Browsing by Subject "Parkinson's disease"

Now showing 1 - 8 of 8
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    Apoptosis and autophagy in nigral neurons of patients with Parkinson's disease
    (Murcia : F. Hernández, 1997) Anglade, P.; Vyas, S.; Javoy-Agid, F.; Herrero Ezquerro, María Trinidad; Michel, P.P.; Marquez, J.; Mouatt-Prigent, A.; Ruberg, M.; Hirsch, E.C.; Agid, Y.
    Parkinson's disease (PD) is a neurodegenerative disorder characterized by progressive cell loss confined mostly to dopaminergic neurons of the substantia nigra. Several factors, including oxidative stress, and decreased activity of complex 1 mitochondrial respiratory chain, are involved in the degenerative process. Yet, the underlying mechanisms leading to dopaminergic cell loss remain elusive. Morphological assessrnent for different modes of cell death: apoptosis, necrosis or autophagic degeneration, can contribute significantly to the understanding of this neurona1 loss. Ultrastructural examination revealed characteristics of apoptosis and autophagic degeneration in melanized neurons of the substantia nigra in PD patients. The results suggest that even at the final stage of the disease, the dopaminergic neurons are undergoing active process of cell death.
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    Cardiac Changes in Parkinson’s Disease: Lessons from Clinical and Experimental Evidence
    (MDPI, 2021-12) Cuenca Bermejo, Lorena; Almela, Pilar; Navarro Zaragoza, Javier; Fernández Villalba, Emiliano; González Cuello, Ana María; Laorden, María Luisa; Herrero, María Trinidad; Enfermería
    Dysautonomia is a common non-motor symptom in Parkinson’s disease (PD). Most dysautonomic symptoms appear due to alterations in the peripheral nerves of the autonomic nervous system, including both the sympathetic and parasympathetic nervous systems. The degeneration of sympathetic nerve fibers and neurons leads to cardiovascular dysfunction, which is highly prevalent in PD patients. Cardiac alterations such as orthostatic hypotension, heart rate variability, modifications in cardiogram parameters and baroreflex dysfunction can appear in both the early and late stages of PD, worsening as the disease progresses. In PD patients it is generally found that parasympathetic activity is decreased, while sympathetic activity is increased. This situation gives rise to an imbalance of both tonicities which might, in turn, promote a higher risk of cardiac damage through tachycardia and vasoconstriction. Cardiovascular abnormalities can also appear as a side effect of PD treatment: L-DOPA can decrease blood pressure and aggravate orthostatic hypotension as a result of a negative inotropic effect on the heart. This unwanted side effect limits the therapeutic use of L-DOPA in geriatric patients with PD and can contribute to the number of hospital admissions. Therefore, it is essential to define the cardiac features related to PD for the monitorization of the heart condition in parkinsonian individuals. This information can allow the application of intervention strategies to improve the course of the disease and the proposition of new alternatives for its treatment to eliminate or reverse the motor and non-motor symptoms, especially in geriatric patients.
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    In situ architecture of neuronal α-Synuclein inclusions
    (Nature Research, ) Trinkaus, Victoria A.; Riera-Tur, Irene; Martínez Sánchez, Antonio; Bauerlein, Felix J.B.; Guo, Qiang; Arzberger, Thomas; Baumeister, Wolfgang; Dudanova, Irina; Hipp, Mark S.; Ulrich Hartl, F.; Fernández-Busnadiego, Rubén; Ingeniería de la Información y las Comunicaciones
    The molecular architecture of α-Synuclein (α-Syn) inclusions, pathognomonic of various neurodegenerative disorders, remains unclear. α-Syn inclusions were long thought to consist mainly of α-Syn fibrils, but recent reports pointed to intracellular membranes as the major inclusion component. Here, we use cryo-electron tomography (cryo-ET) to image neuronal α-Syn inclusions in situ at molecular resolution. We show that inclusions seeded by α-Syn aggregates produced recombinantly or purified from patient brain consist of α-Syn fibrils crisscrossing a variety of cellular organelles. Using gold-labeled seeds, we find that aggregate seeding is predominantly mediated by small α-Syn fibrils, from which cytoplasmic fibrils grow unidirectionally. Detailed analysis of membrane interactions revealed that α-Syn fibrils do not contact membranes directly, and that α-Syn does not drive membrane clustering. Altogether, we conclusively demonstrate that neuronal α-Syn inclusions consist of α-Syn fibrils intermixed with membranous organelles, and illuminate the mechanism of aggregate seeding and cellular interaction.
