Journal articles on the topic 'Neurodegenerative disease'
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Homma, Hidenori, Hikari Tanaka, Kyota Fujita, and Hitoshi Okazawa. "Necrosis Links Neurodegeneration and Neuroinflammation in Neurodegenerative Disease." International Journal of Molecular Sciences 25, no. 7 (March 24, 2024): 3636. http://dx.doi.org/10.3390/ijms25073636.
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The mechanisms of neuronal cell death in neurodegenerative disease remain incompletely understood, although recent studies have made significant advances. Apoptosis was previously considered to be the only mechanism of neuronal cell death in neurodegenerative diseases. However, recent findings have challenged this dogma, identifying new subtypes of necrotic neuronal cell death. The present review provides an updated summary of necrosis subtypes and discusses their potential roles in neurodegenerative cell death. Among numerous necrosis subtypes, including necroptosis, paraptosis, ferroptosis, and pyroptosis, transcriptional repression-induced atypical cell death (TRIAD) has been identified as a potential mechanism of neuronal cell death. TRIAD is induced by functional deficiency of TEAD-YAP and self-amplifies via the release of HMGB1. TRIAD is a feasible potential mechanism of neuronal cell death in Alzheimer’s disease and other neurodegenerative diseases. In addition to induction of cell death, HMGB1 released during TRIAD activates brain inflammatory responses, which is a potential link between neurodegeneration and neuroinflammation.
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Bakir, Sena, Gizem Catalkaya, Fatma D. Ceylan, Haroon Khan, Burcu Guldiken, Esra Capanoglu, and Mohammad A. Kamal. "Role of Dietary Antioxidants in Neurodegenerative Diseases: Where are We Standing?" Current Pharmaceutical Design 26, no. 7 (March 25, 2020): 714–29. http://dx.doi.org/10.2174/1381612826666200107143619.
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: This review presents the potential effects of dietary antioxidants on neurodegenerative diseases. The relationship between autoimmunity and antioxidants, and their preventive effect on neurodegenerative diseases are evaluated. The driven factors of neurodegeneration and the potential effects of natural antioxidants are summarized for Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, spongiform encephalopathy, Huntington’s disease, and amyotrophic lateral sclerosis. The effect of oxidative stress on neurodegenerative diseases and regulative effect of antioxidants on oxidative balance is discussed. This review provides beneficial information for the possible cure of neurodegenerative diseases with dietary intake of antioxidants.
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Marshall Moscon, Savannah L., and James R. Connor. "HFE Mutations in Neurodegenerative Disease as a Model of Hormesis." International Journal of Molecular Sciences 25, no. 6 (March 15, 2024): 3334. http://dx.doi.org/10.3390/ijms25063334.
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Common variants in the iron regulatory protein HFE contribute to systematically increased iron levels, yet the effects in the brain are not fully characterized. It is commonly believed that iron dysregulation is a key contributor to neurodegenerative disease due to iron’s ability to catalyze reactive oxygen species production. However, whether HFE variants exacerbate or protect against neurodegeneration has been heavily debated. Some claim that mutated HFE exacerbates oxidative stress and neuroinflammation, thus predisposing carriers to neurodegeneration-linked pathologies. However, H63D HFE has also been shown to slow the progression of multiple neurodegenerative diseases and to protect against environmental toxins that cause neurodegeneration. These conflicting results showcase the need to further understand the contribution of HFE variants to neurodegenerative disease heterogeneity. Data from mouse models consistently demonstrate robust neuroprotection against toxins known to increase the risk of neurodegenerative disease. This may represent an adaptive, or hormetic, response to increased iron, which leaves cells better protected against future stressors. This review describes the current research regarding the contribution of HFE variants to neurodegenerative disease prognosis in the context of a hormetic model. To our knowledge, this is the first time that a hormetic model for neurodegenerative disease has been presented.
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Abitbol, Arjuna, Brody Mallard, Evelin Tiralongo, and Joe Tiralongo. "Mushroom Natural Products in Neurodegenerative Disease Drug Discovery." Cells 11, no. 23 (December 6, 2022): 3938. http://dx.doi.org/10.3390/cells11233938.
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The variety of drugs available to treat neurodegenerative diseases is limited. Most of these drug’s efficacy is restricted by individual genetics and disease stages and usually do not prevent neurodegeneration acting long after irreversible damage has already occurred. Thus, drugs targeting the molecular mechanisms underlying subsequent neurodegeneration have the potential to negate symptom manifestation and subsequent neurodegeneration. Neuroinflammation is a common feature of neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis, and is associated with the activation of the NLRP3 inflammasome, which in turn leads to neurodegeneration. Inflammasome activation and oligomerisation is suggested to be a major driver of disease progression occurring in microglia. With several natural products and natural product derivatives currently in clinical trials, mushrooms have been highlighted as a rich and largely untapped source of biologically active compounds in both in vitro and in vivo neurodegenerative disease models, partially supported by successful clinical trial evaluations. Additionally, novel high-throughput methods for the screening of natural product compound libraries are being developed to help accelerate the neurodegenerative disease drug discovery process, targeting neuroinflammation. However, the breadth of research relating to mushroom natural product high-throughput screening is limited, providing an exciting opportunity for further detailed investigations.
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Petrozzi, Lucia, Giulia Ricci, Noemi J. Giglioli, Gabriele Siciliano, and Michelangelo Mancuso. "Mitochondria and Neurodegeneration." Bioscience Reports 27, no. 1-3 (June 13, 2007): 87–104. http://dx.doi.org/10.1007/s10540-007-9038-z.
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Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. However, despite the evidence of morphological, biochemical and molecular abnormalities in mitochondria in various tissues of patients with neurodegenerative disorders, the question “is mitochondrial dysfunction a necessary step in neurodegeneration?” is still unanswered. In this review, we highlight some of the major neurodegenerative disorders (Alzheimer's disease, Parkinson's disease, Amyotrophic lateral sclerosis and Huntington's disease) and discuss the role of the mitochondria in the pathogenetic cascade leading to neurodegeneration.
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Brkic, Marjana, Sriram Balusu, Claude Libert, and Roosmarijn E. Vandenbroucke. "Friends or Foes: Matrix Metalloproteinases and Their Multifaceted Roles in Neurodegenerative Diseases." Mediators of Inflammation 2015 (2015): 1–27. http://dx.doi.org/10.1155/2015/620581.
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Neurodegeneration is a chronic progressive loss of neuronal cells leading to deterioration of central nervous system (CNS) functionality. It has been shown that neuroinflammation precedes neurodegeneration in various neurodegenerative diseases. Matrix metalloproteinases (MMPs), a protein family of zinc-containing endopeptidases, are essential in (neuro)inflammation and might be involved in neurodegeneration. Although MMPs are indispensable for physiological development and functioning of the organism, they are often referred to as double-edged swords due to their ability to also inflict substantial damage in various pathological conditions. MMP activity is strictly controlled, and its dysregulation leads to a variety of pathologies. Investigation of their potential use as therapeutic targets requires a better understanding of their contributions to the development of neurodegenerative diseases. Here, we review MMPs and their roles in neurodegenerative diseases: Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), and multiple sclerosis (MS). We also discuss MMP inhibition as a possible therapeutic strategy to treat neurodegenerative diseases.
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Zhang, Minhua, Guangrui Luo, Yanjiao Zhou, Shaohui Wang, and Zhong Zhong. "Phenotypic Screens Targeting Neurodegenerative Diseases." Journal of Biomolecular Screening 19, no. 1 (August 19, 2013): 1–16. http://dx.doi.org/10.1177/1087057113499777.
