The aim of this study was to investigate whether exercise could improve motor behavioral deficits and alter expression of glial fibrillary acidic protein (GFAP) in dorsal striatum in a 6-hydroxydopamine (6-OHDA) rat model of Parkinson’s disease (PD). To this end, animals were randomly divided into 4 groups: sham sedentary (SS, n = 7); sham trained (ST, n=8); lesioned sedentary (LS, n=8) and lesioned trained (LT, n = 8). Rats were unilaterally lesioned with 6-OHDA (10 μg/3 μg) injected into the left medial forebrain bundle and sham groups were only injected with vehicle solution. The treadmill training protocol consisted of running with progressive increase in velocity, 5 days/week, during 4 weeks. Behavioral tasks were applied to asses the motor abilities of all animals prior to 6-OHDA injection and at 8th and 29th days post-injection. The tyrosine hydroxylase (TH - in substantia nigra pars compacta) and GFAP (in dorsal striatum) immunostaining was evaluated by semiquantitative analysis of the intensity (optical density - OD). The 6-OHDA lesion decreased the OD of TH and increased the OD of GFAP. In addition, the 6-OHDA lesion increased the number of ipsilateral rotations induced by methylphenidate (40 mg/kg, i.p., 30 min) and caused motor behavioral deficits. On the other hand, the treadmill training resulted in an increase in maximal exercise capacity in both trained groups (ST and LT). The training was able to reduce the number of ipsilateral rotations and ameliorated the motor behavioral deficits on 8th and 29th days postlesion. Interestingly, the exercise led to a significant increase in OD of GFAP in the LT group while there was no such effect in ST group. Our results indicate that treadmill training can improve motor behavioral deficits and suggest that the effects of exercise may be directly or, indirectly, mediated by astrocytes, as an increase in GFAP was observed in the dorsal striatum. Nevertheless, these are the first data showing an increase in GFAP expression post-exercise in this model and further research is needed to determine the precise action of exercise on astrocytes in Parkinson’s disease.

The aim of this study was to investigate whether exercise could improve motor behavioral deficits and alter expression of glial fibrillary acidic protein (GFAP) in dorsal striatum in a 6-hydroxydopamine (6-OHDA) rat model of Parkinson’s disease (PD). To this end, animals were randomly divided into 4 groups: sham sedentary (SS, n = 7); sham trained (ST, n=8); lesioned sedentary (LS, n=8) and lesioned trained (LT, n = 8). Rats were unilaterally lesioned with 6-OHDA (10 μg/3 μg) injected into the left medial forebrain bundle and sham groups were only injected with vehicle solution. The treadmill training protocol consisted of running with progressive increase in velocity, 5 days/week, during 4 weeks. Behavioral tasks were applied to asses the motor abilities of all animals prior to 6-OHDA injection and at 8th and 29th days post-injection. The tyrosine hydroxylase (TH - in substantia nigra pars compacta) and GFAP (in dorsal striatum) immunostaining was evaluated by semiquantitative analysis of the intensity (optical density - OD). The 6-OHDA lesion decreased the OD of TH and increased the OD of GFAP. In addition, the 6-OHDA lesion increased the number of ipsilateral rotations induced by methylphenidate (40 mg/kg, i.p., 30 min) and caused motor behavioral deficits. On the other hand, the treadmill training resulted in an increase in maximal exercise capacity in both trained groups (ST and LT). The training was able to reduce the number of ipsilateral rotations and ameliorated the motor behavioral deficits on 8th and 29th days postlesion. Interestingly, the exercise led to a significant increase in OD of GFAP in the LT group while there was no such effect in ST group. Our results indicate that treadmill training can improve motor behavioral deficits and suggest that the effects of exercise may be directly or, indirectly, mediated by astrocytes, as an increase in GFAP was observed in the dorsal striatum. Nevertheless, these are the first data showing an increase in GFAP expression post-exercise in this model and further research is needed to determine the precise action of exercise on astrocytes in Parkinson’s disease.

