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PD Progression (pd + progression)
Selected AbstractsAsymmetrical lateral ventricular enlargement in Parkinson's diseaseEUROPEAN JOURNAL OF NEUROLOGY, Issue 4 2009M. M. Lewis Background:, A recent case report suggested the presence of asymmetrical lateral ventricular enlargement associated with motor asymmetry in Parkinson's disease (PD). The current study explored these associations further. Methods:, Magnetic resonance imaging (3T) scans were obtained on 17 PD and 15 healthy control subjects at baseline and 12,43 months later. Baseline and longitudinal lateral ventricular volumetric changes were compared between contralateral and ipsilateral ventricles in PD subjects relative to symptom onset side and in controls relative to their dominant hand. Correlations between changes in ventricular volume and United Parkinson's disease rating scale motor scores (UPDRS-III) whilst on medication were determined. Results:, The lateral ventricle contralateral to symptom onset side displayed a faster rate of enlargement compared to the ipsilateral (P = 0.004) in PD subjects, with no such asymmetry detected (P = 0.312) in controls. There was a positive correlation between ventricular enlargement and worsening motor function assessed by UPDRS-III scores (r = 0.96, P < 0.001). Discussion:, There is asymmetrical lateral ventricular enlargement that is associated with PD motor asymmetry and progression. Further studies are warranted to investigate the underlying mechanism(s), as well as the potential of using volumetric measurements as a marker for PD progression. [source] PPAR-gamma-mediated neuroprotection in a chronic mouse model of Parkinson's diseaseEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2009Nicoletta Schintu Abstract Rosiglitazone is a commonly prescribed insulin-sensitizing drug with a selective agonistic activity on the peroxisome proliferator-activated receptor-gamma (PPAR-,). PPAR-, can modulate inflammatory responses in the brain, and agonists might be beneficial in neurodegenerative diseases. In the present study we used a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine plus probenecid (MPTPp) mouse model of progressive Parkinson's disease (PD) to assess the therapeutic efficacy of rosiglitazone on behavioural impairment, neurodegeneration and inflammation. Mice chronically treated with MPTPp displayed typical features of PD, including impairment of motor and olfactory functions associated with partial loss of tyrosine hydroxylase (TH)-positive neurons in the substantia nigra pars compacta (SNc), decrease of dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC) content and dynorphin (Dyn) mRNA levels in the caudate-putamen (CPu), intense microglial and astroglial response in the SNc and CPu. Chronic rosiglitazone, administered in association with MPTPp, completely prevented motor and olfactory dysfunctions and loss of TH-positive cells in the SNc. In the CPu, loss of striatal DA was partially prevented, whereas decreases in DOPAC content and Dyn were fully counteracted. Moreover, rosiglitazone completely inhibited microglia reactivity in SNc and CPu, as measured by CD11b immunostaining, and partially inhibited astroglial response assessed by glial fibrillary acidic protein immunoreactivity. Measurement of striatal MPP+ levels 2, 4, 6 h and 3 days after chronic treatment indicated that MPTP metabolism was not altered by rosiglitazone. The results support the use of PPAR-, agonists as a putative anti-inflammatory therapy aimed at arresting PD progression, and suggest that assessment in PD clinical trials is warranted. [source] Periodontal attachment loss over 14 years in cleft lip, alveolus and palate (CLAP, CL, CP) subjects not enrolled in a supportive periodontal therapy programJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 9 2003Giovanni E. Salvi Abstract Objectives: (i) To assess the overall and (ii) cleft-associated rate of periodontal disease (PD) progression in subjects with cleft lip, alveolus and palate (CLAP) and (iii) to compare these rates with those of subjects with cleft lip (CL) and cleft palate (CP). Material and methods: Twenty-six subjects not enrolled in a supportive periodontal therapy (SPT) program were examined in 1979, 1987 and 1993. PD progression was assessed as increase in pocket probing depth (PPD in mm) and probing attachment loss (PAL in mm). Results: Extensive plaque accumulation and high