scholarly journals Peroxiredoxins in Neurodegenerative Diseases

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1203
Author(s):  
Monika Szeliga
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Nitrosative Stress ◽  
Current Knowledge ◽  
Lewy Bodies ◽  
Substantial Evidence ◽  
Defense Systems ◽  
Neurodegenerative Process ◽  
Antioxidant Mechanisms ◽  
Lateral Sclerosis

Substantial evidence indicates that oxidative/nitrosative stress contributes to the neurodegenerative diseases. Peroxiredoxins (PRDXs) are one of the enzymatic antioxidant mechanisms neutralizing reactive oxygen/nitrogen species. Since mammalian PRDXs were identified 30 years ago, their significance was long overshadowed by the other well-studied ROS/RNS defense systems. An increasing number of studies suggests that these enzymes may be involved in the neurodegenerative process. This article reviews the current knowledge on the expression and putative roles of PRDXs in neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and dementia with Lewy bodies, multiple sclerosis, amyotrophic lateral sclerosis and Huntington’s disease.

scholarly journals Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease

Antioxidants ◽  
2019 ◽  
Vol 8 (9) ◽  
pp. 333 ◽  
Author(s):  
Aimee N. Winter ◽  
Paula C. Bickford
Keyword(s):  
Neurodegenerative Diseases ◽  
Nitrosative Stress ◽  
Therapeutic Potential ◽  
Stress Protein ◽  
Motor Impairments ◽  
Oxidative And Nitrosative Stress ◽  
Beneficial Effects ◽  
Neuronal Populations ◽  
Neurodegenerative Process ◽  
Lateral Sclerosis

Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS), are characterized by the death of neurons within specific regions of the brain or spinal cord. While the etiology of many neurodegenerative diseases remains elusive, several factors are thought to contribute to the neurodegenerative process, such as oxidative and nitrosative stress, excitotoxicity, endoplasmic reticulum stress, protein aggregation, and neuroinflammation. These processes culminate in the death of vulnerable neuronal populations, which manifests symptomatically as cognitive and/or motor impairments. Until recently, most treatments for these disorders have targeted single aspects of disease pathology; however, this strategy has proved largely ineffective, and focus has now turned towards therapeutics which target multiple aspects underlying neurodegeneration. Anthocyanins are unique flavonoid compounds that have been shown to modulate several of the factors contributing to neuronal death, and interest in their use as therapeutics for neurodegeneration has grown in recent years. Additionally, due to observations that the bioavailability of anthocyanins is low relative to that of their metabolites, it has been proposed that anthocyanin metabolites may play a significant part in mediating the beneficial effects of an anthocyanin-rich diet. Thus, in this review, we will explore the evidence evaluating the neuroprotective and therapeutic potential of anthocyanins and their common metabolites for treating neurodegenerative diseases.

scholarly journals Differential levels of Neurofilament Light protein in cerebrospinal fluid in patients with a wide range of neurodegenerative disorders

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
C. Delaby ◽  
D. Alcolea ◽  
M. Carmona-Iragui ◽  
I. Illán-Gala ◽  
E. Morenas-Rodríguez ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Lewy Bodies ◽  
Csf Biomarkers ◽  
Neurofilament Light ◽  
Cognitively Normal ◽  
Wide Range ◽  
Lateral Sclerosis ◽  
Neuroaxonal Degeneration

Abstract Cerebrospinal fluid (CSF) biomarkers are useful in the diagnosis and the prediction of progression of several neurodegenerative diseases. Among them, CSF neurofilament light (NfL) protein has particular interest, as its levels reflect neuroaxonal degeneration, a common feature in various neurodegenerative diseases. In the present study, we analyzed NfL levels in the CSF of 535 participants of the SPIN (Sant Pau Initiative on Neurodegeneration) cohort including cognitively normal participants, patients with Alzheimer disease (AD), Down syndrome (DS), frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), dementia with Lewy bodies (DLB), progressive supranuclear palsy (PSP) and corticobasal syndrome (CBS). We evaluated the differences in CSF NfL accross groups and its association with other CSF biomarkers and with cognitive scales. All neurogenerative diseases showed increased levels of CSF NfL, with the highest levels in patients with ALS, FTD, CBS and PSP. Furthermore, we found an association of CSF NfL levels with cognitive impairment in patients within the AD and FTD spectrum and with AD pathology in DLB and DS patients. These results have implications for the use of NfL as a marker in neurodegenerative diseases.

