Article
Biochemistry & Molecular Biology
Alessandra Mingione, Francesca Pivari, Nicoletta Plotegher, Michele Dei Cas, Aida Zulueta, Tommaso Bocci, Marco Trinchera, Elisabetta Albi, Vittorio Maglione, Anna Caretti, Luigi Bubacco, Rita Paroni, Daniele Bottai, Riccardo Ghidoni, Paola Signorelli
Summary: Parkinson's disease is associated with alpha-synuclein aggregation and lipid-protein inclusion formation, leading to impaired autophagy, protein aggregation, and inflammation. Myr treatment may help improve these conditions by reducing intracellular aggregates and inflammation.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Review
Biochemistry & Molecular Biology
Tapan Behl, Piyush Madaan, Aayush Sehgal, Sukhbir Singh, Md Khalid Anwer, Hafiz A. Makeen, Mohammed Albratty, Syam Mohan, Simona Bungau
Summary: This article discusses the etiology, oxidative stress, autophagy, programmed cell death, and other important roles in the pathogenesis of Parkinson's disease, emphasizing the crucial role of iron and copper in the development of Parkinson's disease. Metal chelators may have the potential to reduce oxidative stress levels by scavenging metal ions, thereby preventing or slowing down the progression of Parkinson's disease.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Review
Pharmacology & Pharmacy
Yumin Wang, Shuang Wu, Qiang Li, Weihong Lang, Wenjing Li, Xiaodong Jiang, Zhirong Wan, Jichao Chen, Hongquan Wang
Summary: This review summarizes the recent updates and knowledge of the molecular mechanisms underlying the neuroprotective effects of epigallocatechin 3-gallate (EGCG) derived from green tea extract in Parkinson's disease (PD). The review highlights the pleiotropic effects of EGCG, including anti-apoptotic, anti-oxidative stress, anti-inflammatory, modulation of dopamine production, and inhibition of alpha-synuclein aggregation, which make it a promising neuroprotective compound for the treatment of PD.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Multidisciplinary Sciences
Daniel J. Apicco, Evgeny Shlevkov, Catherine L. Nezich, David T. Tran, Edward Guilmette, Justin W. Nicholatos, Collin M. Bantle, Yi Chen, Kelly E. Glajch, Neeta A. Abraham, Lan T. Dang, G. Campbell Kaynor, Ellen A. Tsai, Khanh-Dung H. Nguyen, Joost Groot, YuTing Liu, Andreas Weihofen, Jessica A. Hurt, Heiko Runz, Warren D. Hirst
Summary: ITPKB is negatively regulating alpha-synuclein aggregation by inhibiting ER-to-mitochondria calcium transport, suggesting modulation of this pathway as a potential therapeutic strategy for sporadic PD.
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
(2021)
Article
Medicine, Research & Experimental
Qingyu Ren, Xin Jiang, Shanshan Zhang, Xin Gao, Yam Nath Paudel, Pengyu Zhang, Rongchun Wang, Kechun Liu, Meng Jin
Summary: In this study, it was found that YIAEDAER peptide extracted from Neptunea arthritica cumingii has potential therapeutic effects on MPTP-induced PD-like condition by modulating multiple genes related to autophagy and oxidative stress.
BIOMEDICINE & PHARMACOTHERAPY
(2022)
Review
Biochemistry & Molecular Biology
Sasanka Chakrabarti, Marco Bisaglia
Summary: Parkinson's disease is a chronic neurodegenerative condition that affects over 1% of people over the age of 65. It is characterized by the degeneration of specific neurons responsible for motor symptoms. The underlying mechanisms, including redox alterations, mitochondrial dysfunctions, and neuroinflammation, are not fully understood. This review explores the role of dopamine and its oxidation chemistry in the pathogenesis of Parkinson's disease, including the formation of free radicals and toxic metabolites.
Review
Biochemistry & Molecular Biology
Ritu Soni, Jigna Shah
Summary: Parkinson's disease is a progressive neurodegenerative disorder associated with metabolic syndrome, which may contribute to the development of the disease through various pathological pathways.
ACS CHEMICAL NEUROSCIENCE
(2022)
Review
Biochemistry & Molecular Biology
Engila Khan, Ikramul Hasan, M. Emdadul Haque
Summary: Disease modeling in non-human subjects is crucial for clinical research. Animal models are necessary to replicate the disease process and understand the etiology and pathophysiology. Parkinson's disease, with its progressive nature and various disabilities, has specific pathological hallmarks that involve misfolded protein accumulation and degeneration of neurons. Extensive research has been conducted on Parkinson's disease animal models, including pharmacological and genetic manipulation induction. This review summarizes and discusses commonly used Parkinson's disease animal model systems, as well as their applications and limitations.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Multidisciplinary Sciences
Richa Singh, Walia Zahra, Saumitra Sen Singh, Hareram Birla, Aaina Singh Rathore, Priyanka Kumari Keshri, Hagera Dilnashin, Shekhar Singh, Surya Pratap Singh
Summary: Major pathological features of Parkinson's disease (PD) include oxidative stress, alpha-synuclein aggregation, mitochondrial dysfunction, apoptosis of dopaminergic neurons, and downregulation of neurotrophic factors. Trophic factor-based neuroprotective medicines have been of interest for treating PD symptoms. Rotenone inhibits mitochondrial complex I, leading to ROS overproduction and alpha-synuclein aggregation. BDNF and TrkB interaction triggers neuronal cell development and differentiation through Akt and GSK-3 beta. The homeostasis of these signaling cascades is compromised in PD. Oleuropein (OLE) from olive leaves shows antioxidative properties and was found to be neuroprotective in a PD mouse model. OLE improved motor impairment, upregulated CREB regulation, phosphorylated Akt and GSK-3 beta, reduced mitochondrial dysfunction, and downregulated proapoptotic markers. OLE may be used as a therapeutic agent for PD by regulating BDNF/CREB/Akt signaling pathway.
