Circadian rhythm alterations affecting the pathology of neurodegenerative diseases

The circadian rhythm is a nearly 24‐h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation a...

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Published inJournal of neurochemistry Vol. 168; no. 8; pp. 1475 - 1489
Main Authors Canever, Jaquelini Betta, Queiroz, Letícia Yoshitome, Soares, Ericks Sousa, Avelar, Núbia Carelli Pereira, Cimarosti, Helena Iturvides
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.08.2024
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Abstract The circadian rhythm is a nearly 24‐h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation and memory consolidation. Dysregulation in the circadian rhythm can negatively impact human health, resulting in cardiovascular and metabolic diseases, psychiatric disorders, and premature death. Emerging evidence points to a relationship between the dysregulation circadian rhythm and neurodegenerative diseases, suggesting that the alterations in circadian function might play crucial roles in the pathogenesis and progression of neurodegenerative diseases. Better understanding this association is of paramount importance to expand the knowledge on the pathophysiology of neurodegenerative diseases, as well as, to provide potential targets for the development of new interventions based on the dysregulation of circadian rhythm. Here we review the latest findings on dysregulation of circadian rhythm alterations in Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, spinocerebellar ataxia and multiple‐system atrophy, focusing on research published in the last 3 years. Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), spinocerebellar ataxia (SCA), and multiple‐system atrophy (MSA) dysregulate clock genes, which leads to sleep disturbances and can also exacerbate these diseases. In PD, the decrease in clock genes leads to oxidative stress. In AD, this disturbance leads to an increase in tau phosphorylation. In HD, it intensifies the accumulation of mutant huntingtin, and in MSA, it impairs dopaminergic signaling. These alterations act as a feedback loop, exacerbating neurodegenerative diseases.
AbstractList Abstract The circadian rhythm is a nearly 24‐h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation and memory consolidation. Dysregulation in the circadian rhythm can negatively impact human health, resulting in cardiovascular and metabolic diseases, psychiatric disorders, and premature death. Emerging evidence points to a relationship between the dysregulation circadian rhythm and neurodegenerative diseases, suggesting that the alterations in circadian function might play crucial roles in the pathogenesis and progression of neurodegenerative diseases. Better understanding this association is of paramount importance to expand the knowledge on the pathophysiology of neurodegenerative diseases, as well as, to provide potential targets for the development of new interventions based on the dysregulation of circadian rhythm. Here we review the latest findings on dysregulation of circadian rhythm alterations in Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, spinocerebellar ataxia and multiple‐system atrophy, focusing on research published in the last 3 years. image
The circadian rhythm is a nearly 24-h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation and memory consolidation. Dysregulation in the circadian rhythm can negatively impact human health, resulting in cardiovascular and metabolic diseases, psychiatric disorders, and premature death. Emerging evidence points to a relationship between the dysregulation circadian rhythm and neurodegenerative diseases, suggesting that the alterations in circadian function might play crucial roles in the pathogenesis and progression of neurodegenerative diseases. Better understanding this association is of paramount importance to expand the knowledge on the pathophysiology of neurodegenerative diseases, as well as, to provide potential targets for the development of new interventions based on the dysregulation of circadian rhythm. Here we review the latest findings on dysregulation of circadian rhythm alterations in Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, spinocerebellar ataxia and multiple-system atrophy, focusing on research published in the last 3 years.The circadian rhythm is a nearly 24-h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation and memory consolidation. Dysregulation in the circadian rhythm can negatively impact human health, resulting in cardiovascular and metabolic diseases, psychiatric disorders, and premature death. Emerging evidence points to a relationship between the dysregulation circadian rhythm and neurodegenerative diseases, suggesting that the alterations in circadian function might play crucial roles in the pathogenesis and progression of neurodegenerative diseases. Better understanding this association is of paramount importance to expand the knowledge on the pathophysiology of neurodegenerative diseases, as well as, to provide potential targets for the development of new interventions based on the dysregulation of circadian rhythm. Here we review the latest findings on dysregulation of circadian rhythm alterations in Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, spinocerebellar ataxia and multiple-system atrophy, focusing on research published in the last 3 years.
