The role of excitatory amino acids in experimental models of Parkinson's disease

1994 ◽  
Vol 8 (1-2) ◽  
pp. 39-71 ◽  
Author(s):  
K. Ossowska
Keyword(s):  
Parkinson’S Disease ◽  
Amino Acids ◽  
Parkinson's Disease ◽  
Excitatory Amino Acids ◽  
Experimental Models

Excitatory amino acids and Parkinson's disease

1990 ◽  
Vol 13 (2) ◽  
pp. 46 ◽  
Author(s):  
Werner J. Schmidt ◽  
Michael Bubser ◽  
Wolfgang Hauber
Keyword(s):  
Parkinson’S Disease ◽  
Amino Acids ◽  
Parkinson's Disease ◽  
Excitatory Amino Acids

scholarly journals Parkinson’s Disease-Related Genes and Lipid Alteration

2021 ◽  
Vol 22 (14) ◽  
pp. 7630
Author(s):  
Milena Fais ◽  
Antonio Dore ◽  
Manuela Galioto ◽  
Grazia Galleri ◽  
Claudia Crosio ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Mechanisms ◽  
Neurodegenerative Disorder ◽  
Clinical Manifestations ◽  
Alpha Synuclein ◽  
Experimental Models ◽  
Protein Clearance ◽  
Genetic And Environmental Factors

Parkinson’s disease (PD) is a complex and progressive neurodegenerative disorder with a prevalence of approximately 0.5–1% among those aged 65–70 years. Although most of its clinical manifestations are due to a loss of dopaminergic neurons, the PD etiology is largely unknown. PD is caused by a combination of genetic and environmental factors, and the exact interplay between genes and the environment is still debated. Several biological processes have been implicated in PD, including mitochondrial or lysosomal dysfunctions, alteration in protein clearance, and neuroinflammation, but a common molecular mechanism connecting the different cellular alterations remains incompletely understood. Accumulating evidence underlines a significant role of lipids in the pathological pathways leading to PD. Beside the well-described lipid alteration in idiopathic PD, this review summarizes the several lipid alterations observed in experimental models expressing PD-related genes and suggests a possible scenario in relationship to the molecular mechanisms of neuronal toxicity. PD could be considered a lipid-induced proteinopathy, where alteration in lipid composition or metabolism could induce protein alteration—for instance, alpha-synuclein accumulation—and finally neuronal death.

A short overview on the role of α-synuclein and proteasome in experimental models of Parkinson’s disease

2006 ◽  
pp. 105-109 ◽  
Author(s):  
F. S. Giorgi ◽  
A. Bandettini di Poggio ◽  
G. Battaglia ◽  
A. Pellegrini ◽  
L. Murri ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Experimental Models ◽  
Short Overview

scholarly journals Novel insights into the antioxidant role of tauroursodeoxycholic acid in experimental models of Parkinson's disease

2017 ◽  
Vol 1863 (9) ◽  
pp. 2171-2181 ◽  
Author(s):  
Alexandra I. Rosa ◽  
Inês Fonseca ◽  
Maria João Nunes ◽  
Sara Moreira ◽  
Elsa Rodrigues ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Experimental Models ◽  
Tauroursodeoxycholic Acid

scholarly journals Hippocampal and Reticulo-Thalamic Parvalbumin Interneurons and Synaptic Re-Organization during Sleep Disorders in the Rat Models of Parkinson’s Disease Neuropathology

2021 ◽  
Vol 22 (16) ◽  
pp. 8922
Author(s):  
Ljiljana Radovanovic ◽  
Jelena Petrovic ◽  
Jasna Saponjic
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Sleep Disorders ◽  
Rem Sleep ◽  
Experimental Models ◽  
Rat Models ◽  
Parvalbumin Interneurons ◽  
First Time ◽  
Local Sleep

We investigated the alterations of hippocampal and reticulo-thalamic (RT) GABAergic parvalbumin (PV) interneurons and their synaptic re-organizations underlying the prodromal local sleep disorders in the distinct rat models of Parkinson’s disease (PD). We demonstrated for the first time that REM sleep is a predisposing state for the high-voltage sleep spindles (HVS) induction in all experimental models of PD, particularly during hippocampal REM sleep in the hemiparkinsonian models. There were the opposite underlying alterations of the hippocampal and RT GABAergic PV+ interneurons along with the distinct MAP2 and PSD-95 expressions. Whereas the PD cholinopathy enhanced the number of PV+ interneurons and suppressed the MAP2/PSD-95 expression, the hemiparkinsonism with PD cholinopathy reduced the number of PV+ interneurons and enhanced the MAP2/PSD-95 expression in the hippocampus. Whereas the PD cholinopathy did not alter PV+ interneurons but partially enhanced MAP2 and suppressed PSD-95 expression remotely in the RT, the hemiparkinsonism with PD cholinopathy reduced the PV+ interneurons, enhanced MAP2, and did not change PSD-95 expression remotely in the RT. Our study demonstrates for the first time an important regulatory role of the hippocampal and RT GABAergic PV+ interneurons and the synaptic protein dynamic alterations in the distinct rat models of PD neuropathology.

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