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Neurodegenerative diseases affect millions of people worldwide, and the incidences increase as the population ages. Disease-modifying therapy that prevents or slows disease progression is still lacking, making neurodegenerative diseases an area of high unmet medical need. Target-based drug discovery for disease-modifying agents has been ongoing for many years, without much success due to incomplete understanding of the molecular mechanisms underlying neurodegeneration. Phenotypic screening, starting with a disease-relevant phenotype to screen for compounds that change the outcome of biological pathways rather than activities at certain specific targets, offers an alternative approach to find small molecules or targets that modulate the key characteristics of neurodegeneration. Phenotypic screens that focus on amelioration of disease-specific toxins, protection of neurons from degeneration, or promotion of neuroregeneration could be potential fertile grounds for discovering therapeutic agents for neurodegenerative diseases. In this review, we will summarize the progress of compound screening using these phenotypic-based strategies for this area, with a highlight on unique considerations for disease models, assays, and screening methodologies. We will further provide our perspectives on how best to use phenotypic screening to develop drug leads for neurodegenerative diseases.
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Lemieszewska, Marta, Agnieszka Zabłocka, and Joanna Rymaszewska. "Parkinson’s disease: Etiopathogenesis, molecular basis and potential treatment opportunities." Postępy Higieny i Medycyny Doświadczalnej 73 (May 15, 2019): 256–68. http://dx.doi.org/10.5604/01.3001.0013.2021.
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Neurodegenerative diseases affect the life quality and lifespan of aging populations. Among all forms of neurodegenerative diseases, Parkinson’s disease (PD) has a massive impact on the elderly. Oxidative stress and mitochondrial dysfunction are the main causes of neurodegeneration and progression of PD. Oxidative stress, which plays a vital role in the pathophysiology of PD, is related to the dysfunction of cellular antioxidant mechanisms as a result of enhanced production of reactive oxygen species. A large number of studies have utilized oxidative stress biomarkers to investigate the severity of neurodegeneration and medications are available, but these only treat the symptoms. Extensive studies scientifically validated the beneficial effect of natural products against neurodegenerative diseases, using suitable animal models. The review focuses on the role of oxidative stress in the pathogenesis of Parkinson’s disease and the protective potential of natural products against neurodegeneration.
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Belyakin, Sergey, and Sergey Shuteev. "Application of a Time-Delay Model of the Plykin - Newhouse Attractor to Study the Dynamics of Neuro - Degeneration by Electroencephalography of the Brain." Psychology and Mental Health Care 6, no. 2 (January 22, 2022): 01–06. http://dx.doi.org/10.31579/2637-8892/153.
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Neurodegeneration is the progressive loss of structure or function of neurons, which may ultimately involve cell death. Many neurodegenerative diseases-such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, and prion diseases-occur as a result of neurodegenerative processes. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable. Biomedical research has revealed many similarities between these diseases at the sub-cellular level, including atypical protein assemblies (like proteopathy) and induced cell death. These similarities suggest that advances against one neurodegenerative disease might ameliorate other diseases as well. In this report, an autonomous physical system is used, which is represented by a Smale Williams hyperbolic type attractor. Dynamics and evolution of neurodegeneration The Plykin-Newkhoz attractor model with the Piragas method is applied
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Doudet, D. J. "Neurodegenerative Disease." Molecular Imaging and Biology 9, no. 4 (April 20, 2007): 159–60. http://dx.doi.org/10.1007/s11307-007-0099-y.
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Desai, Shyamal, Meredith Juncker, and Catherine Kim. "Regulation of mitophagy by the ubiquitin pathway in neurodegenerative diseases." Experimental Biology and Medicine 243, no. 6 (January 9, 2018): 554–62. http://dx.doi.org/10.1177/1535370217752351.
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Mitophagy is a cellular process by which dysfunctional mitochondria are degraded via autophagy. Increasing empirical evidence proposes that this mitochondrial quality-control mechanism is defective in neurons of patients with various neurodegenerative diseases such as Ataxia Telangiectasia, Alzheimer’s disease, Parkinson’s disease, and Amyotrophic Lateral Sclerosis. Accumulation of defective mitochondria and the production of reactive oxygen species due to defective mitophagy have been identified as causes underlying neurodegenerative disease pathogenesis. However, the reason mitophagy is defective in most neurodegenerative diseases is unclear. Like mitophagy, defects in the ubiquitin/26S proteasome pathway have been linked to neurodegeneration, resulting in the characteristic protein aggregates often seen in neurons of affected patients. Although initiation of mitophagy requires a functional ubiquitin pathway, whether defects in the ubiquitin pathway are causally responsible for defective mitophagy is not known. In this mini-review, we introduce mitophagy and ubiquitin pathways and provide a summary of our current understanding of the regulation of mitophagy by the ubiquitin pathway. We will then briefly review empirical evidence supporting mitophagy defects in neurodegenerative diseases. The review will conclude with a discussion of the constitutively elevated expression of ubiquitin-like protein Interferon-Stimulated Gene 15 (ISG15), an antagonist of the ubiquitin pathway, as a potential cause of defective mitophagy in neurodegenerative diseases. Impact statement Neurodegenerative diseases place an enormous burden on patients and caregivers globally. Over six million people in the United States alone suffer from neurodegenerative diseases, all of which are chronic, incurable, and with causes unknown. Identifying a common molecular mechanism underpinning neurodegenerative disease pathology is urgently needed to aid in the design of effective therapies to ease suffering, reduce economic cost, and improve the quality of life for these patients. Although the development of neurodegeneration may vary between neurodegenerative diseases, they have common cellular hallmarks, including defects in the ubiquitin-proteasome system and mitophagy. In this review, we will provide a summary of our current understanding of the regulation of mitophagy by the ubiquitin pathway and discuss the potential of targeting mitophagy and ubiquitin pathways for the treatment of neurodegeneration.
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Coppedè, Fabio, Michelangelo Mancuso, Gabriele Siciliano, Lucia Migliore, and Luigi Murri. "Genes and the Environment in Neurodegeneration." Bioscience Reports 26, no. 5 (November 9, 2006): 341–67. http://dx.doi.org/10.1007/s10540-006-9028-6.
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Neurodegenerative diseases are a heterogeneous group of pathologies which includes complex multifactorial diseases, monogenic disorders and disorders for which inherited, sporadic and transmissible forms are known. Factors associated with predisposition and vulnerability to neurodegenerative disorders may be described usefully within the context of gene–environment interplay. There are many identified genetic determinants for neurodegeneration, and it is possible to duplicate many elements of recognized human neurodegenerative disorders in animal models of the disease. However, there are similarly several identifiable environmental influences on outcomes of the genetic defects; and the course of a progressive neurodegenerative disorder can be greatly modified by environmental elements. In this review we highlight some of the major neurodegenerative disorders (Alzheimer's disease, Parkinson's disease, Amyotrophic lateral sclerosis, Huntington's disease, and prion diseases.) and discuss possible links of gene–environment interplay including, where implicated, mitochondrial genes.
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Juranek, Judyta, Rashmi Ray, Marta Banach, and Vivek Rai. "Receptor for advanced glycation end-products in neurodegenerative diseases." Reviews in the Neurosciences 26, no. 6 (December 1, 2015): 691–98. http://dx.doi.org/10.1515/revneuro-2015-0003.