SCIENTIFIC REPORTS
(2023)
Review
Biochemistry & Molecular Biology
Abbie T. Rodger, Maryam A. L. Nasser, Wayne G. Carter
Summary: Currently, there are no pharmacological treatments that can completely stop or reverse the progression of Parkinson's Disease (PD). Therefore, there is a need for neuroprotective therapies. This systematic review examines the effectiveness of anti-a-synuclein (a-syn) therapies in preventing PD progression in preclinical models and human clinical trials. The review found that novel preclinical anti-a-syn therapeutics reduced a-syn aggregations and protected against dopaminergic neuronal loss. Completed clinical trials showed significant tolerability and efficacy in reducing a-syn and minimal adverse effects. Overall, this review highlights the potential of anti-a-syn therapies in both preclinical and clinical settings to reduce a-syn accumulation and potentially slow down PD progression.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Review
Clinical Neurology
Zixuan Chen, Madiha Rasheed, Yulin Deng
Summary: Mitochondrial dysfunction plays a crucial role in the pathogenesis of Parkinson's disease, influenced by a combination of genetic and environmental factors. The complex relationship between oxidative stress, alpha-synuclein aggregation, endogenous neurotoxins release, and epigenetic modifications leads to a vicious cycle of mitochondrial damage and neuronal degeneration. Understanding these interactions may offer potential for future diagnostic biomarkers and targeted drug therapies in Parkinson's disease management.
Review
Neurosciences
Si-Tong Feng, Zhen-Zhen Wang, Yu-He Yuan, Hong-Mei Sun, Nai-Hong Chen, Yi Zhang
Summary: The review highlights the critical role of mitochondrial dysfunction in Parkinson's disease, with various Parkinson's proteins being associated with this dysfunction and oxidative stress. The interaction between alpha-synuclein and tau proteins amplifies neurotoxic effects on mitochondria, while oxidative stress caused by dysfunction favors the formation of protein aggregates and plays a key role in PD progression.
EUROPEAN JOURNAL OF NEUROSCIENCE
(2021)
Article
Biochemistry & Molecular Biology
Fabio Schifano, Simone Dell'Acqua, Stefania Nicolis, Luigi Casella, Enrico Monzani
Summary: The study explores the interplay between α-Synuclein (aS), dopamine (DA), and iron in Parkinson's disease etiology. At high DA:Fe molar ratios, the formation of the [Fe-III(DA)(2)](-) complex hinders the interaction with aS peptides. However, at lower ratios, the peptide competes with one of the two coordinated DA molecules. Post-translational modifications of the peptide, such as oxidation and phosphorylation, play crucial roles in aS aggregation and affinity for iron(III). Moreover, the presence of a membrane-like environment enhances the peptide's effect on DA oxidation and complex formation and decomposition.
Review
Neurosciences
Laura Mahoney-Sanchez, Hind Bouchaoui, Scott Ayton, David Devos, James A. Duce, Jean-Christophe Devedjian
Summary: Parkinson's Disease is a common neurodegenerative disorder with motor impairments and non-motor symptoms. Pathological features include dopaminergic neuronal death, alpha-synuclein deposition, iron accumulation, oxidative stress, and lipid peroxidation damage. Targeting pathways like ferroptosis could have therapeutic potential in treating PD.
PROGRESS IN NEUROBIOLOGY
(2021)
Article
Neurosciences
Alberto Delaidelli, Mette Richner, Lixiang Jiang, Amelia van der Laan, Ida Bergholdt Jul Christiansen, Nelson Ferreira, Jens R. Nyengaard, Christian B. Vaegter, Poul H. Jensen, Ian R. Mackenzie, Poul H. Sorensen, Asad Jan
Summary: The pathological accumulation of alpha-synuclein impairs redox homeostasis in the nervous system, leading to nuclear NRF2 accumulation and alterations in NRF2-responsive genes. Using a transgenic mouse model, it was observed that neuronal populations with phosphorylated aSyn showed increased nuclear NRF2 and abnormal anti-oxidant and inflammatory gene response in the affected neuraxis. Boosting neuronal anti-oxidant response may be a promising strategy to mitigate neurodegeneration in PD and related diseases.
ACTA NEUROPATHOLOGICA COMMUNICATIONS
(2021)
Article
Biochemistry & Molecular Biology
Pei-Yang Gao, Ya-Nan Ou, Yi-Ming Huang, Zhi-Bo Wang, Yan Fu, Ya-Hui Ma, Qiong-Yao Li, Li-Yun Ma, Rui-Ping Cui, Yin-Chu Mi, Lan Tan, Jin-Tai Yu
Summary: Liver function may play a role in the progression of Alzheimer's disease. The study found that as AD progressed, certain liver function markers increased while others decreased. The relationship between liver function and CSF AD biomarkers indicates a potential mediation effect on cognition.
JOURNAL OF NEUROCHEMISTRY
(2024)