Made available in DSpace on 2014-06-11T19:22:52Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-12-13Bitstream added on 2014-06-13T19:08:24Z : No. of bitstreams: 1 caetano_mjd_me_rcla.pdf: 817407 bytes, checksum: f99f3e12cec3f7e3ecd3ea982d13c044 (MD5) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Andar é essencial para o desempenho das funções diárias. No entanto, as alterações morfofuncionais decorrentes do processo de envelhecimento podem comprometer o equilíbrio durante o andar e gerar instabilidade. Este comprometimento é ainda mais acentuado em idosos com doença de Parkinson devido aos distúrbios motores ocasionados pela doença. Neste contexto, os objetivos do presente estudo foram: 1) analisar as características espaço-temporais e os ângulos articulares de indivíduos idosos neurologicamente sadios e com doença de Parkinson idiopática andando livremente e em condições de restrição na largura e na altura da superfície de suporte; 2) relacionar estes parâmetros com as pontuações nas escalas de H&Y e UPDRS (apenas para os pacientes) e com a incidência de queda recente (1 ano) e pontuações na Escala de Equilíbrio Funcional de Berg (para ambos os grupos). Participaram 16 idosos distribuídos em dois grupos: oito idosos neurologicamente sadios e oito com doença de Parkinson idiopática. As características espaço-temporais e os ângulos articulares andando livremente e em condições de restrição na largura e na altura da superfície de suporte foram investigados por meio de ferramenta cinemática. Pacientes com doença de Parkinson apresentaram valores médios significativamente menores que os idosos neurologicamente sadios em relação à duração da fase de balanço e ao comprimento e velocidade da passada e maiores para a duração do duplo suporte devido à hipocinesia, à dificuldade no controle do equilíbrio e ao próprio relacionamento entre as variáveis. As restrições impostas pela superfície de suporte geraram alterações nas características espaço-temporais e angulares do andar dos idosos de ambos os grupos, devido à necessidade de adotar uma estratégia cautelosa que facilite o controle da locomoção, garantindo estabilidade, e ao medo de cair imposto pelas demandas da tarefa,... / Walking is crucial for the performance of daily living activities. However, morpho and functional changes due to the aging process can compromise the balance during walking and generate instability. It is more pronounced in elderly patients with Parkinson’s disease due to the motor signs/symptoms of the disease. In this context, the aims of this study were: 1) to analyze the spatial and temporal parameters and joint angles of healthy elderly and with Parkinson’s disease during free walking and under width and height constraints of the support surface; 2) to correlate these parameters with the scores in H&Y scale and UPDRS (only for patients) and with the occurrence of recent fall (1 year) and the scores in the Berg Functional Balance Scale (for both groups). Sixteen elderly were distributed in two groups: 8 healthy elderly and 8 idiopathic Parkinson’s disease patients. Both the spatial and temporal parameters of gait and joint angles were investigated by means of kinematics tools during free walking and under width and height constraints of the support surface. Parkinson’s disease patients showed significantly lower mean values than healthy elderly for swing phase duration, stride length and stride velocity, and higher double support duration due to the hipokinesia, the difficulty in balance control, and the relationship among the gait variables. The support surface constraints changed the gait spatial and temporal parameters and joint angles in both groups due to the necessity to perform a cautious walking strategy that can facilitate the locomotor control, preventing instability, and the fear of falling enforced by the task demands, specially when width and height constraints were associated. The scores in H&Y and UPDRS were not correlated to the gait parameters of the Parkinson’s disease patients probably because the scales did not reflect the gait performance of patients under medication. There were a relationship among the gait .

The aim of this study was to investigate whether exercise could improve motor behavioral deficits and alter expression of glial fibrillary acidic protein (GFAP) in dorsal striatum in a 6-hydroxydopamine (6-OHDA) rat model of Parkinson’s disease (PD). To this end, animals were randomly divided into 4 groups: sham sedentary (SS, n = 7); sham trained (ST, n=8); lesioned sedentary (LS, n=8) and lesioned trained (LT, n = 8). Rats were unilaterally lesioned with 6-OHDA (10 μg/3 μg) injected into the left medial forebrain bundle and sham groups were only injected with vehicle solution. The treadmill training protocol consisted of running with progressive increase in velocity, 5 days/week, during 4 weeks. Behavioral tasks were applied to asses the motor abilities of all animals prior to 6-OHDA injection and at 8th and 29th days post-injection. The tyrosine hydroxylase (TH - in substantia nigra pars compacta) and GFAP (in dorsal striatum) immunostaining was evaluated by semiquantitative analysis of the intensity (optical density - OD). The 6-OHDA lesion decreased the OD of TH and increased the OD of GFAP. In addition, the 6-OHDA lesion increased the number of ipsilateral rotations induced by methylphenidate (40 mg/kg, i.p., 30 min) and caused motor behavioral deficits. On the other hand, the treadmill training resulted in an increase in maximal exercise capacity in both trained groups (ST and LT). The training was able to reduce the number of ipsilateral rotations and ameliorated the motor behavioral deficits on 8th and 29th days postlesion. Interestingly, the exercise led to a significant increase in OD of GFAP in the LT group while there was no such effect in ST group. Our results indicate that treadmill training can improve motor behavioral deficits and suggest that the effects of exercise may be directly or, indirectly, mediated by astrocytes, as an increase in GFAP was observed in the dorsal striatum. Nevertheless, these are the first data showing an increase in GFAP expression post-exercise in this model and further research is needed to determine the precise action of exercise on astrocytes in Parkinson’s disease.

