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

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.

Download Full-text

Neurobiology of sleep: the role of dopamine in Parkinson’s disease-related sleep disorders

Non-motor Symptoms of Parkinson's Disease ◽

10.1093/med/9780199684243.003.0013 ◽

2014 ◽

pp. 209-220

Author(s):

Lynn Marie Trotti ◽

David B. Rye

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Sleep Disorders

Download Full-text

Role of DHA metabolites in protective effects of DHA supplementation in the brains of rotenone-induced rat models of Parkinson’s disease

10.3390/iecbm2020-08583 ◽

2020 ◽

Author(s):

Ami Oguro ◽

Yasuhiro Ishihara

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Protective Effects ◽

Rat Models

Download Full-text

Mitochondrial Metabolism as Target of the Neuroprotective Role of Erythropoietin in Parkinson’s Disease

Antioxidants ◽

10.3390/antiox10010121 ◽

2021 ◽

Vol 10 (1) ◽

pp. 121

Author(s):

Federica Rey ◽

Sara Ottolenghi ◽

Toniella Giallongo ◽

Alice Balsari ◽

Carla Martinelli ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Extracellular Acidification ◽

Atp Levels ◽

Transmission Electron ◽

First Time ◽

Glycolytic Rate

Existing therapies for Parkinson’s disease (PD) are only symptomatic. As erythropoietin (EPO) is emerging for its benefits in neurodegenerative diseases, here, we test the protective effect driven by EPO in in vitro (SH-SY5Y cells challenged by MPP+) and in vivo (C57BL/6J mice administered with MPTP) PD models. EPO restores cell viability in both protective and restorative layouts, enhancing the dopaminergic recovery. Specifically, EPO rescues the PD-induced damage to mitochondria, as shown by transmission electron microscopy, Mitotracker assay and PINK1 expression. Moreover, EPO promotes a rescue of mitochondrial respiration while markedly enhancing the glycolytic rate, as shown by the augmented extracellular acidification rate, contributing to elevated ATP levels in MPP+-challenged cells. In PD mice, EPO intrastriatal infusion markedly improves the outcome of behavioral tests. This is associated with the rescue of dopaminergic markers and decreased neuroinflammation. This study demonstrates cellular and functional recovery following EPO treatment, likely mediated by the 37 Kda isoform of the EPO-receptor. We report for the first time, that EPO-neuroprotection is exerted through restoring ATP levels by accelerating the glycolytic rate. In conclusion, the redox imbalance and neuroinflammation associated with PD may be successfully treated by EPO.

Download Full-text

Prodromal local sleep disorders in a rat model of Parkinson’s disease cholinopathy, hemiparkinsonism and hemiparkinsonism with cholinopathy

Behavioural Brain Research ◽

10.1016/j.bbr.2020.112957 ◽

2021 ◽

Vol 397 ◽

pp. 112957

Author(s):

Jelena Petrovic ◽

Ljiljana Radovanovic ◽

Jasna Saponjic

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Sleep Disorders ◽

Rat Model ◽

Local Sleep

Download Full-text

Diagnosing REM sleep behaviour disorder in patients with Parkinson's disease: The role of screening questionnaires and of measures of REM sleep without atonia

Sleep Medicine ◽

10.1016/j.sleep.2015.02.004 ◽

2015 ◽

Vol 16 ◽

pp. S2-S3

Author(s):

M. Figorilli ◽

R. Ferri ◽

B. Pereira ◽

P. Beudin ◽

F. Marrosu ◽

...

Keyword(s):

Parkinson’S Disease ◽

Parkinson's Disease ◽

Rem Sleep ◽

Behaviour Disorder ◽

Sleep Behaviour ◽

Rem Sleep Without Atonia ◽

Rem Sleep Behaviour Disorder ◽

Screening Questionnaires

Download Full-text

Parkinson’s Disease-Related Genes and Lipid Alteration

International Journal of Molecular Sciences ◽

10.3390/ijms22147630 ◽

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.

Download Full-text