Chronobiology of Parkinson's disease: Past, present and future

Asadpoordezaki, Ziba; Coogan, Andrew N.; Henley, Beverley M.

doi:10.1111/ejn.15859

Cited by 12 publications

(6 citation statements)

References 230 publications

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“…Along with understanding the role of circadian rhythm disruption in PD and facilitating research on the interplay between neurodegeneration and circadian rhythm disruption, there is a new perspective for therapeutic potential (Table 3). 133 Some simple approaches already exist, such as the effect of high-intensity exercise, which not only improves sleep efficiency but also improves circadian rhythm. 134 Similarly, light therapy has already been explored in PD.…”

Section: Therapeutic Potential Of Circadian Rhythm Regulationmentioning

confidence: 99%

Fighting Against the Clock: Circadian Disruption and Parkinson’s Disease

Chen,

Wang,

Lewis

et al. 2024

JMD

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Circadian disruption is being increasingly recognized as a critical factor in the development and progression of Parkinson’s disease (PD). This review aims to provide an in-depth overview of the relationship between circadian disruption and PD by exploring the molecular, cellular, and behavioral aspects of this interaction. This review will include a comprehensive understanding of how the clock gene system and transcription–translation feedback loops function and how they are diminished in PD. The article also discusses the role of clock genes in the regulation of circadian rhythms, as well as the impact of clock gene dysregulation on mitochondrial function, oxidative stress, and neuroinflammation, including the microbiota-gut-brain axis, which have all been proposed as being crucial mechanisms in the pathophysiology of PD. Finally, this review highlights potential therapeutic strategies targeting the clock gene system and circadian rhythm for the treatment of PD.

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Section: Therapeutic Potential Of Circadian Rhythm Regulationmentioning

confidence: 99%

Fighting Against the Clock: Circadian Disruption and Parkinson’s Disease

Chen,

Wang,

Lewis

et al. 2024

JMD

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“…On the other hand, a large number of studies has pointed to an age-related loss of the pineal function in both animals and humans (e.g. : elderly individuals, and preclinical and clinical patients with agingrelated pathologies, such as Alzheimer's disease and Parkinson's disease) [4,43,45,[49][50][51]. This loss has been linked to some or all the following features: anatomical abnormalities, reduced number of pinealocytes and variable numbers of glial cells, fibrosis, calcification, inflammation, altered CG expression and clock functionality, disconnection from the master circadian clock at the hypothalamic SCN, and impaired sympathetic regulation [49][50][51][52][53][54].…”

Section: Sympathetic Dysfunctionmentioning

confidence: 99%

“…: elderly individuals, and preclinical and clinical patients with agingrelated pathologies, such as Alzheimer's disease and Parkinson's disease) [4,43,45,[49][50][51]. This loss has been linked to some or all the following features: anatomical abnormalities, reduced number of pinealocytes and variable numbers of glial cells, fibrosis, calcification, inflammation, altered CG expression and clock functionality, disconnection from the master circadian clock at the hypothalamic SCN, and impaired sympathetic regulation [49][50][51][52][53][54]. Sympathetic dysregulation may involve the loss of nerve terminals, as well as age-induced neuroaxonal dystrophy (NAD) of distal axons, altered denervation supersensitivity, and a decrease in adrenoceptor reception and responsiveness, among other mechanisms (Figure 2) [53,55].…”

Section: Sympathetic Dysfunctionmentioning

confidence: 99%

“…Acute and chronic MEL supplementation, in both early and late stages of these conditions, also warrants further investigation. The use of exogenous MEL supplements represents, however, a promising remedial therapy especially for those patients in preclinical phases due to both its chronobiotic and its cytoprotective properties [51,56,57].…”

Section: Sympathetic Dysfunctionmentioning

confidence: 99%

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Sympathetic Innervation of the Mammalian Pineal Gland: Its Involvement in Ontogeny and Physiology, and in Pineal Dysfunction