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AbstractThis review, for the first time, aims to summarize the current knowledge in the emerging field of RAGE (receptor for advanced glycation end-products) studies in neurodegeneration and neurodegenerative diseases. RAGE, a member of the multiligand cell surface immunoglobulin family, has been implicated in numerous pathological conditions – from diabetes and cardiovascular diseases to tumors and neurodegenerative disorders, such as Alzheimer’s disease, familial amyloid polyneuropathy, diabetic neuropathy, Parkinson’s disease, and Huntington’s disease. Until now, the detailed mechanisms of the contribution of RAGE to neurodegeneration remain elusive; however, mounting evidence suggests that its detrimental actions are triggered by its ligand interactions and contribute to increased neuroinflammation, neuronal degeneration, and apoptosis. Deciphering the role of RAGE in neurodegenerative disorders will be a milestone in our basic understanding of the mechanisms involved in the pathogenesis of neurodegeneration, helping to delineate molecular links between complex RAGE signaling pathways and neuronal dysfunction and neurodegeneration.
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Rezak, Michael, and Mamede de Carvalho. "Disease modification in neurodegenerative diseases." Neurology 94, no. 1 (December 2, 2019): 12–13. http://dx.doi.org/10.1212/wnl.0000000000008690.
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Tchekalarova, Jana, and Rumiana Tzoneva. "Oxidative Stress and Aging as Risk Factors for Alzheimer’s Disease and Parkinson’s Disease: The Role of the Antioxidant Melatonin." International Journal of Molecular Sciences 24, no. 3 (February 3, 2023): 3022. http://dx.doi.org/10.3390/ijms24033022.
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Aging and neurodegenerative diseases share common hallmarks, including mitochondrial dysfunction and protein aggregation. Moreover, one of the major issues of the demographic crisis today is related to the progressive rise in costs for care and maintenance of the standard living condition of aged patients with neurodegenerative diseases. There is a divergence in the etiology of neurodegenerative diseases. Still, a disturbed endogenous pro-oxidants/antioxidants balance is considered the crucial detrimental factor that makes the brain vulnerable to aging and progressive neurodegeneration. The present review focuses on the complex relationships between oxidative stress, autophagy, and the two of the most frequent neurodegenerative diseases associated with aging, Alzheimer’s disease (AD) and Parkinson’s disease (PD). Most of the available data support the hypothesis that a disturbed antioxidant defense system is a prerequisite for developing pathogenesis and clinical symptoms of ADs and PD. Furthermore, the release of the endogenous hormone melatonin from the pineal gland progressively diminishes with aging, and people’s susceptibility to these diseases increases with age. Elucidation of the underlying mechanisms involved in deleterious conditions predisposing to neurodegeneration in aging, including the diminished role of melatonin, is important for elaborating precise treatment strategies for the pathogenesis of AD and PD.
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Hrelia, Patrizia, Giulia Sita, Marina Ziche, Emma Ristori, Angela Marino, Marika Cordaro, Raffaella Molteni, et al. "Common Protective Strategies in Neurodegenerative Disease: Focusing on Risk Factors to Target the Cellular Redox System." Oxidative Medicine and Cellular Longevity 2020 (August 3, 2020): 1–18. http://dx.doi.org/10.1155/2020/8363245.
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Neurodegenerative disease is an umbrella term for different conditions which primarily affect the neurons in the human brain. In the last century, significant research has been focused on mechanisms and risk factors relevant to the multifaceted etiopathogenesis of neurodegenerative diseases. Currently, neurodegenerative diseases are incurable, and the treatments available only control the symptoms or delay the progression of the disease. This review is aimed at characterizing the complex network of molecular mechanisms underpinning acute and chronic neurodegeneration, focusing on the disturbance in redox homeostasis, as a common mechanism behind five pivotal risk factors: aging, oxidative stress, inflammation, glycation, and vascular injury. Considering the complex multifactorial nature of neurodegenerative diseases, a preventive strategy able to simultaneously target multiple risk factors and disease mechanisms at an early stage is most likely to be effective to slow/halt the progression of neurodegenerative diseases.
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Talan, Jamie. "Disease Mechanisms-Neurodegenerative Disease." Neurology Today 18, no. 16 (August 2018): 1. http://dx.doi.org/10.1097/01.nt.0000544621.18582.bc.
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Talan, Jamie. "Disease Mechanisms-Neurodegenerative Disease." Neurology Today 18, no. 19 (October 2018): 51–53. http://dx.doi.org/10.1097/01.nt.0000547371.17110.51.
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Nimmo, Jacqui, Robert A. J. Byrne, Nikoleta Daskoulidou, Lewis M. Watkins, Sarah M. Carpanini, Wioleta M. Zelek, and B. Paul Morgan. "The complement system in neurodegenerative diseases." Clinical Science 138, no. 6 (March 2024): 387–412. http://dx.doi.org/10.1042/cs20230513.
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Abstract Complement is an important component of innate immune defence against pathogens and crucial for efficient immune complex disposal. These core protective activities are dependent in large part on properly regulated complement-mediated inflammation. Dysregulated complement activation, often driven by persistence of activating triggers, is a cause of pathological inflammation in numerous diseases, including neurological diseases. Increasingly, this has become apparent not only in well-recognized neuroinflammatory diseases like multiple sclerosis but also in neurodegenerative and neuropsychiatric diseases where inflammation was previously either ignored or dismissed as a secondary event. There is now a large and rapidly growing body of evidence implicating complement in neurological diseases that cannot be comprehensively addressed in a brief review. Here, we will focus on neurodegenerative diseases, including not only the ‘classical’ neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, but also two other neurological diseases where neurodegeneration is a neglected feature and complement is implicated, namely, schizophrenia, a neurodevelopmental disorder with many mechanistic features of neurodegeneration, and multiple sclerosis, a demyelinating disorder where neurodegeneration is a major cause of progressive decline. We will discuss the evidence implicating complement as a driver of pathology in these diverse diseases and address briefly the potential and pitfalls of anti-complement drug therapy for neurodegenerative diseases.
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Stoklund Dittlau, Katarina, and Kristine Freude. "Astrocytes: The Stars in Neurodegeneration?" Biomolecules 14, no. 3 (February 28, 2024): 289. http://dx.doi.org/10.3390/biom14030289.
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Today, neurodegenerative disorders like Alzheimer’s disease (AD), Parkinson’s disease (PD), frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS) affect millions of people worldwide, and as the average human lifespan increases, similarly grows the number of patients. For many decades, cognitive and motoric decline has been explained by the very apparent deterioration of neurons in various regions of the brain and spinal cord. However, more recent studies show that disease progression is greatly influenced by the vast population of glial cells. Astrocytes are traditionally considered star-shaped cells on which neurons rely heavily for their optimal homeostasis and survival. Increasing amounts of evidence depict how astrocytes lose their supportive functions while simultaneously gaining toxic properties during neurodegeneration. Many of these changes are similar across various neurodegenerative diseases, and in this review, we highlight these commonalities. We discuss how astrocyte dysfunction drives neuronal demise across a wide range of neurodegenerative diseases, but rather than categorizing based on disease, we aim to provide an overview based on currently known mechanisms. As such, this review delivers a different perspective on the disease causes of neurodegeneration in the hope to encourage further cross-disease studies into shared disease mechanisms, which might ultimately disclose potentially common therapeutic entry points across a wide panel of neurodegenerative diseases.
