Time course of nigrostriatal degeneration in parkinson's disease

1976 ◽  
Vol 38 (3-4) ◽  
pp. 277-301 ◽  
Author(s):  
P. Riederer ◽  
St. Wuketich
2003 ◽  
Vol 28 (3) ◽  
pp. 209-218 ◽  
Author(s):  
Wassilios Meissner ◽  
Caroline Prunier ◽  
Denis Guilloteau ◽  
Sylvie Chalon ◽  
Christian E. Gross ◽  
...  

2021 ◽  
pp. 1-11
Author(s):  
Karoline Knudsen ◽  
Tatyana D. Fedorova ◽  
Jacob Horsager ◽  
Katrine B. Andersen ◽  
Casper Skjærbæk ◽  
...  

Background: We have hypothesized that Parkinson’s disease (PD) comprises two subtypes. Brain-first, where pathogenic α-synuclein initially forms unilaterally in one hemisphere leading to asymmetric nigrostriatal degeneration, and body-first with initial enteric pathology, which spreads through overlapping vagal innervation leading to more symmetric brainstem involvement and hence more symmetric nigrostriatal degeneration. Isolated REM sleep behaviour disorder has been identified as a strong marker of the body-first type. Objective: To analyse striatal asymmetry in [18F]FDOPA PET and [123I]FP-CIT DaT SPECT data from iRBD patients, de novo PD patients with RBD (PD +RBD) and de novo PD patients without RBD (PD - RBD). These groups were defined as prodromal body-first, de novo body-first, and de novo brain-first, respectively. Methods: We included [18F]FDOPA PET scans from 21 iRBD patients, 11 de novo PD +RBD, 22 de novo PD - RBD, and 18 controls subjects. Also, [123I]FP-CIT DaT SPECT data from iRBD and de novo PD patients with unknown RBD status from the PPPMI dataset was analysed. Lowest putamen specific binding ratio and putamen asymmetry index (AI) was defined. Results: Nigrostriatal degeneration was significantly more symmetric in patients with RBD versus patients without RBD or with unknown RBD status in both FDOPA (p = 0.001) and DaT SPECT (p = 0.001) datasets. Conclusion: iRBD subjects and de novo PD +RBD patients present with significantly more symmetric nigrostriatal dopaminergic degeneration compared to de novo PD - RBD patients. The results support the hypothesis that body-first PD is characterized by more symmetric distribution most likely due to more symmetric propagation of pathogenic α-synuclein compared to brain-first PD.


Synapse ◽  
1999 ◽  
Vol 31 (2) ◽  
pp. 134-139 ◽  
Author(s):  
Sylvie Chalon ◽  
Patrick Emond ◽  
Sylvie Bodard ◽  
Marie-Paule Vilar ◽  
Cynthia Thiercelin ◽  
...  

1997 ◽  
Vol 12 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Ilan Ziv ◽  
Rina Zilkha-Falb ◽  
Daniel Offen ◽  
Anat Shirvan ◽  
Ari Barzilai ◽  
...  

2009 ◽  
Vol 25 (1) ◽  
pp. 25-39 ◽  
Author(s):  
CA Dodd ◽  
BG Klein

The pyrethroid insecticide permethrin and the organophosphate insecticide chlorpyrifos can experimentally produce Parkinson’s disease (PD)-associated changes in the dopaminergic nigrostriatal pathway, short of frank degeneration, although at doses considerably higher than from a likely environmental exposure. The ability of permethrin (200 mg/kg), chlorpyrifos (50 mg/kg), or combined permethrin + chlorpyrifos to facilitate nigrostriatal damage in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg/kg) C57BL/6 mouse model of PD was investigated in three separate experiments. Tyrosine hydroxylase (TH) and glial fibrillary acidic protein (GFAP) immunohistochemistry assessed nigrostriatal degeneration or nigrostriatal damage more subtle than frank degeneration. Four fields in the dorsolateral caudate-putamen were examined at two rostrocaudal locations. The dopaminergic neurotoxin MPTP decreased striatal TH immunopositive neuropil and increased GFAP immunopositive neuropil. Neither permethrin nor chlorpyrifos, alone or in combination, altered the effects of MPTP upon TH or GFAP immunostaining. Permethrin alone increased striatal GFAP immunopositive neuropil but not when combined with chlorpyrifos treatment. Therefore, combined administration of the two insecticides appeared to protect against an increase in a neuropathological indicator of striatal damage seen with permethrin treatment alone. Differences compared with analysis of entire striatum emphasize the value of varying the topographic focus used to assess nigrostriatal degeneration in studies of insecticides in PD.


2009 ◽  
Vol 152 (2) ◽  
pp. 195-200 ◽  
Author(s):  
Friederike Sixel-Döring ◽  
Claudia Trenkwalder ◽  
Christoph Kappus ◽  
Dieter Hellwig

1998 ◽  
Vol 245 (10) ◽  
pp. 659-664 ◽  
Author(s):  
T. Müller ◽  
Wilfried Kuhn ◽  
Thomas Büttner ◽  
Ernst Eising ◽  
H. Coenen ◽  
...  

2007 ◽  
Vol 13 (7) ◽  
pp. 438-442 ◽  
Author(s):  
Zoltan Keresztenyi ◽  
Peter Valkovič ◽  
Thomas Eggert ◽  
Ulrich Steude ◽  
Joachim Hermsdörfer ◽  
...  

2018 ◽  
Vol 79 (5-6) ◽  
pp. 281-286 ◽  
Author(s):  
Hisayoshi Oka ◽  
Atuso Nakahara ◽  
Tadashi Umehara

Introduction: Cardiovascular autonomic failure is commonly associated with Parkinson’s disease (PD), affecting the daily lives of patients. Rotigotine was recently reported not to influence cardiovascular autonomic responses in contrast to other dopaminergic drugs. The effect of rotigotine on daily blood pressure (BP) fluctuations might reflect autonomic failure in patients with PD. Methods: Twenty-five PD patients who were receiving rotigotine and 12 patients not receiving rotigotine were recruited. Systolic BP during the daytime and nighttime was measured by 24-h BP monitoring at an interval of 2 years. The patients were divided into 3 groups according to the BP fluctuation type: dippers (nocturnal fall in BP ≥10%), non-dippers (0–10%), and risers (< 0%). The time course of BP was compared between the patients given rotigotine and those not given rotigotine. Results: Among the 25 patients who received rotigotine, the BP type worsened in 2 patients, was unchanged in 16 patients, and improved in 7 patients. Among the 12 patients who were not receiving rotigotine, the BP type worsened in 5 patients, was unchanged in 4 patients, and improved only in 3 patients (p = 0.042). Conclusion: Rotigotine improves the abnormal circadian rhythm of BP in patients with PD. Rotigotine was suggested to have favorable effects on cardiovascular autonomic responses and circadian rhythm in patients with PD.


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