scholarly journals Novel Approaches for the Treatment of Alzheimer’s and Parkinson’s Disease

2019 ◽  
Vol 20 (3) ◽  
pp. 719 ◽  
Author(s):  
Michiel Van Bulck ◽  
Ana Sierra-Magro ◽  
Jesus Alarcon-Gil ◽  
Ana Perez-Castillo ◽  
Jose Morales-Garcia
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Current Knowledge ◽  
Chronic Illnesses ◽  
Aging Brain ◽  
Therapeutic Approaches ◽  
Neurodegenerative Process ◽  
Age Related ◽  
Parkinson’S Diseases ◽  
Current Therapies

Neurodegenerative disorders affect around one billion people worldwide. They can arise from a combination of genomic, epigenomic, metabolic, and environmental factors. Aging is the leading risk factor for most chronic illnesses of old age, including Alzheimer’s and Parkinson’s diseases. A progressive neurodegenerative process and neuroinflammation occur, and no current therapies can prevent, slow, or halt disease progression. To date, no novel disease-modifying therapies have been shown to provide significant benefit for patients who suffer from these devastating disorders. Therefore, early diagnosis and the discovery of new targets and novel therapies are of upmost importance. Neurodegenerative diseases, like in other age-related disorders, the progression of pathology begins many years before the onset of symptoms. Many efforts in this field have led to the conclusion that exits some similar events among these diseases that can explain why the aging brain is so vulnerable to suffer neurodegenerative diseases. This article reviews the current knowledge about these diseases by summarizing the most common features of major neurodegenerative disorders, their causes and consequences, and the proposed novel therapeutic approaches.

scholarly journals Cellular Mechanisms of Melatonin: Insight from Neurodegenerative Diseases

Biomolecules ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1158 ◽  
Author(s):  
Dongmei Chen ◽  
Tao Zhang ◽  
Tae Ho Lee
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Cellular Mechanisms ◽  
Wide Range ◽  
Public Health Challenge ◽  
Cumulative Evidence ◽  
The Brain ◽  
Lateral Sclerosis

Neurodegenerative diseases are the second most common cause of death and characterized by progressive impairments in movement or mental functioning in the central or peripheral nervous system. The prevention of neurodegenerative disorders has become an emerging public health challenge for our society. Melatonin, a pineal hormone, has various physiological functions in the brain, including regulating circadian rhythms, clearing free radicals, inhibiting biomolecular oxidation, and suppressing neuroinflammation. Cumulative evidence indicates that melatonin has a wide range of neuroprotective roles by regulating pathophysiological mechanisms and signaling pathways. Moreover, melatonin levels are decreased in patients with neurodegenerative diseases. In this review, we summarize current knowledge on the regulation, molecular mechanisms and biological functions of melatonin in neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, vascular dementia and multiple sclerosis. We also discuss the clinical application of melatonin in neurodegenerative disorders. This information will lead to a better understanding of the regulation of melatonin in the brain and provide therapeutic options for the treatment of various neurodegenerative diseases.

scholarly journals Human Monocytes Plasticity in Neurodegeneration

Biomedicines ◽  
2021 ◽  
Vol 9 (7) ◽  
pp. 717
Author(s):  
Ilenia Savinetti ◽  
Angela Papagna ◽  
Maria Foti
Keyword(s):  
Neurodegenerative Disorders ◽  
Current Knowledge ◽  
Neurological Diseases ◽  
Surface Marker ◽  
First Line ◽  
Surface Marker Expression ◽  
Physiological Properties ◽  
Attractive Therapeutic Target ◽  
The Brain ◽  
Lateral Sclerosis