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Mohd Sairazi, Nur Shafika, and K. N. S. Sirajudeen. "Natural Products and Their Bioactive Compounds: Neuroprotective Potentials against Neurodegenerative Diseases." Evidence-Based Complementary and Alternative Medicine 2020 (February 14, 2020): 1–30. http://dx.doi.org/10.1155/2020/6565396.
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In recent years, natural products, which originate from plants, animals, and fungi, together with their bioactive compounds have been intensively explored and studied for their therapeutic potentials for various diseases such as cardiovascular, diabetes, hypertension, reproductive, cancer, and neurodegenerative diseases. Neurodegenerative diseases, including Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis are characterized by the progressive dysfunction and loss of neuronal structure and function that resulted in the neuronal cell death. Since the multifactorial pathological mechanisms are associated with neurodegeneration, targeting multiple mechanisms of actions and neuroprotection approach, which involves preventing cell death and restoring the function to damaged neurons, could be promising strategies for the prevention and therapeutic of neurodegenerative diseases. Natural products have emerged as potential neuroprotective agents for the treatment of neurodegenerative diseases. This review focused on the therapeutic potential of natural products and their bioactive compounds to exert a neuroprotective effect on the pathologies of neurodegenerative diseases.
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Oizumi, Hideki, Yoko Sugimura, Tomoko Totsune, Iori Kawasaki, Saki Ohshiro, Toru Baba, Teiko Kimpara, et al. "Plasma sphingolipid abnormalities in neurodegenerative diseases." PLOS ONE 17, no. 12 (December 16, 2022): e0279315. http://dx.doi.org/10.1371/journal.pone.0279315.
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Background In recent years, there has been increasing evidence that several lipid metabolism abnormalities play an important role in the pathogenesis of neurodegenerative diseases. However, it is still unclear which lipid metabolism abnormalities play the most important role in neurodegenerative diseases. Plasma lipid metabolomics (lipidomics) has been shown to be an unbiased method that can be used to explore lipid metabolism abnormalities in neurodegenerative diseases. Plasma lipidomics in neurodegenerative diseases has been performed only in idiopathic Parkinson’s disease (IPD) and Alzheimer’s disease (AD), and comprehensive studies are needed to clarify the pathogenesis. Methods In this study, we investigated plasma lipids using lipidomics in individuals with neurodegenerative diseases and healthy controls (CNs). Plasma lipidomics was evaluated by liquid chromatography-tandem mass spectrometry (LC–MS/MS) in those with IPD, dementia with Lewy bodies (DLB), multiple system atrophy (MSA), AD, and progressive supranuclear palsy (PSP) and CNs. Results The results showed that (1) plasma sphingosine-1-phosphate (S1P) was significantly lower in all neurodegenerative disease groups (IPD, DLB, MSA, AD, and PSP) than in the CN group. (2) Plasma monohexylceramide (MonCer) and lactosylceramide (LacCer) were significantly higher in all neurodegenerative disease groups (IPD, DLB, MSA, AD, and PSP) than in the CN group. (3) Plasma MonCer levels were significantly positively correlated with plasma LacCer levels in all enrolled groups. Conclusion S1P, Glucosylceramide (GlcCer), the main component of MonCer, and LacCer are sphingolipids that are biosynthesized from ceramide. Recent studies have suggested that elevated GlcCer and decreased S1P levels in neurons are related to neuronal cell death and that elevated LacCer levels induce neurodegeneration by neuroinflammation. In the present study, we found decreased plasma S1P levels and elevated plasma MonCer and LacCer levels in those with neurodegenerative diseases, which is a new finding indicating the importance of abnormal sphingolipid metabolism in neurodegeneration.
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Mendsaikhan, Anarmaa, Ikuo Tooyama, and Douglas G. Walker. "Microglial Progranulin: Involvement in Alzheimer’s Disease and Neurodegenerative Diseases." Cells 8, no. 3 (March 11, 2019): 230. http://dx.doi.org/10.3390/cells8030230.
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Neurodegenerative diseases such as Alzheimer’s disease have proven resistant to new treatments. The complexity of neurodegenerative disease mechanisms can be highlighted by accumulating evidence for a role for a growth factor, progranulin (PGRN). PGRN is a glycoprotein encoded by the GRN/Grn gene with multiple cellular functions, including neurotrophic, anti-inflammatory and lysosome regulatory properties. Mutations in the GRN gene can lead to frontotemporal lobar degeneration (FTLD), a cause of dementia, and neuronal ceroid lipofuscinosis (NCL), a lysosomal storage disease. Both diseases are associated with loss of PGRN function resulting, amongst other features, in enhanced microglial neuroinflammation and lysosomal dysfunction. PGRN has also been implicated in Alzheimer’s disease (AD). Unlike FTLD, increased expression of PGRN occurs in brains of human AD cases and AD model mice, particularly in activated microglia. How microglial PGRN might be involved in AD and other neurodegenerative diseases will be discussed. A unifying feature of PGRN in diseases might be its modulation of lysosomal function in neurons and microglia. Many experimental models have focused on consequences of PGRN gene deletion: however, possible outcomes of increasing PGRN on microglial inflammation and neurodegeneration will be discussed. We will also suggest directions for future studies on PGRN and microglia in relation to neurodegenerative diseases.
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Bi, Mingxia, Chang Liu, Yulin Wang, and Shuang-Jiang Liu. "Therapeutic Prospect of New Probiotics in Neurodegenerative Diseases." Microorganisms 11, no. 6 (June 8, 2023): 1527. http://dx.doi.org/10.3390/microorganisms11061527.
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Increasing clinical and preclinical evidence implicates gut microbiome (GM) dysbiosis as a key susceptibility factor for neurodegenerative disorders, including Alzheimer’s disease (AD) and Parkinson’s disease (PD). In recent years, neurodegenerative diseases have been viewed as being driven not solely by defects in the brain, and the role of GM in modulating central nervous system function via the gut–brain axis has attracted considerable interest. Encouraged by current GM research, the development of new probiotics may lead to tangible impacts on the treatment of neurodegenerative disorders. This review summarizes current understandings of GM composition and characteristics associated with neurodegenerative diseases and research demonstrations of key molecules from the GM that affect neurodegeneration. Furthermore, applications of new probiotics, such as Clostridium butyricum, Akkermansia muciniphila, Faecalibacterium prausnitzii, and Bacteroides fragilis, for the remediation of neurodegenerative diseases are discussed.
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Prajapati, Anil Kumar, Akshmita Gairola, and Mustakim Mansuri. "Insulin resistance and neurodegenerative diseases." IP International Journal of Comprehensive and Advanced Pharmacology 9, no. 2 (June 15, 2024): 87–90. http://dx.doi.org/10.18231/j.ijcaap.2024.013.
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Insulin resistance is a condition where normal or elevated insulin levels fail to elicit the expected biological response, with significant implications for neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). Despite extensive research, the precise cellular mechanisms driving insulin resistance and its role in neurodegeneration remain elusive. Insights into insulin signaling dysregulation, amyloid-beta accumulation, neuroinflammation, and impaired mitochondrial function shed light on the complex interplay between insulin resistance and neurodegeneration. Various therapeutic strategies targeting insulin resistance, including insulin interventions, GLP-1 analogs, intranasal insulin, and lifestyle interventions, offer promising avenues for mitigating disease progression. This review provides a comprehensive overview of insulin resistance and its association with neurodegenerative disorders, highlighting key molecular and cellular insights, therapeutic approaches, and future directions.
