Parkinsonism-plus syndromes

Jankovic, Joseph

doi:10.1002/mds.870040512

Cited by 58 publications

(12 citation statements)

References 110 publications

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“…All other categories of parkinsonism (non-PD parkinsonism), including vascular parkinsonism, Parkinson-plus syndromes or unspecified (ie, the exact type of non-PD parkinsonism was not certain) 15 16…”

Section: Methodsmentioning

confidence: 99%

Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population based study

Benito‐León

Louis

Bermejo‐Pareja

2008

Journal of Neurology, Neurosurgery & Psychiatry

218

152

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Section: Methodsmentioning

confidence: 99%

Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population based study

Benito‐León

Louis

Bermejo‐Pareja

2008

Journal of Neurology, Neurosurgery & Psychiatry

218

152

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“…(Jankovic, 1989;Rajput et al, 1991;Duvoisin and Golbe, 1991). The main biochemical characteristic of Parkinson's disease is the dopamine deficiency in the caudate-putamen nuclei due to the loss of dopaminergic neurons caused by degeneration of the nigrostriatal pathway.…”

Section: Introductionmentioning

confidence: 94%

Cerebrospinal monoamine metabolites and amino acid content in patients with parkinsonian syndrome and rats lesioned with MPP+

Espino¹,

Ambrosio

Bartrons

et al. 1994

J Neural Transm Gen Sect

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Monoamine metabolites and amino acid concentration in cerebrospinal fluid (CSF) of 33 untreated patients with parkinsonian syndrome, and 20 control patients without specific neurological symptoms have been compared with those obtained in cerebrospinal fluid of rats intrastriatally lesioned with 1-methyl-4-phenylpyridinium ion (MPP+) and sham operated animals. Homovanillic acid content was found to be significantly lower in patients with severe parkinsonism (motor score of UPDRS > 24), but not in patients with mild symptoms (motor score < or = 24). A correlation between the loss of striatal dopamine and the decrease in cerebrospinal homovanillic acid has been established in rats treated with MPP+. The extrapolation of these results to those obtained from human patients could be important in assessing the degree of striatal dopamine loss shown by humans with parkinsonian syndrome at the moment of clinical diagnosis. No significant differences were found between the other monoamine metabolites analyzed and free amino acid content in human and rat CSF.

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“…Usually, ~80-85% of Parkinsonism patients are found to have these typical features of idiopathic PD (IDP), whereas the remaining 15-20% patients belong to the other category of neurodegenerative disorders [29]. Some patients who are clinically diagnosed as having IPD with additional or atypical clinical features are currently classified as having Parkinsonism plus syndromes (PPS) [36]. It has been emphasized that several differences exist between typical IPD and PPS in the pattern of extrapyramidal features, pattern of onset of illness, and therapeutic responses [37].…”

Section: -Synuclein and Pdmentioning

confidence: 99%

α-Synuclein Misfolding and Neurodegenerative Diseases

Uversky

2008

CPPS

184

159

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Alpha-synuclein is an abundant presynaptic brain protein, misfolding, aggregation and fibrillation of which are implicated as critical factors in several neurodegenerative diseases. The list of the well-known synucleinopathies includes such devastating disorders as Parkinson's disease, Lewy body variant of Alzheimer's disease, diffuse Lewy body disease, dementia with Lewy bodies, multiple system atrophy, and neurodegeneration with brain iron accumulation type I. The precise functions of alpha-synuclein remain elusive, but there are evidence indicating its involvement in regulation vesicular release and/or turnover and synaptic function in the central nervous system. It might play a role in neuronal plasticity responses, bind fatty acids, regulate certain enzymes, transporters, and neurotransmitter vesicles, be involved in neuronal survival and even can act as a molecular chaperone. Structurally, alpha-synuclein is an illustrative member of the rapidly growing family of natively unfolded (or intrinsically disordered) proteins and considerable knowledge has been accumulated about its structural properties and conformational behavior. The molecular mechanisms underlying misfolding, aggregation and fibrillation of alpha-synuclein and the role of various environmental and genetic factors in stimulation and inhibition of these processes are relatively well understood. Here, the main structural features of alpha-synuclein, its functions, and involvement in various human diseases are summarized providing a foundation for better understanding of the biochemistry, biophysics and neuropathology of alpha-synuclein aggregation.

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Parkinsonism-plus syndromes

Cited by 58 publications

References 110 publications

Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population based study

Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population based study

Cerebrospinal monoamine metabolites and amino acid content in patients with parkinsonian syndrome and rats lesioned with MPP+

α-Synuclein Misfolding and Neurodegenerative Diseases

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Parkinsonism-plus syndromes

Cited by 58 publications

References 110 publications

Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population based study

Risk of incident Parkinson's disease and parkinsonism in essential tremor: a population based study

Cerebrospinal monoamine metabolites and amino acid content in patients with parkinsonian syndrome and rats lesioned with MPP+

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α-Synuclein Misfolding and Neurodegenerative Diseases