Monocytes play a crucial role in immunity and tissue homeostasis. They constitute the first line of defense during the inflammatory process, playing a role in the pathogenesis and progression of diseases, making them an attractive therapeutic target. They are heterogeneous in morphology and surface marker expression, which suggest different molecular and physiological properties. Recent evidences have demonstrated their ability to enter the brain, and, as a consequence, their hypothetical role in different neurodegenerative diseases. In this review, we will discuss the current knowledge about the correlation between monocyte dysregulation in the brain and/or in the periphery and neurological diseases in humans. Here we will focus on the most common neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and multiple sclerosis.

scholarly journals Neuroinflammation in neurodegenerative disorders: the roles of microglia and astrocytes

2020 ◽  
Vol 9 (1) ◽  
Author(s):  
Hyuk Sung Kwon ◽  
Seong-Ho Koh
Keyword(s):  
Central Nervous System ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Inflammatory Responses ◽  
Therapeutic Drugs ◽  
M1 Phenotype ◽  
The Central Nervous System ◽  
The Relationship ◽  
Lateral Sclerosis ◽  
M2 Phenotype

AbstractNeuroinflammation is associated with neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Microglia and astrocytes are key regulators of inflammatory responses in the central nervous system. The activation of microglia and astrocytes is heterogeneous and traditionally categorized as neurotoxic (M1-phenotype microglia and A1-phenotype astrocytes) or neuroprotective (M2-phenotype microglia and A2-phenotype astrocytes). However, this dichotomized classification may not reflect the various phenotypes of microglia and astrocytes. The relationship between these activated glial cells is also very complicated, and the phenotypic distribution can change, based on the progression of neurodegenerative diseases. A better understanding of the roles of microglia and astrocytes in neurodegenerative diseases is essential for developing effective therapies. In this review, we discuss the roles of inflammatory response in neurodegenerative diseases, focusing on the contributions of microglia and astrocytes and their relationship. In addition, we discuss biomarkers to measure neuroinflammation and studies on therapeutic drugs that can modulate neuroinflammation.

Traumatic brain injury: a risk factor for neurodegenerative diseases

2016 ◽  
Vol 27 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Rajaneesh Gupta ◽  
Nilkantha Sen
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Chronic Traumatic Encephalopathy ◽  
Disease Process ◽  
Acute Effects ◽  
Secondary Progressive ◽  
Lateral Sclerosis

AbstractTraumatic brain injury (TBI), a major global health and socioeconomic problem, is now established as a chronic disease process with a broad spectrum of pathophysiological symptoms followed by long-term disabilities. It triggers multiple and multidirectional biochemical events that lead to neurodegeneration and cognitive impairment. Recent studies have presented strong evidence that patients with TBI history have a tendency to develop proteinopathy, which is the pathophysiological feature of neurodegenerative disorders such as Alzheimer disease (AD), chronic traumatic encephalopathy (CTE), and amyotrophic lateral sclerosis (ALS). This review mainly focuses on mechanisms related to AD, CTE, and ALS that are induced after TBI and their relevance to the advancement of these neurodegenerative diseases. This review encompasses acute effects and chronic neurodegenerative consequences after TBI for a better understanding of TBI-induced neuronal death and to design therapies that will effectively treat patients in the primary or secondary progressive stages.