Bakgrund: Parkinsons sjukdom är en kronisk progredierande neurodegenerativ sjukdom och är den näst största i dess slag. Sjukdomen kan ge uttryck i både motoriska och icke-motoriska symtom. Genom sjukdomsförloppet genomgår personen olika faser som medför förlust av både mentala och kroppsliga funktioner. Förlusten av funktionerna ger en generellt sämre livskvalitet än hos andra personer. Syfte: Syftet med litteraturöversikten var att belysa symtomens påverkan på livskvaliteten hos personer med Parkinsons sjukdom. Metod: En allmän litteraturstudie baserad på tio kvalitativa studier. Resultat: Resultatet visar på att personer som lever med Parkinsons sjukdom har en komplex livssituation. De fysiska symtom som sjukdomen kännetecknas av ger svårigheter i vardagen. Resultatet visar också att den psykiska hälsan blir väsentligt påverkad i samband med detta. En följd av de fysiska och psykiska symtomen kan leda till social isolering, och tillsammans kan dessa skapa en kedjereaktion som leder till en försämrad livskvalitet. Slutsats och förslag på forskning: De motoriska symtomen är det mest påfrestande med att leva med Parkinsons sjukdom och bidrar starkt till en minskad livskvalitet. Därför behövs vidare omvårdnadsforskning för personer med Parkinsons sjukdom samt vilka omvårdnadsåtgärder som skulle kunna leda till förbättrad livskvalitet. / Background: Parkinson's disease is a chronic progressive neurodegenerative disease and is the second largest of its kind. The disease expresses both motor and non-motor symptoms. Through the course of the disease, the person undergoes different phases that cause loss of both mental and physical functions. The loss of functions gives a generally poorer quality of life than other people. Aim: The aim of the literature review was to highlight the effects of the symptoms on quality of life for people with Parkinson's disease. Method: A general literature study based on ten qualitative studies. Result: The result shows that people who are living with Parkinson's disease, lives in a complex life situation. The physical symptoms that the disease is characterized by creates difficulties in everyday life. The result also shows that mental health is significantly affected in this regard. A consequence of the physical and mental symptoms can lead to social isolation, and together they can create a chain reaction that leads to a deteriorating quality of life. Conclusion and Suggestions for Research: The motor symptoms are the most profound of living with Parkinson's disease and contribute significantly to a reduced quality of life. Therefore, nursing research is needed for people with Parkinson's disease as well as nursing measures that could lead to improved quality of life.

La maladie de Parkinson (MP) est caractérisée par une perte dopaminergique dans le striatum, structure sous-corticale impliquée dans le contrôle moteur, la mémoire et les comportements émotionnels. Les interneurones cholinergiques (ChIs) striataux jouent un rôle clef dans cette réorganisation pathologique du striatum en modulant l’activité des neurones de projection striataux (MSNs). Ce travail vise à étudier l’implication des ChIs et des récepteurs muscariniques (mAChRs) dans les mécanismes qui sous-tendent l’expression des déficits moteurs, cognitifs et émotionnels dans différents modèles de la MP chez la souris. L’inhibition optogénétique des ChIs réduit les déficits moteurs (akinésie, asymétrie posturale, déficit sensori-moteur). Les enregistrements électrophysiologiques montrent que l’inhibition des ChIs réduit l’excitabilité des MSNs et rétablit l’équilibre d’activité des deux voies de sortie striatale. Ces effets antiparkinsoniens sont reproduits par le blocage pharmacologique striatal des mAChRs M1 et M4. Ils sont dus à une action préférentielle de l’ACh sur les mAChRs au niveau des MSNs à l’origine de la voie striatonigrale puisqu’ils disparaissent chez des souris invalidées pour les récepteurs M4 exprimés dans ces neurones. La photoinhibition des ChIs réduit les déficits mnésiques et l’anxiété. L’antagoniste des mAChRs M1 réduit l’anxiété mais est inefficace sur les déficits mnésiques, suggérant que d’autres récepteurs cholinergiques striataux puissent être engagés dans les fonctions mnésiques. L’ensemble de nos résultats apporte un éclairage nouveau sur l’implication des ChIs striataux dans le fonctionnement physiologique et pathologique du striatum. / Parkinson’s disease (PD) is characterized by a dopamiergic loss into the striatum, a subcortical structure involved in motor control, memory and emotional behaviors. Striatal cholinergic interneurons (ChIs) play a key role in this pathological reorganization of the striatal circuitry by modulating striatal projection neurons (MSNs). This study aims to investigate the involvement of ChIs and muscarinic receptors (mAChRs) in the mechanisms underlying the expression of motor, cognitive and emotional deficits observed in different models of PD in mice. ChIs optogenetic inhibition reduced motor deficits (akinesia, postural asymmetry, sensorimotor deficit). Electrophysiological recordings show that ChIs photoinhibition reduces MSNs excitability and restores the balance between the two striatal output pathways. These antiparkinsonian effects are reproduced by pharmacological intrastriatal blockade of M1 and M4 mAChRs. They are due to a preferential action of ACh on mAChRs expressed on striatonigral MSNs since the deficits disappear in mutant mice that lack M4 mAChRs only in these neurons. ChIs photoinhibition also reduces memory deficits and anxiety. M1 mAChRs antagonist reduces anxiety but is inefficient on memory deficits, suggesting that other cholinergic receptors might be involved in striatal memory functions. Overall, these results give new insights on the role of cholinergic interneurons in the normal and pathological functioning of the striatum.