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Murai, Toshiyuki, and Satoru Matsuda. "Integrated Multimodal Omics and Dietary Approaches for the Management of Neurodegeneration." Epigenomes 7, no. 3 (September 1, 2023): 20. http://dx.doi.org/10.3390/epigenomes7030020.
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Neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease, are caused by a combination of multiple events that damage neuronal function. A well-characterized biomarker of neurodegeneration is the accumulation of proteinaceous aggregates in the brain. However, the gradually worsening symptoms of neurodegenerative diseases are unlikely to be solely due to the result of a mutation in a single gene, but rather a multi-step process involving epigenetic changes. Recently, it has been suggested that a fraction of epigenetic alternations may be correlated to neurodegeneration in the brain. Unlike DNA mutations, epigenetic alterations are reversible, and therefore raise the possibilities for therapeutic intervention, including dietary modifications. Additionally, reactive oxygen species may contribute to the pathogenesis of Alzheimer’s disease and Parkinson’s disease through epigenetic alternation. Given that the antioxidant properties of plant-derived phytochemicals are likely to exhibit pleiotropic effects against ROS-mediated epigenetic alternation, dietary intervention may be promising for the management of neurodegeneration in these diseases. In this review, the state-of-the-art applications using single-cell multimodal omics approaches, including epigenetics, and dietary approaches for the identification of novel biomarkers and therapeutic approaches for the treatment of neurodegenerative diseases are discussed.
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Winter, Aimee N., and Paula C. Bickford. "Anthocyanins and Their Metabolites as Therapeutic Agents for Neurodegenerative Disease." Antioxidants 8, no. 9 (August 22, 2019): 333. http://dx.doi.org/10.3390/antiox8090333.
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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.
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Bolus, Harris, Kassi Crocker, Grace Boekhoff-Falk, and Stanislava Chtarbanova. "Modeling Neurodegenerative Disorders in Drosophila melanogaster." International Journal of Molecular Sciences 21, no. 9 (April 26, 2020): 3055. http://dx.doi.org/10.3390/ijms21093055.
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Drosophila melanogaster provides a powerful genetic model system in which to investigate the molecular mechanisms underlying neurodegenerative diseases. In this review, we discuss recent progress in Drosophila modeling Alzheimer’s Disease, Parkinson’s Disease, Amyotrophic Lateral Sclerosis (ALS), Huntington’s Disease, Ataxia Telangiectasia, and neurodegeneration related to mitochondrial dysfunction or traumatic brain injury. We close by discussing recent progress using Drosophila models of neural regeneration and how these are likely to provide critical insights into future treatments for neurodegenerative disorders.
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Vyawhare, Puja G., Gayatri M. Ahire, Neelam M. Yadav, and Dr Rupali R. Tasgaonkar. "Neurodegenerative Disorder." International Journal for Research in Applied Science and Engineering Technology 11, no. 4 (April 30, 2023): 824–28. http://dx.doi.org/10.22214/ijraset.2023.50032.
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Abstract: Neurodegenerative disorders of the nervous System that Can primarily Characterized by neuron loss. Neurodegenerative diseases Such as Alzheimer, parkinson, Huntington, Amyotrophic lateral sclerosis and Multiple sclerosis are known as Lou Gehrig's disease.The huge body of evidence disorders arise by multifactorial conditions. Alzheimer's and parkinson's disease are most common neurodegenretive disorder. It includes generation of New neurons, the Phenotypic level of essential functions: Sensory & motor, and congnitive abilities. The therapeutic interventions directed toward treatement of these Neurodegenerative diseases. Multiple sclerosis is treated manly immune - suppressers, speed of recovery from relapse and slow down the disease. The neurodegenretive disease have a some therapies like a steam therapy, gene transfer therepy, and the multitarget directed ligands has promising to find new therapies for neurodegenerative disorder , in the Nanotechnology have a great potential for neurotheraputic modalities. The nanomedicines administer from several routes like olfactory, oral and 4 systemic etc. The brain there is the one or more targeting changes for the diseae modifying treatement that is slow disease progression in the Alzheimer’s disease , in the Amyotrophic lateral sclerosis Antisense treatement in the development to reduce superoxide dismutase and the huntington’s disease are monoconal antibody in development to blocked the Semaphorin 4D.
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Joseph, JT. "The Amygdala in Neurodegeneration." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 48, s1 (May 2021): S5—S6. http://dx.doi.org/10.1017/cjn.2021.97.
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The amygdala is a key anatomic structure that has multiple different nuclei and is involved in several critical aspects of cognition and systemic functions. Several different neurodegenerative diseases have major pathological effects on distinct amygdala nuclei. This presentation will describe the classic and characteristic anatomic distributions in the amygdala of “pure” Alzheimer disease and “pure” Lewy body disease, as well as “normal aging”. In addition, data will be presented on how these classic distributions are altered in either “mixed dementias” or in some atypical forms of neurodegeneration. Amygdala pathology will also be illustrated in several other neurodegenerative diseases. The implications of the differing anatomic distributions in different neurodegenerative diseases will be discussed.LEARNING OBJECTIVESThis presentation will enable the learner to:Recognize key anatomic divisions of the amygdala 1.Describe how different neurodegenerative diseases affect the amygdala2.Consider how anatomic specificity of protein aggregation is important in the classification of neurodegenerative diseases
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Kong, Yew Rong, Kai Ching Tay, Yi Xiang Su, Choon Kwang Wong, Wen Nee Tan, and Kooi Yeong Khaw. "Potential of Naturally Derived Alkaloids as Multi-Targeted Therapeutic Agents for Neurodegenerative Diseases." Molecules 26, no. 3 (January 30, 2021): 728. http://dx.doi.org/10.3390/molecules26030728.
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Alkaloids are a class of secondary metabolites that can be derived from plants, fungi and marine sponges. They are widely known as a continuous source of medicine for the management of chronic disease including cancer, diabetes and neurodegenerative diseases. For example, galanthamine and huperzine A are alkaloid derivatives currently being used for the symptomatic management of neurodegenerative disease. The etiology of neurodegenerative diseases is polygenic and multifactorial including but not limited to inflammation, oxidative stress and protein aggregation. Therefore, natural-product-based alkaloids with polypharmacology modulation properties are potentially useful for further drug development or, to a lesser extent, as nutraceuticals to manage neurodegeneration. This review aims to discuss and summarise recent developments in relation to naturally derived alkaloids for neurodegenerative diseases.
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Adler, Gabrielle L., Kelvin Le, YuHong Fu, and Woojin Scott Kim. "Human Endogenous Retroviruses in Neurodegenerative Diseases." Genes 15, no. 6 (June 5, 2024): 745. http://dx.doi.org/10.3390/genes15060745.
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Human endogenous retroviruses (HERVs) are DNA transposable elements that have integrated into the human genome via an ancestral germline infection. The potential importance of HERVs is underscored by the fact that they comprise approximately 8% of the human genome. HERVs have been implicated in the pathogenesis of neurodegenerative diseases, a group of CNS diseases characterized by a progressive loss of structure and function of neurons, resulting in cell death and multiple physiological dysfunctions. Much evidence indicates that HERVs are initiators or drivers of neurodegenerative processes in multiple sclerosis and amyotrophic lateral sclerosis, and clinical trials have been designed to target HERVs. In recent years, the role of HERVs has been explored in other major neurodegenerative diseases, including frontotemporal dementia, Alzheimer’s disease and Parkinson’s disease, with some interesting discoveries. This review summarizes and evaluates the past and current research on HERVs in neurodegenerative diseases. It discusses the potential role of HERVs in disease manifestation and neurodegeneration. It critically reviews antiretroviral strategies used in the therapeutic intervention of neurodegenerative diseases.
