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Development of early diagnosis of Parkinson’s disease and comprehensive economic analysis of the effect of its implementation

This approach can also be used to verify blood markers identified in patients at the clinical stage of PD. It is also evident that the complex socioeconomic factors influencing the incidence of PD is different in developed versus developing countries. The societal and medical costs of Parkinson’s are huge and efforts to improve early preclinical

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Parkinson’s Disease: Alterations in Iron and Redox Biology as a Key to Unlock Therapeutic Strategies

 This dysfunction could then drive alterations in iron trafficking that attempt to rescue energy deficits such as the increased iron uptake to provide iron for key electron transport proteins. Considering the increased iron-loading in PD brains, therapies utilizing limited iron chelation have shown success. Greater therapeutic advancements should be possible once the exact molecular pathways

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The Relationship of Rapid Eye Movement Sleep Behavior Disorder and Freezing of Gait in Parkinson’s Disease

Rapid eye movement sleep behavior disorder (RBD) contributes to injury due to the alteration of the expected atonia during rapid eye movement (REM) sleep. It occurs before the overt signs of Parkinson’s disease (PD). The co-expression of PD and RBD is characterized by non-tremor predominant subtype and higher incidence of freezing. Freezing of gait (FOG)

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Spectrum of Non-Motor Symptoms in Parkinson’s Disease

Parkinson’s disease is predominantly classified as a movement disorder. Beyond the textbook definition of rigidity, tremors, and bradykinesia, Parkinson’s disease encompasses an entire entity of non-motor symptom complexes that can precede the motor features by many years. Despite their significant clinical importance, the awareness of non-motor symptoms is quite negligible. Sleep disorders, gastrointestinal dysfunction, olfactory

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REST protects dopaminergic neurons from mitochondrial and α-synuclein oligomer pathology in an alpha synuclein overexpressing BAC-transgenic mouse model

Finally, decreased α-synuclein oligomer accumulation and mitochondrial dysfunction in mice correlated with nuclear REST and PGC-1α in protected SN GABAergic neurons, when compared to vulnerable dopaminergic neurons. Our findings show that increased levels of α-synuclein oligomers cause dopaminergic neuronal-specific dysfunction through mitochondrial toxicity, which can be attenuated by REST in an early model of Parkinsonian

REST protects dopaminergic neurons from mitochondrial and α-synuclein oligomer pathology in an alpha synuclein overexpressing BAC-transgenic mouse model Read More »