Background: In Parkinson’s disease (PD), alpha-synuclein accumulation in cutaneous autonomic pilomotor and sudomotor nerve fibers has been linked to autonomic nervous system disturbances even in the early stages of the disease. This study aims to assess the association between alpha-synuclein-mediated structural autonomic nerve fiber damage and function in PD, elucidate the role of neuropathy progression during the early disease stages, and test reproducibility and external validity of pilomotor function assessment using quantitative pilomotor axon-reflex test and sudomotor function via quantitative direct and indirect test of sudomotor function. Methods/design: A prospective controlled study will be conducted at four study sites in Europe and the USA. Fifty-two male and female patients with idiopathic PD (Hoehn and Yahr 1–2) and 52 age- and sex-matched healthy controls will be recruited. Axon-reflex-mediated pilomotor erection will be induced by iontophoresis of phenylephrine on the dorsal forearm. Silicone impressions of the response will be obtained, scanned, and quantified for pilomotor muscle impressions by number, impression size, and area of axon-reflex spread. Axon-reflex-mediated sweating following acetylcholine iontophoresis will be quantified for number and size of droplets and axon-reflex spread. Sympathetic skin responses, autonomic and motor symptoms will be evaluated. Tests will be performed at baseline, after 2 weeks, 1, 2, and 3 years. Skin biopsies will be obtained at baseline and after 3 years and will be analyzed for nerve fiber density and alpha-synuclein accumulation. Discussion: We anticipate that progression of autonomic nerve dysfunction assessed via pilomotor and sudomotor axon-reflex tests is related to progression of autonomic symptom severity and alpha-synuclein deposition. Potential applications of the techniques include interventional studies evaluating disease-modifying approaches and clinical assessment of autonomic dysfunction in patients with PD.

No description available.

Background/Aims: The diagnostic value of olfactory testing for the discrimination of tremor-dominant Parkinson’s disease (PD) from other tremor disorders remains enigmatic. We evaluated whether olfactory testing can accurately detect PD in tremor patients. Methods: A retrospective analysis of 299 consecutive subjects referred for the differential diagnosis of a tremor disorder was done. Olfactory testing was performed using ‘Sniffin’ Sticks’, resulting in a composite TDI score of odor threshold (T), discrimination (D), and identification (I). Receiver operating curve (ROC) plots were used to calculate sensitivity/specificity for the detection of PD. Results: Of all subjects, 167 (55.9%) had PD and 85 (28.4%) had essential tremor (ET). The mean TDI score in PD was significantly reduced compared to those in ET and other tremor disorders with no differences between ET and other tremor disorders. ROC analysis revealed strong correlations of TDI scores with PD [area under the curve: 0.85 (95% CI: 0.80–0.89); p < 0.001]. The highest Youden index was observed for a TDI score <25 (Youden index: 0.58). Using this cutoff score and that generated from normative data of healthy controls, the TDI score provided high sensitivity (negative predictive value) and specificity (positive predictive value) of approximately 80% for detecting PD. Conclusion: Olfactory testing is a useful, easily applied and inexpensive diagnostic test which is helpful to detect PD among tremor patients.

Background: Epidemiological data on the prevalence of Parkinson’s disease (PD) in Germany are limited. The aims of this study were to estimate the age- and gender-specific prevalence of PD in Germany as well as the severity and illness duration. Summary: A systematic literature search was performed in 5 different databases. European studies were included if they reported age- and gender-specific numbers of prevalence rates of PD. Meta-analytic approaches were applied to derive age- and gender-specific pooled prevalence estimates. Data of 4 German outpatient samples were incorporated to calculate the proportion of patients with PD in Germany grouped by Hoehn and Yahr (HY) stages and disease duration. In the German population, 178,169 cases of PD were estimated (prevalence: 217.22/100,000). The estimated relative illness duration was 40% with less than 5 years, 31% with 5–9 years, and 29% with more than 9 years. The proportions for different HY stages were estimated at 13% (I), 30% (II), 35% (III), 17% (IV), and 4% (V), respectively. Key Message: We provide an up-to-date estimation of age and gender-specific as well as severity-based prevalence figures for PD in Germany. Further community studies are needed to estimate population-based severity distributions and distributions of non-motor symptoms in PD.