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Jo, Seong-Lae, Hyun Yang, Kang-Joo Jeong, Hye-Won Lee, and Eui-Ju Hong. "Neuroprotective Effects of Ecklonia cava in a Chronic Neuroinflammatory Disease Model." Nutrients 15, no. 8 (April 21, 2023): 2007. http://dx.doi.org/10.3390/nu15082007.
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Inflammation is a natural defense mechanism against noxious stimuli, but chronic inflammation can lead to various chronic diseases. Neuroinflammation in the central nervous system plays an important role in the development and progression of neurodegenerative diseases. Polyphenol-rich natural products, such as Ecklonia cava (E. cava), are known to have anti-inflammatory and antioxidant properties and can provide treatment strategies for neurodegenerative diseases by controlling neuroinflammation. We investigated the effects of an E. cava extract on neuroinflammation and neurodegeneration under chronic inflammatory conditions. Mice were pretreated with E. cava extract for 19 days and then exposed to E. cava with lipopolysaccharide (LPS) for 1 week. We monitored pro-inflammatory cytokines levels in the serum, inflammation-related markers, and neurodegenerative markers using Western blotting and qRT-PCR in the mouse cerebrum and hippocampus. E. cava reduced pro-inflammatory cytokine levels in the blood and brain of mice with LPS-induced chronic inflammation. We also measured the activity of genes related to neuroinflammation and neurodegeneration. Surprisingly, E. cava decreased the activity of markers associated with inflammation (NF-kB and STAT3) and a neurodegenerative disease marker (glial fibrillary acidic protein, beta-amyloid) in the cerebrum and hippocampus of mice. We suggest that E. cava extract has the potential as a protective agent against neuroinflammation and neurodegenerative diseases.
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Fischer, Roman, and Olaf Maier. "Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–18. http://dx.doi.org/10.1155/2015/610813.
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Neuroinflammation and mitochondrial dysfunction are common features of chronic neurodegenerative diseases of the central nervous system. Both conditions can lead to increased oxidative stress by excessive release of harmful reactive oxygen and nitrogen species (ROS and RNS), which further promote neuronal damage and subsequent inflammation resulting in a feed-forward loop of neurodegeneration. The cytokine tumor necrosis factor (TNF), a master regulator of the immune system, plays an important role in the propagation of inflammation due to the activation and recruitment of immune cells via its receptor TNF receptor 1 (TNFR1). Moreover, TNFR1 can directly induce oxidative stress by the activation of ROS and RNS producing enzymes. Both TNF-induced oxidative stress and inflammation interact and cooperate to promote neurodegeneration. However, TNF plays a dual role in neurodegenerative disease, since stimulation via its second receptor, TNFR2, is neuroprotective and promotes tissue regeneration. Here we review the interrelation of oxidative stress and inflammation in the two major chronic neurodegenerative diseases, Alzheimer’s and Parkinson’s disease, and discuss the dual role of TNF in promoting neurodegeneration and tissue regeneration via its two receptors.
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de Paula, Caroline Zocatelli, Bruno Daniel Correia Gonçalves, and Luciene Bruno Vieira. "An Overview of Potential Targets for Treating Amyotrophic Lateral Sclerosis and Huntington’s Disease." BioMed Research International 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/198612.
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Neurodegenerative diseases affect millions of people worldwide. Progressive damage or loss of neurons, neurodegeneration, has severe consequences on the mental and physical health of a patient. Despite all efforts by scientific community, there is currently no cure or manner to slow degeneration progression. We review some treatments that attempt to prevent the progress of some of major neurodegenerative diseases: Amyotrophic Lateral Sclerosis and Huntington’s disease.
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Limongi, Dolores, and Sara Baldelli. "Redox Imbalance and Viral Infections in Neurodegenerative Diseases." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/6547248.
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Reactive oxygen species (ROS) are essential molecules for many physiological functions and act as second messengers in a large variety of tissues. An imbalance in the production and elimination of ROS is associated with human diseases including neurodegenerative disorders. In the last years the notion that neurodegenerative diseases are accompanied by chronic viral infections, which may result in an increase of neurodegenerative diseases progression, emerged. It is known in literature that enhanced viral infection risk, observed during neurodegeneration, is partly due to the increase of ROS accumulation in brain cells. However, the molecular mechanisms of viral infection, occurring during the progression of neurodegeneration, remain unclear. In this review, we discuss the recent knowledge regarding the role of influenza, herpes simplex virus type-1, and retroviruses infection in ROS/RNS-mediated Parkinson’s disease (PD), Alzheimer’s disease (AD), and amyotrophic lateral sclerosis (ALS).
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Li, Bei, Meiling Chen, and Caihong Zhu. "Neuroinflammation in Prion Disease." International Journal of Molecular Sciences 22, no. 4 (February 23, 2021): 2196. http://dx.doi.org/10.3390/ijms22042196.
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Neuroinflammation, typically manifest as microglial activation and astrogliosis accompanied by transcriptomic alterations, represents a common hallmark of various neurodegenerative conditions including prion diseases. Microglia play an overall neuroprotective role in prion disease, whereas reactive astrocytes with aberrant phenotypes propagate prions and contribute to prion-induced neurodegeneration. The existence of heterogeneous subpopulations and dual functions of microglia and astrocytes in prion disease make them potential targets for therapeutic intervention. A variety of neuroinflammation-related molecules are involved in prion pathogenesis. Therapeutics targeting neuroinflammation represents a novel approach to combat prion disease. Deciphering neuroinflammation in prion disease will deepen our understanding of pathogenesis of other neurodegenerative disorders.
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Carvalho Piasentim, Joao Vitor, and Samya Nogueira Asseiss. "The Role of MicroRNAs in regulating genes related to neurodegenerative diseases." International Journal of Molecular Biology Open Access 7, no. 1 (July 1, 2024): 81–82. http://dx.doi.org/10.15406/ijmboa.2024.07.00174.
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Neurodegenerative diseases pose significant challenges to public health worldwide. MicroRNAs (miRNAs) have emerged as critical regulators of gene expression and are implicated in the pathogenesis of various neurodegenerative disorders. This review comprehensively explores the current understanding of how miRNAs influence gene networks involved in Alzheimer disease, Parkinson disease and amyotrophic lateral sclerosis. We discuss the mechanisms by which miRNAs modulate disease associated genes, their potential as diagnostic biomarkers, and therapeutic targets in neurodegeneration.
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Sarparast, Morteza, Devon Dattmore, Jamie Alan, and Kin Sing Stephen Lee. "Cytochrome P450 Metabolism of Polyunsaturated Fatty Acids and Neurodegeneration." Nutrients 12, no. 11 (November 16, 2020): 3523. http://dx.doi.org/10.3390/nu12113523.
