Clinical and Pathological Features of Parkinson’s Disease

2014 ◽  
pp. 205-220 ◽  
Author(s):  
Susanne A. Schneider ◽  
Jose A. Obeso
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Pathological Features ◽  
Clinical And Pathological Features

scholarly journals TGF-β/Smad3 Signalling Modulates GABA Neurotransmission: Implications in Parkinson’s Disease

2020 ◽  
Vol 21 (2) ◽  
pp. 590 ◽  
Author(s):  
Mª Muñoz ◽  
Nerea de la Fuente ◽  
Amelia Sánchez-Capelo
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Basal Ganglia ◽  
Side Effects ◽  
Pathological Features ◽  
Therapeutic Approaches ◽  
Brain Nuclei ◽  
Dopaminergic Neurodegeneration ◽  
Cognitive Alterations ◽  
Gaba Neurotransmission

γ-Aminobutiryc acid (GABA) is found extensively in different brain nuclei, including parts involved in Parkinson’s disease (PD), such as the basal ganglia and hippocampus. In PD and in different models of the disorder, an increase in GABA neurotransmission is observed and may promote bradykinesia or L-Dopa-induced side-effects. In addition, proteins involved in GABAA receptor (GABAAR) trafficking, such as GABARAP, Trak1 or PAELR, may participate in the aetiology of the disease. TGF-β/Smad3 signalling has been associated with several pathological features of PD, such as dopaminergic neurodegeneration; reduction of dopaminergic axons and dendrites; and α-synuclein aggregation. Moreover, TGF-β/Smad3 intracellular signalling was recently shown to modulate GABA neurotransmission in the context of parkinsonism and cognitive alterations. This review provides a summary of GABA neurotransmission and TGF-β signalling; their implications in PD; and the regulation of GABA neurotransmission by TGF-β/Smad3. There appear to be new possibilities to develop therapeutic approaches for the treatment of PD using GABA modulators.

P3-167 Specific association of small heat shock proteins with the pathological features of Alzheimer's and Parkinson's disease brains

2004 ◽  
Vol 25 ◽  
pp. S403
Author(s):  
Micha M. Wilhelmus ◽  
Irene Otte-Höller ◽  
Rob A.I. de Vos ◽  
Ernst Jansen Steur ◽  
Pieter Wesseling ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Small Heat Shock Proteins ◽  
Pathological Features ◽  
Specific Association ◽  
Shock Proteins

scholarly journals Pathological features of cerebral cortical capillaries are doubled in Alzheimer's disease and Parkinson's disease

2000 ◽  
Vol 100 (4) ◽  
pp. 395-402 ◽  
Author(s):  
E. Farkas ◽  
G. I. De Jong ◽  
R. A. I. de Vos ◽  
E. N. H. Jansen Steur ◽  
P. G. M. Luiten
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Pathological Features ◽  
Cortical Capillaries

scholarly journals Human α-synuclein overexpression in a mouse model of Parkinson’s disease leads to vascular pathology, blood brain barrier leakage and pericyte activation

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Osama Elabi ◽  
Abderahim Gaceb ◽  
Robert Carlsson ◽  
Thomas Padel ◽  
Rana Soylu-Kucharz ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mouse Model ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Vascular Pathology ◽  
Motor Deficit ◽  
Pathological Features ◽  
Vessel Morphology ◽  
Blood Brain

AbstractThe pathological hallmark of Parkinson’s disease (PD) is the formation of Lewy bodies containing aggregated alpha-synuclein (α-syn). Although PD is associated with these distinct histological changes, other pathological features such as microvascular alterations have been linked to neurodegeneration. These changes need to be investigated as they create a hostile brain microenvironment and may contribute to the development and progression of the disease. We use a human α-syn overexpression mouse model that recapitulates some of the pathological features of PD in terms of progressive aggregation of human α-syn, impaired striatal dopamine fiber density, and an age-dependent motor deficit consistent with an impaired dopamine release. We demonstrate for the first time in this model a compromised blood–brain barrier integrity and dynamic changes in vessel morphology from angiogenesis at earlier stages to vascular regression at later stages. The vascular alterations are accompanied by a pathological activation of pericytes already at an early stage without changing overall pericyte density. Our data support and further extend the occurrence of vascular pathology as an important pathophysiological aspect in PD. The model used provides a powerful tool to investigate disease-modifying factors in PD in a temporal sequence that might guide the development of new treatments.

Evaluation of Efferent Auditory System and Hearing Quality in Parkinson's Disease: Is the Difficulty in Speech Understanding in Complex Listening Conditions Related to Neural Degeneration or Aging?

2020 ◽  
pp. 1-9
Author(s):  
Nuriye Yıldırım Gökay ◽  
Bülent Gündüz ◽  
Fatih Söke ◽  
Recep Karamert
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Auditory System ◽  
Otoacoustic Emissions ◽  
Pure Tone ◽  
Pure Tone Audiometry ◽  
Auditory Pathway ◽  
Normal Hearing ◽  
System Function ◽  
Distortion Product

Purpose The effects of neurological diseases on the auditory system have been a notable issue for investigators because the auditory pathway is closely associated with neural systems. The purposes of this study are to evaluate the efferent auditory system function and hearing quality in Parkinson's disease (PD) and to compare the findings with age-matched individuals without PD to present a perspective on aging. Method The study included 35 individuals with PD (mean age of 48.50 ± 8.00 years) and 35 normal-hearing peers (mean age of 49 ± 10 years). The following tests were administered for all participants: the first section of the Speech, Spatial and Qualities of Hearing Scale; pure-tone audiometry, speech audiometry, tympanometry, and acoustic reflexes; and distortion product otoacoustic emissions (DPOAEs) and contralateral suppression of DPOAEs. SPSS Version 25 was used for statistical analyses, and values of p < .05 were considered statistically significant. Results There were no statistically significant differences in the pure-tone audiometry thresholds and DPOAE responses between the individuals with PD and their normal-hearing peers ( p = .732). However, statistically significant differences were found between the groups in suppression levels of DPOAEs and hearing quality ( p < .05). In addition, a statistically significant and positive correlation was found between the amount of suppression at some frequencies and the Speech, Spatial and Qualities of Hearing Scale scores. Conclusions This study indicates that medial olivocochlear efferent system function and the hearing quality of individuals with PD were affected adversely due to the results of PD pathophysiology on the hearing system. For optimal intervention and follow-up, tasks related to hearing quality in daily life can also be added to therapies for PD.

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