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    Induction system of neural and muscle lineage cells from bone marrow stromal cells; a new strategy for tissue reconstruction in degenerative diseases
    (Murcia : F. Hernández, 2009) Kitada, Masaaki; Dezawa, Mari
    Since bone marrow stromal cells (MSCs) are easily accessible both from healthy donors and patients, and can be expanded on a therapeutic scale, they have attracted attention for cell-based therapy. MSCs contribute to the protection of host tissue after transplantation by Immune modulation and trophic effect. They also have an ability to differentiate into other cell kinds that will replenish lost cells in the degenerated tissue. This review discusses the potential of MSCs for tissue reconstruction in neuro- and muscledegenerative diseases and their differentiation capacity into functional cells.
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    Investigación en enfermedades neurodegenerativas. Evitando la epidemia "silenciosa" del siglo XXI.
    (Murcia : Servicio de Publicaciones de la Universidad de Murcia, 2008) Herrero Ezquerro, María Trinidad; Departamentos y Servicios::Departamentos de la UMU::Anatomía Humana y Psicobiología
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    MiRNAs participate in the diagnosis, pathogenesis and therapy of Parkinson's disease
    (Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Lu, Xuexin; Cui, Zhijie; Liu, Shuang; Yin, Feng
    MicroRNAs (miRNAs), one kind of posttranscriptional modification, mediate transcriptional silencing of various metabolic enzymes that are involved in various life processes, including Parkinson’s disease. At present, the pathogenesis of Parkinson's disease is not clear, although many studies suggest that miRNAs play a very important role in the progress of Parkinsonism. This paper reviews the biological characteristics of miRNAs and summarizes the progress of miRNAs in reference to the diagnosis and pathogenesis of Parkinson’s disease. It even considers miRNAs as a potential target for Parkinson’s disease therapy
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    Pathological changes in dendrites of substantia nigra neurons in Parkinson's disease: a Golgi study
    (Murcia : F. Hernández, 1991) Patt, Stephan; Gertz, Hermann-Josef; Gerhard, Lieselotte; Cervós-Navarro, J.
    Neurons of the substantia nigra show severe morphological changes in Parkinson's disease. Pathological alterations of cell bodies have been described, whereas those of neuronal processes have hardly been investigated. Golgi impregnation has been the chosen method for demonstrating neuronal processes and dendritic and somatic spines. We therefore used the Golgi-Braitenberg method to qualitatively and semi-quantitatively study the substantia nigra of eight patients with Parkinson's disease compared with eight control cases. Golgi impregnation of substantia nigra neurons was good in al1 control cases. In full agreement with the analysis of Braak and Braak (1986) three neuronal types within the substantia nigra were found. In cases of Parkinson's disease, severe pathological changes such as decrease of dendritic length, loss of dendritic spines and severa1 types of dendritic varicosities were found only in the melanin-containing pars compacta neurons. Pars reticulata nerve cells were intact. These findings support the predominant role played by the dopaminergic efferent pathway in the degenerative process. The afferent pathway was not affected. This suggests that the substantia nigra lesion is primary in Parkinson's disease. Loss of neurons found in H & E sections corresponded to a lesser amount of impregnated pars compacta neurons in cases with Parkinson's disease when compared to controls. Evidences exist that the duration of the disease may be related to the extent of pathologically altered Golgi-impregnated pars compacta cells. The amount of Lewy bodies in H & E sections corresponded to the quantity of round varicosities in impregnated pars compacta neurons. These round dendritic varicosities were considered to be Lewy body inclusions. They seem to have no influence on the dendritic spine density and morphology in most cases.
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    The synergetic effect of edaravone and scutellarin in the MPP(+)-induced cell model of Parkinson's disease
    (Universidad de Murcia, Departamento Histología e Histopatología, 2025) Wei Wei; Wu Jing; Zhang Dandan; Xu Shoucheng; Wang Yi; Li Xuezhong; Yu Ming; Chen Xiaopeng; Biología Celular e Histología
    Parkinson's disease (PD) is a limb movement disorder caused by the degeneration of brain neurons and seriously affects the quality of life of the elderly. However, the current drugs are symptomatic treatments that cannot prevent or delay the development of the disease. Targeted therapy for pathogenesis may be the direction of development in the future. Oxidative stress and the inflammatory response are involved in the pathogenesis of PD. Edaravone and scutellarin have been studied in antioxidant and anti-inflammatory reactions. The focus of this study is whether there is synergy between the two and its mechanism. Through research, we found that edaravone and scutellarin at different dose combinations have synergistic effects in 1-methyl-4-phenylpyridinium (MPP+)-induced PC12 cells using the Chou-Talalay joint index method. According to the CompuSyn software calculation, the results showed that the combination index (CI) of the combined application of 15 μM edaravone and 15 μM scutellarin was the lowest, indicating that the synergistic effect was the best. Compared with the single drug, the synergy increased superoxide dismutase (SOD) and reduced glutathione (GSH) levels, reduced the levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and enhanced the anti-apoptosis ability in the MPP(+) induced cell model of PD.