The circadian rhythm is a nearly 24‐h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation and memory consolidation. Dysregulation in the circadian rhythm can negatively impact human health, resulting in cardiovascular and metabolic diseases, psychiatric disorders, and premature death. Emerging evidence points to a relationship between the dysregulation circadian rhythm and neurodegenerative diseases, suggesting that the alterations in circadian function might play crucial roles in the pathogenesis and progression of neurodegenerative diseases. Better understanding this association is of paramount importance to expand the knowledge on the pathophysiology of neurodegenerative diseases, as well as, to provide potential targets for the development of new interventions based on the dysregulation of circadian rhythm. Here we review the latest findings on dysregulation of circadian rhythm alterations in Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, spinocerebellar ataxia and multiple‐system atrophy, focusing on research published in the last 3 years. Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), spinocerebellar ataxia (SCA), and multiple‐system atrophy (MSA) dysregulate clock genes, which leads to sleep disturbances and can also exacerbate these diseases. In PD, the decrease in clock genes leads to oxidative stress. In AD, this disturbance leads to an increase in tau phosphorylation. In HD, it intensifies the accumulation of mutant huntingtin, and in MSA, it impairs dopaminergic signaling. These alterations act as a feedback loop, exacerbating neurodegenerative diseases.
The circadian rhythm is a nearly 24-h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and genetic factors. It is responsible for maintaining body homeostasis and it is critical for essential functions, such as metabolic regulation and memory consolidation. Dysregulation in the circadian rhythm can negatively impact human health, resulting in cardiovascular and metabolic diseases, psychiatric disorders, and premature death. Emerging evidence points to a relationship between the dysregulation circadian rhythm and neurodegenerative diseases, suggesting that the alterations in circadian function might play crucial roles in the pathogenesis and progression of neurodegenerative diseases. Better understanding this association is of paramount importance to expand the knowledge on the pathophysiology of neurodegenerative diseases, as well as, to provide potential targets for the development of new interventions based on the dysregulation of circadian rhythm. Here we review the latest findings on dysregulation of circadian rhythm alterations in Parkinson's disease, Alzheimer's disease, Huntington's disease, amyotrophic lateral sclerosis, multiple sclerosis, spinocerebellar ataxia and multiple-system atrophy, focusing on research published in the last 3 years.
Author Avelar, Núbia Carelli Pereira
Queiroz, Letícia Yoshitome
Cimarosti, Helena Iturvides
Soares, Ericks Sousa
Canever, Jaquelini Betta
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  organization: Federal University of Santa Catarina
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Issue 8
Keywords Huntington's disease
Alzheimer's disease
amyotrophic lateral sclerosis
spinocerebellar ataxia
synucleinopathies
multiple sclerosis
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Aging and Neurodegeneration: from molecular mechanisms to therapeutic interventions
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  ident: e_1_2_10_93_1
  article-title: Circadian rhythm alterations in an in vitro cellular model of spinocerebellar ataxia type 17
  publication-title: Movement Disorders
  contributor:
    fullname: Motolese F.
– ident: e_1_2_10_96_1
  doi: 10.1111/bpa.13028
– ident: e_1_2_10_119_1
  doi: 10.1002/jnr.24505
– ident: e_1_2_10_74_1
  doi: 10.1016/j.expneurol.2010.12.011
– ident: e_1_2_10_129_1
  doi: 10.1159/000324374
– ident: e_1_2_10_45_1
  doi: 10.1038/nrdp.2017.71
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Snippet The circadian rhythm is a nearly 24‐h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and...
The circadian rhythm is a nearly 24-h oscillation found in various physiological processes in the human brain and body that is regulated by environmental and...
Abstract The circadian rhythm is a nearly 24‐h oscillation found in various physiological processes in the human brain and body that is regulated by...
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SubjectTerms Alzheimer's disease
Amyotrophic lateral sclerosis
Animals
Ataxia
Atrophy
Circadian rhythm
Circadian Rhythm - physiology
Circadian rhythms
Disease
Genetic factors
Homeostasis
Humans
Huntington's disease
Huntingtons disease
Immunological memory
Machado-Joseph disease
Mental disorders
Metabolic disorders
Metabolism
Movement disorders
Multiple sclerosis
Neurodegenerative diseases
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Neurodegenerative Diseases - physiopathology
Parkinson's disease
Pathogenesis
Physiological effects
spinocerebellar ataxia
synucleinopathies
Title Circadian rhythm alterations affecting the pathology of neurodegenerative diseases
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjnc.15883
https://www.ncbi.nlm.nih.gov/pubmed/37358003
https://www.proquest.com/docview/3085848613/abstract/
https://www.proquest.com/docview/2829705082/abstract/
Volume 168
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