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Due to the aging population in the world, neurodegenerative diseases have become a serious public health issue that greatly impacts patients’ quality of life and adds a huge economic burden. Even after decades of research, there is no effective curative treatment for neurodegenerative diseases. Polyunsaturated fatty acids (PUFAs) have become an emerging dietary medical intervention for health maintenance and treatment of diseases, including neurodegenerative diseases. Recent research demonstrated that the oxidized metabolites, particularly the cytochrome P450 (CYP) metabolites, of PUFAs are beneficial to several neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease; however, their mechanism(s) remains unclear. The endogenous levels of CYP metabolites are greatly affected by our diet, endogenous synthesis, and the downstream metabolism. While the activity of omega-3 (ω-3) CYP PUFA metabolites and omega-6 (ω-6) CYP PUFA metabolites largely overlap, the ω-3 CYP PUFA metabolites are more active in general. In this review, we will briefly summarize recent findings regarding the biosynthesis and metabolism of CYP PUFA metabolites. We will also discuss the potential mechanism(s) of CYP PUFA metabolites in neurodegeneration, which will ultimately improve our understanding of how PUFAs affect neurodegeneration and may identify potential drug targets for neurodegenerative diseases.
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Nainu, Firzan, Emil Salim, Rangga Meidianto Asri, Aki Hori, and Takayuki Kuraishi. "Neurodegenerative disorders and sterile inflammation: lessons from a Drosophila model." Journal of Biochemistry 166, no. 3 (June 28, 2019): 213–21. http://dx.doi.org/10.1093/jb/mvz053.
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Abstract Central nervous system (CNS)-related disorders, including neurodegenerative diseases, are common but difficult to treat. As effective medical interventions are limited, those diseases will likely continue adversely affecting people’s health. There is evidence that the hyperactivation of innate immunity is a hallmark of most neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and polyglutamine diseases. In mammalian and fly CNS, the presence of noninfectious ligands, including danger-associated molecular patterns, is recognized by (micro)glial cells, inducing the expression of proinflammatory cytokines. Such inflammation may contribute to the onset and progression of neurodegenerative states. Studies using fruit flies have shed light on the types of signals, receptors and cells responsible for inducing the inflammation that leads to neurodegeneration. Researchers are using fly models to assess the mechanisms of sterile inflammation in the brain and its link to progressive neurodegeneration. Given the similarity of its physiological system and biochemical function to those of mammals, especially in activating and regulating innate immune signalling, Drosophila can be a versatile model system for studying the mechanisms and biological significance of sterile inflammatory responses in the pathogenesis of neurodegenerative diseases. Such knowledge would greatly facilitate the quest for a novel effective treatment for neurodegenerative diseases.
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Okesina, A. A., M. S. Ajao, M. O. Buhari, A. M. Afodun, K. B. Okesina, R. Y. Usman, F. A. Sulaimon, and B. P. Kolawole. "Activation of pro-apoptotic cells, reactive astrogliosis and hyperphosphorylation of tau protein in trimethyltin-induced hippocampal injury in rats." Anatomy Journal of Africa 9, no. 2 (August 21, 2020): 1782–88. http://dx.doi.org/10.4314/aja.v9i2.198924.
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Neurodegenerative diseases cause neural cells to lose both the functional and sensory abilities as a result of genetic factors, proteopathies and mitochondrial dysfunction. Neurodegeneration forms the basis of most neurodegenerative disorders for example Alzheimer’s disease, Huntington’s diseases, and Parkinson’s diseases. The mechanism that underlines the process of neurodegeneration is not well understood. Understanding the process and mechanism involved in neurodegeneration might offer a better therapeutic approach to positively manage cases of neurodegenerative diseases. Therefore, this study’s target was to create an animal model to study neurodegeneration. Sixteen adult male Wistar rats were used in the study and divided into two groups. Control (0.2 mL of normal saline (NS)), and trimethyltin-treated (TMT, 8 mg/kg stat dose only). These animals underwent perfusion with 4% paraformaldehyde, brain excision and analysis of p53 antigen, GFAP and Bielshowsky on these tissues. The results showed that animals in the control group showed presence of activated p53 antigen, reactive astrogliosis, neurofibrillary tangles, and amyloid plaques within the cytoplasm of the hippocampal cells. Cornus Ammonis (CA2) and (CA3) showed more of the trimethylrtin injury than CA1 and CA4. This study thus revealed that, intra-peritoneal administration of single dose of 8mg/kg of trimethyltin can offer an attractive disease model to study some neurodegenerative diseases.
Keywords: p53 antigen, Bielshowsky, Glia fibrillary acidic protein, Trimethyltin, Hippocampus,
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Ruffini, Nicolas, Susanne Klingenberg, Susann Schweiger, and Susanne Gerber. "Common Factors in Neurodegeneration: A Meta-Study Revealing Shared Patterns on a Multi-Omics Scale." Cells 9, no. 12 (December 8, 2020): 2642. http://dx.doi.org/10.3390/cells9122642.
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Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) are heterogeneous, progressive diseases with frequently overlapping symptoms characterized by a loss of neurons. Studies have suggested relations between neurodegenerative diseases for many years (e.g., regarding the aggregation of toxic proteins or triggering endogenous cell death pathways). We gathered publicly available genomic, transcriptomic, and proteomic data from 177 studies and more than one million patients to detect shared genetic patterns between the neurodegenerative diseases on three analyzed omics-layers. The results show a remarkably high number of shared differentially expressed genes between the transcriptomic and proteomic levels for all conditions, while showing a significant relation between genomic and proteomic data between AD and PD and AD and ALS. We identified a set of 139 genes being differentially expressed in several transcriptomic experiments of all four diseases. These 139 genes showed overrepresented gene ontology (GO) Terms involved in the development of neurodegeneration, such as response to heat and hypoxia, positive regulation of cytokines and angiogenesis, and RNA catabolic process. Furthermore, the four analyzed neurodegenerative diseases (NDDs) were clustered by their mean direction of regulation throughout all transcriptomic studies for this set of 139 genes, with the closest relation regarding this common gene set seen between AD and HD. GO-Term and pathway analysis of the proteomic overlap led to biological processes (BPs), related to protein folding and humoral immune response. Taken together, we could confirm the existence of many relations between Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis on transcriptomic and proteomic levels by analyzing the pathways and GO-Terms arising in these intersections. The significance of the connection and the striking relation of the results to processes leading to neurodegeneration between the transcriptomic and proteomic data for all four analyzed neurodegenerative diseases showed that exploring many studies simultaneously, including multiple omics-layers of different neurodegenerative diseases simultaneously, holds new relevant insights that do not emerge from analyzing these data separately. Furthermore, the results shed light on processes like the humoral immune response that have previously been described only for certain diseases. Our data therefore suggest human patients with neurodegenerative diseases should be addressed as complex biological systems by integrating multiple underlying data sources.
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Al-Chalabi, Ammar. "Preventing neurodegenerative disease." Brain 144, no. 5 (May 1, 2021): 1279–80. http://dx.doi.org/10.1093/brain/awab151.
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Alidoust, Leila, and Adele Jafari. "Exosomes: Future Perspective in Neurodegenerative Diseases." Caspian Journal of Neurological Sciences 6, no. 4 (October 1, 2020): 251–58. http://dx.doi.org/10.32598/cjns.6.23.4.
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Neurodegeneration is a progressive and irreversible loss of neuronal cells in specific regions of the brain. Alzheimer Diseases (AD) Parkinson Disease (PD) are the most common forms of neurodegenerative diseases in older people. Exosomes are extracellular nanovesicles that have a key role in physiological processes such as intercellular communication, cell migration, angiogenesis, and anti-tumor immunity. Mounting evidence indicates the role of exosomes in neurodegenerative disorders as possible carriers of disease particles. They have several different potential applications thanks to their unique structure and functions. The present review summarizes recent studies on exosome potentials as a biomarker and therapeutic tool in neurodegenerative diseases. It also provides an overview of the structure and function of exosomes.