frequencies of gingival units bleeding on probing were observed at all three examinations. A statistically significant increase in mean PPD of 0.57±0.21 mm (SD) in both groups as well as a statistically significant loss of PAL of 1.85±0.23 mm (SD) in the CLAP group and of 1.72±0.21 mm (SD) in the CL/CP group occurred over the observation period (p<0.05). In subjects with CLAP, statistically significant increases in PPD and loss of PAL were recorded over time at sites adjacent to the cleft as well as at control sites (p<0.05). Over 14 years, however, PPD increased 1.72±1.08 mm (SD) at cleft sites versus 0.72±1.14 mm (SD) at control sites (p<0.05), and PAL amounted to 3.19±1.35 mm (SD) at cleft sites versus 2.41±1.52 mm (SD) at control sites (p<0.05). Conclusion: Both the CLAP and the CL/CP subjects are at high risk for PD progression if no SPT program is provided. This also suggests that alveolar cleft sites in subjects with high plaque and gingival inflammation scores underwent more periodontal tissue destruction than control sites over a 14-year period. Zusammenfassung Ziele: 1. Beurteilung der gesamten und 2. der mit der Spalte assoziierten Progressionsrate der Parodontalerkrankung (PD) bei Patienten mit Lippen-Kiefer-Gaumenspalten (CLAP) und 3. der Vergleich dieser Progressionsraten mit denen von Patienten mit Lippenspalten (CL) sowie Gaumenspalten (CP). Material und Methoden: 26 Patienten, die nicht an einem SPT-Programm teilnahmen wurden in 1979, 1987 und 1993 untersucht. Die PD-Progression wurde über die Zunahme der Sondierungstiefe (PPD in mm) und den klinischen Attachmentverlust (PAL in mm) beurteilt. Ergebnisse: Bei allen drei Untersuchungszeitpunkten wurde eine ausgedehnte Plaqueakkumulation und eine große Häufigkeit von Gingivabereichen, die bei Sondierung bluteten beobachtet. Während der Beobachtungsperiode fand in beiden Gruppen ein statistisch signifikanter Anstieg der mittleren PPD von 0.57±0.21 mm (SD) als auch ein statistisch signifikanter Attachmentverlust von 1.85±0.23 mm (SD) in der CLAP-Gruppe sowie von 1.72±0.21 mm (SD) in der CL/CP-Gruppe statt (p<0.05). Bei den Patienten mit CLAP wurde im Laufe der Zeit sowohl an den Parodontien neben der Spalte als auch an den Kontrollstellen (p<0.05) ein statistisch signifikanter Anstieg der PPD und Attachmentverlust registriert. Während der 14 Jahre jedoch nahm die PPD an Stellen mit Spalte um 1.72±1.08 mm (SD) zu im Gegensatz zu den Kontrollstellen (p<0.05) wo dieser Wert 0.72±1.14 mm (SD) betrug. Für den Attachmentverlust lag dieser Wert bei 3.19±1.35 mm (SD) an den Stellen mit Spalte im Gegensatz zu den Kontrollstellen (p<0.05) mit 2.41±1.52 mm (SD). Schlussfolgerung: Wenn keine parodontale Erhaltungstherapie zur Verfügung gestellt wird haben beide Personen, die mit CLAP und die mit CL/CP ein hohes Risiko hinsichtlich der Parodontitisprogression. Dies läßt annehmen, dass bei Personen mit viel Plaque und ausgeprägter Entzündung der Gingiva, die Stellen mit Kieferspalten während einer 14-jährigen Zeitperiode eine stärkere Zerstörung der parodontalen Gewebe erfahren als die Kontrollstellen. Résumé Les buts de cette étude ont été de suivre la progression du taux de la maladie parodontale associée au bec de lièvre (CLAP) et de comparer ces taux avec ceux de sujets ayant lèvre fendue (CL) et palais fendu (CP). Vingt-six sujets non-soumis à un programme parodontal de maintien (SPT) ont été examinés en 1979, 1987 et 1993. La progression PD a été enregistrée telle une augmentation de la profondeur au sondage (PPD en mm) et une perte d'attache au sondage (PAL en mm). Une énorme accumulation de plaque dentaire et de très hautes fréquences dans les nombres d'unités gingivales avec saignement au sondage ont été observées lors des trois examens. Une augmentation statistiquement significative dans la moyenne PPD de 0.57±0.21 mm (SD) dans les deux groupes ainsi qu'une perte significative de PAL de 1.85±0.23 mm (SD) dans le groupe CLAP et de 1.72±0.21 mm (SD) dans le groupe CL/CP apparaîssaient durant cette période d'observation (p<0.05). Chez les sujets avec CLAP, les augmentations statistiquement significatives de PPD et la perte de PAL ont été enregistrées avec le temps sur les sites adjacents au bec de lièvre ainsi qu'au niveau des sites contrôles (p<0.05). Sur les quatorze années, cependant, PPD augmentait de 1.72±1.08 mm (SD) au niveau des sites bec de lièvre vs 0.72±1.14 mm (SD) au niveau des contrôles (p<0.05), et PAL s'élevait à 3.19±1.35 mm (SD) au