Avila,

L. Freites,

Vásquez

et al. 2023

Topics in Autonomic Nervous System

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In mammals, the melatonin-producing pineal gland (PG) receives sympathetic innervation from the superior cervical ganglia (SCG). This chapter describes the role of this innervation on the PG’s ontogeny and rhythmic function, along with consequences to physiology when this regulation is disrupted. The PG and the SCG are components of the circadian timing system (CTS). Therefore, the overall CTS is described, including its oscillatory basis, its synchronization to the light: dark (L:D) cycles, and the dissemination of timing cues to all cells throughout the body. Pineal cellular composition and heterogeneity, cell-cell interactions, and the molecular mechanisms involved in the circadian rhythm of melatonin (MEL), are discussed. The SCG’s bilateral placement among surrounding anatomical landmarks, as well as their afferent and efferent connections, are described and illustrated. In addition, the SCG-related surgical models and the state-of-the art technology used to investigate the connection between SCG and PG are presented. Perspectives and gaps in our understanding are also discussed. We hope this chapter inspires readers to delve deeper into the field of the pineal gland and its main messenger, melatonin, as well as MEL’s impact in health and disease, including as a remedial therapy.

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“…[5] Amyloids are insoluble protein aggregates that accumulate in different organs and tissues and can lead to several debilitating diseases. There are more than 20 different human diseases known that are linked to amyloid formation including Alzheimer's disease (AD), [6] Parkinson's disease (PD), [7] and type-2 diabetes. [8,9] In addition to proteinaceous amyloids, small metabolites, that is, nucleosides, amino acids and glycolipids have recently been found to form amyloid-like toxic structures linked to different inborn errors of metabolism (IEM) diseases.…”

Section: Introductionmentioning

confidence: 99%

Ultra‐Small ATP‐Decorated Gold Nanoparticles for Targeting Amyloid Fibrils in Neurodegenerative Diseases

Kumar,

Kumar

et al. 2023

Adv Funct Materials

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Ultrafine Gold nanoparticles (Au NPs) functionalized with various biomolecules constitute an alternative to antibodies as anti‐amyloidogenic agents. However, generating stable ultrafine Au NPs with high surface activity is challenging. Here, the capacity of phosphate groups in biomolecules is used to stabilize Au NPs. The characteristics of Au NPs decorated with adenosine mono‐, di‐, and tri‐phosphate are compared as well as adenosine and peptide nucleic acid‐containing adenosine as controls. Among them, ATP‐Au NPs are found to be superior having small size (2–4 nm) and stability (for several months) when analysed by spectroscopy and electron microscopy. Spectroscopy analysis also revealed that each ATP‐stabilized Au NP is decorated with 7–8 molecules of ATP. ThT binding analysis and TEM imaging showed that the ATP‐Au NPs efficiently prevented amyloid fibril formation in vitro by Aβ‐42, α‐Synuclein as well as by the Glucosylceramide metabolite, and disaggregated their pre‐formed fibrils. NMR analysis revealed the interaction of the ATP‐Au NPs with the amyloid fibrils. The ATP‐Au NPs are safe toward cultured SH‐SY5Y cells and when co‐incubated with α‐Synuclein amyloids inhibited their cytotoxicity and readily enter the cells to inhibit formation of amyloid fibrils within them. The results indicates the pharmacological potentials of ATP decorated Au NPs.

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Chronobiology of Parkinson's disease: Past, present and future

Cited by 12 publications

References 230 publications

Fighting Against the Clock: Circadian Disruption and Parkinson’s Disease

Fighting Against the Clock: Circadian Disruption and Parkinson’s Disease

Sympathetic Innervation of the Mammalian Pineal Gland: Its Involvement in Ontogeny and Physiology, and in Pineal Dysfunction

Ultra‐Small ATP‐Decorated Gold Nanoparticles for Targeting Amyloid Fibrils in Neurodegenerative Diseases

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