Pesticides and Neurodegenerative Disorders

2017 ◽  
Author(s):  
John W. McBurney
Keyword(s):  
Neurodegenerative Disorders ◽  
Neuronal Degeneration ◽  
Lewy Bodies ◽  
Food Choices ◽  
Medical Professionals ◽  
Mitochondrial Toxicity ◽  
Oxygen Species ◽  
Pesticide Exposures ◽  
Global Population ◽  
Lateral Sclerosis

Neurodegenerative diseases, which are characterized by neuronal degeneration, include Alzheimer disease (AD), Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS). Their worldwide prevalence is increasing as the global population ages. The causes reflect interactions between genetics and environmental factors such as increasing urbanization, industrialization, and widespread use of chemicals, including insecticides, fungicides, and herbicides. Epidemiologic data suggest that exposure to many of these pesticides increases the risk of neurodegeneration. The best-defined mechanism for this association is mitochondrial toxicity resulting in increased reactive oxygen species. In PD and AD, the associated accumulation of aggregates of insoluble, misfolded proteins results in the formation of Lewy bodies and neurofibrillary tangles, respectively. Pesticide exposures can be reduced by modifying food choices and applying integrated pest management in schools, businesses, and homes. Medical professionals can counsel patients about limiting exposure to pesticides and decreasing the risk of neurodegenerative disorders.

Sleep disorders in neurodegenerative diseases other than Parkinson disease and multiple system atrophy

2017 ◽  
Author(s):  
Raffaele Manni ◽  
Michele Terzaghi
Keyword(s):  
Neurodegenerative Diseases ◽  
Sleep Disorders ◽  
Neurodegenerative Disorders ◽  
Sleep Problems ◽  
Lewy Bodies ◽  
Corticobasal Degeneration ◽  
Spinocerebellar Ataxias ◽  
Age Related ◽  
Key Points ◽  
Sleep Alterations

This chapter examines sleep–wake disturbances occurring in the most common neurodegenerative disorders. It reviews sleep alterations in Alzheimer disease and dementia with Lewy bodies. It also discusses sleep problems in progressive supranuclear palsy, corticobasal degeneration, Huntington disease, and spinocerebellar ataxias. Status dissociatus as an extreme form of sleep alteration in advanced neurodegenerative diseases is also considered. The chapter reviews the key points for the treatment of disrupted sleep in neurodegenerative disorders, with a focus on pharmacological and nonpharmacological interventions to improve sleep continuity. It also summarizes paraphysiological age-related changes in sleep patterns and discusses indications and procedures for clinical and instrumental assessment of sleep disorders in neurodegenerative disorders.

scholarly journals Kynurenic Acid Levels are Increased in the CSF of Alzheimer’s Disease Patients

Biomolecules ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 571 ◽  
Author(s):  
Marta González-Sánchez ◽  
Javier Jiménez ◽  
Arantzazu Narváez ◽  
Desiree Antequera ◽  
Sara Llamas-Velasco ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurodegenerative Disorders ◽  
Healthy Subjects ◽  
Kynurenic Acid ◽  
Kynurenine Pathway ◽  
Healthy Controls ◽  
Specific Increase ◽  
Normal Controls ◽  
Lateral Sclerosis

Kynurenic acid (KYNA) is a product of the tryptophan (TRP) metabolism via the kynurenine pathway (KP). This pathway is activated in neurodegenerative disorders, such as Alzheimer´s disease (AD). KYNA is primarily produced by astrocytes and is considered neuroprotective. Thus, altered KYNA levels may suggest an inflammatory response. Very recently, significant increases in KYNA levels were reported in cerebrospinal fluid (CSF) from AD patients compared with normal controls. In this study, we assessed the accuracy of KYNA in CSF for the classification of patients with AD, cognitively healthy controls, and patients with a variety of other neurodegenerative diseases, including frontotemporal dementia (FTD), amyotrophic lateral sclerosis (ALS), and progressive supranuclear palsy (PSP). Averaged KYNA concentration in CSF was higher in patients with AD when compared with healthy subjects and with all the other differentially diagnosed groups. There were no significant differences in KYNA levels in CSF between any other neurodegenerative groups and controls. These results suggest a specific increase in KYNA concentration in CSF from AD patients not seen in other neurodegenerative diseases.

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