niveau des sites bec de lièvre vs 2.41±1.52 mm au niveau des contrôles (p<0.05). Tant les sujets CLAP que les CL/CP étaient à haut risque pour la progression PD si un programme SPT n'était pas suivi. Ceci suggère également que les sites alvéolaires associés au bec de lièvre avec des scores de plaque et de gingivite importants s'accompagnaient de plus de destruction que les sites contrôles sur une période de quatorze années. [source] A double-blind, placebo-controlled study to assess the mitochondria-targeted antioxidant MitoQ as a disease-modifying therapy in Parkinson's diseaseMOVEMENT DISORDERS, Issue 11 2010Barry J. Snow MD Abstract Multiple lines of evidence point to mitochondrial oxidative stress as a potential pathogenic cause for Parkinson's disease (PD). MitoQ is a powerful mitochondrial antioxidant. It is absorbed orally and concentrates within mitochondria where it has been shown to protect against oxidative damage. We enrolled 128 newly diagnosed untreated patients with PD in a double-blind study of two doses of MitoQ compared with placebo to explore the hypothesis that, over 12 months, MitoQ would slow the progression of PD as measured by clinical scores, particularly the Unified Parkinson Disease Rating Scale. We showed no difference between MitoQ and placebo on any measure of PD progression. MitoQ does not slow the progression of PD, and this finding should be taken into account when considering the oxidative stress hypothesis for the pathogenesis of PD. © 2010 Movement Disorder Society [source] Uric acid in Parkinson's diseaseMOVEMENT DISORDERS, Issue 12 2008Ilana Schlesinger MD Abstract Recent studies have provided evidence that uric acid may play a role in the development and progression of Parkinson's disease (PD). Uric acid is a natural antioxidant that may reduce oxidative stress, a mechanism thought to play a role in the pathogenesis of PD. Higher levels of serum urate (SU) may have a neuroprotective effect. High SU levels reduced the risk of developing PD and correlated with slower PD progression. Among PD patients SU levels were lower as compared with controls. The manipulation of SU levels holds promise in the treatment of PD. It is possible that a high purine diet in patients with PD may slow progression of the disease. Milk and meat consumption as well as exercise modify the risk of developing PD possibly through their influence on SU levels. In this article, we review the association between PD and SU levels and its implication on the management of PD. © 2008 Movement Disorder Society [source] Biomarkers for Parkison's disease: Tools to assess Parkinson's disease onset and progression,ANNALS OF NEUROLOGY, Issue S2 2008Kenneth Marek MD Reliable and well-validated biomarkers for PD to identify individuals "at risk" before motor symptoms, accurately diagnose individuals at the threshold of clinical PD, and monitor PD progression throughout its course would dramatically accelerate research into both PD cause and therapeutics. Biomarkers offer the potential to provide a window onto disease mechanism, potentially generating therapeutic targets for disease. In particular, biomarkers enable investigation of the premotor period of PD before typical symptoms are manifest, but while degeneration has already begun. Given the multiple genetic causes for PD already identified, the marked variability in the loss of dopaminergic markers measured by imaging at motor symptom onset and the clear heterogeneity of clinical symptoms in PD onset and clinical progression, it is likely many biomarkers with a focus ranging from clinical symptoms to PD pathobiology to molecular genetic mechanisms will be necessary to fully map PD risk and progression. Biomarkers are also critical in new drug development for PD, both in early validation studies to assess drug dosing and to determine drug penetrance into the brain, and in later efficacy studies to complement PD clinical outcomes. During the past two decades, much progress has been made in identifying and assessing PD biomarkers, but as yet, no fully validated biomarker for PD is currently available. Nonetheless, there is increasing evidence that molecular genetics, focused -omic (proteomic, metabolomic, and transcriptomic) assessment of blood and cerebrospinal fluid, and advanced in vivo brain imaging will provide critical clues to assist in the diagnosis and medical management of PD patients. Ann Neurol 2008;64 (suppl):S111,S121 [source] | ||||||||||