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Wang, Bo, and Xiao-Ping Wang. "Does Ceruloplasmin Defend Against Neurodegenerative Diseases?" Current Neuropharmacology 17, no. 6 (May 9, 2019): 539–49. http://dx.doi.org/10.2174/1570159x16666180508113025.
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Ceruloplasmin (CP) is the major copper transport protein in plasma, mainly produced by the liver. Glycosylphosphatidylinositol-linked CP (GPI-CP) is the predominant form expressed in astrocytes of the brain. A growing body of evidence has demonstrated that CP is an essential protein in the body with multiple functions such as regulating the homeostasis of copper and iron ions, ferroxidase activity, oxidizing organic amines, and preventing the formation of free radicals. In addition, as an acute-phase protein, CP is induced during inflammation and infection. The fact that patients with genetic disorder aceruloplasminemia do not suffer from tissue copper deficiency, but rather from disruptions in iron metabolism shows essential roles of CP in iron metabolism rather than copper. Furthermore, abnormal metabolism of metal ions and oxidative stress are found in other neurodegenerative diseases, such as Wilson’s disease, Alzheimer’s disease and Parkinson’s disease. Brain iron accumulation and decreased activity of CP have been shown to be associated with neurodegeneration. We hypothesize that CP may play a protective role in neurodegenerative diseases. However, whether iron accumulation is a cause or a result of neurodegeneration remains unclear. Further research on molecular mechanisms is required before a consensus can be reached regarding a neuroprotective role for CP in neurodegeneration. This review article summarizes the main physiological functions of CP and the current knowledge of its role in neurodegenerative diseases.
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Schmidt, Sissel Ida, Morten Blaabjerg, Kristine Freude, and Morten Meyer. "RhoA Signaling in Neurodegenerative Diseases." Cells 11, no. 9 (May 1, 2022): 1520. http://dx.doi.org/10.3390/cells11091520.
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Ras homolog gene family member A (RhoA) is a small GTPase of the Rho family involved in regulating multiple signal transduction pathways that influence a diverse range of cellular functions. RhoA and many of its downstream effector proteins are highly expressed in the nervous system, implying an important role for RhoA signaling in neurons and glial cells. Indeed, emerging evidence points toward a role of aberrant RhoA signaling in neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. In this review, we summarize the current knowledge of RhoA regulation and downstream cellular functions with an emphasis on the role of RhoA signaling in neurodegenerative diseases and the therapeutic potential of RhoA inhibition in neurodegeneration.
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Krey, Lea, Meret Koroni Huber, Günter U. Höglinger, and Florian Wegner. "Can SARS-CoV-2 Infection Lead to Neurodegeneration and Parkinson’s Disease?" Brain Sciences 11, no. 12 (December 18, 2021): 1654. http://dx.doi.org/10.3390/brainsci11121654.
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The SARS-CoV-2 pandemic has affected the daily life of the worldwide population since 2020. Links between the newly discovered viral infection and the pathogenesis of neurodegenerative diseases have been investigated in different studies. This review aims to summarize the literature concerning COVID-19 and Parkinson’s disease (PD) to give an overview on the interface between viral infection and neurodegeneration with regard to this current topic. We will highlight SARS-CoV-2 neurotropism, neuropathology and the suspected pathophysiological links between the infection and neurodegeneration as well as the psychosocial impact of the pandemic on patients with PD. Some evidence discussed in this review suggests that the SARS-CoV-2 pandemic might be followed by a higher incidence of neurodegenerative diseases in the future. However, the data generated so far are not sufficient to confirm that COVID-19 can trigger or accelerate neurodegenerative diseases.
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Morén, Constanza, Ruth Mary deSouza, Darly Milena Giraldo, and Christopher Uff. "Antioxidant Therapeutic Strategies in Neurodegenerative Diseases." International Journal of Molecular Sciences 23, no. 16 (August 19, 2022): 9328. http://dx.doi.org/10.3390/ijms23169328.
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The distinguishing pathogenic features of neurodegenerative diseases include mitochondrial dysfunction and derived reactive oxygen species generation. The neural tissue is highly sensitive to oxidative stress and this is a prominent factor in both chronic and acute neurodegeneration. Based on this, therapeutic strategies using antioxidant molecules towards redox equilibrium have been widely used for the treatment of several brain pathologies. Globally, polyphenols, carotenes and vitamins are among the most typical exogenous antioxidant agents that have been tested in neurodegeneration as adjunctive therapies. However, other types of antioxidants, including hormones, such as the widely used melatonin, are also considered neuroprotective agents and have been used in different neurodegenerative contexts. This review highlights the most relevant mitochondrial antioxidant targets in the main neurodegenerative disorders including Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease and also in the less represented amyotrophic lateral sclerosis, as well as traumatic brain injury, while summarizing the latest randomized placebo-controlled trials.
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Yang, Junzheng. "Stem Cells Applications in Neurodegenerative Diseases." Epidemiology International Journal 7, no. 4 (2023): 1–6. http://dx.doi.org/10.23880/eij-16000267.
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Neurodegenerative diseases are a kind of diseases caused by progressive loss of neuronal structure and function and glial cell homeostasis imbalance, there are many kinds of neurodegenerative diseases include Alzheimer's disease (AD), Parkinson's disease (PD); Huntington's disease (HD) and amyotrophic lateral sclerosis (ALS). So far, due to the lack of ideal treatment methods, it seriously threats to human health especially the elder population. Recently, with the rapid development of regenerative medicine, stem cells rely on their advantages including self-renewing capability, low immunogenicity, migration and homing capabilities, and stem cell derivatives including stem cells derived extracellular vesicles and stem cell-derived organoids, it provides unlimited application possibilities for the treatment of neurodegenerative diseases. In this review, we will summarize the recent research progress on the preclinical and clinical applications of stem cells in neurodegenerative diseases, hope that the reviews may provide some useful clues for researchers.
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Iemmolo, Matilda, Giulio Ghersi, and Giulia Bivona. "The Cytokine CX3CL1 and ADAMs/MMPs in Concerted Cross-Talk Influencing Neurodegenerative Diseases." International Journal of Molecular Sciences 24, no. 9 (April 28, 2023): 8026. http://dx.doi.org/10.3390/ijms24098026.
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Neuroinflammation plays a fundamental role in the development and progression of neurodegenerative diseases. It could therefore be said that neuroinflammation in neurodegenerative pathologies is not a consequence but a cause of them and could represent a therapeutic target of neuronal degeneration. CX3CL1 and several proteases (ADAMs/MMPs) are strongly involved in the inflammatory pathways of these neurodegenerative pathologies with multiple effects. On the one hand, ADAMs have neuroprotective and anti-apoptotic effects; on the other hand, they target cytokines and chemokines, thus causing inflammatory processes and, consequently, neurodegeneration. CX3CL1 itself is a cytokine substrate for the ADAM, ADAM17, which cleaves and releases it in a soluble isoform (sCX3CL1). CX3CL1, as an adhesion molecule, on the one hand, plays an inhibiting role in the pro-inflammatory response in the central nervous system (CNS) and shows neuroprotective effects by binding its membrane receptor (CX3CR1) present into microglia cells and maintaining them in a quiescent state; on the other hand, the sCX3CL1 isoform seems to promote neurodegeneration. In this review, the dual roles of CX3CL1 and ADAMs/MMPs in different neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (MH), and multiple sclerosis (MS), are investigated.