : | Anglais |
EA : | Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD. |
CC : | 002B17; 002B17G |
FD : | Maladie de Parkinson; Pathologie du système nerveux; Protéine PrP; Prion |
FG : | Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central |
ED : | Parkinson disease; Nervous system diseases; Prion protein; Prion |
EG : | Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease |
SD : | Parkinson enfermedad; Sistema nervioso patología; Protéina PrP; Prion |
LO : | INIST-20953.354000191622890130 |
ID : | 11-0264654 |
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Pascal:11-0264654Le document en format XML
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD.</div>
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<ET>Parkinson's Disease, Proteins, and Prions: Milestones</ET>
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