Journal articles: 'Neurodegenerative'

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Marín López, Alejandra Guadalupe, Justo Murguía Castillo, Rafael De Jesús Macías Vélez, and Martha Catalina Rivera Cervantes. "Neurodegeneración aguda y crónica un continuo en el establecimiento de los desórdenes neurodegenerativos." e-CUCBA 10, no. 19 (December 22, 2022): 175–82. http://dx.doi.org/10.32870/ecucba.vi19.277.

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As worldwide human population grows in number and gets older, disabilities derived from neurological disorders become morepresent. In addition to the lack of efforts directed to preventive actions against the occurrence and establishment of a neurologicaldisorder, will lead governmental institutions to face an increasing requirement for treatment and rehabilitations programs to dealwith consequences caused by these disorders. Demonstrating the importance that neuroscientists focus on the design of newparadigms that allow the identification of a potential prophylactic and therapeutic treatment for these disorders, is a key step. In thepresent work, authors did an overall bibliographical review and general description of the mechanisms involved on acute andchronic neurodegenerative damage, trying to show the common points on both kind of damage. Therefore, to identify andsubstantiate the key characteristics that link degenerative progression from an acute damage to the establishment of a chronicalneurological disorder. Highlighting the value of early interventions on acute neurological damage, centered on neuroprotection viacell signaling pathways that could mediate or prevent neuronal damage. Consequently, to spot and notice the repercussions andtranscendence that research in therapeutic strategies focus on mimic and potentiate the compensatory response unchained after aneurological damage, is a key factor to find new treatments for these disorders.

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Mandel, Silvia, and Moussa B. H. Youdim. "Catechin polyphenols: neurodegeneration and neuroprotection in neurodegenerative diseases." Free Radical Biology and Medicine 37, no. 3 (August 2004): 304–17. http://dx.doi.org/10.1016/j.freeradbiomed.2004.04.012.

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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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Bischof, Gérard N. "Tau-PET Bildgebung der Demenzerkrankungen." Angewandte Nuklearmedizin 45, no. 04 (December 2022): 266–72. http://dx.doi.org/10.1055/a-1712-6020.

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ZusammenfassungDie Ablagerung von Tau-Proteinen ist ein grundlegendes pathophysiologisches Merkmal vieler neurodegenerativer Demenzerkrankungen. Die Entwicklung sensitiver Tau-PET Tracer in den letzten Jahren hat die Lokalisation von Tau-Ablagerungen in unterschiedlichen klinischen neurodegenerativen Phänotypen in vivo ermöglicht. Bei der Alzheimer Demenz sind die räumlichen Muster der Tau-Pathologie in temporalen, parietalen und frontalen Regionen mit der Neurodegeneration und klinischen Symptomatik korreliert. Des Weiteren zeigen sich Zusammenhänge mit der Schwere der kognitiven Beeinträchtigung und der gemessenen Tau-Last, sodass Tau-PET in Zukunft einen hohen Nutzen in der klinischen Anwendung zugesprochen werden könnte. Bei primären Tauopathien, neurodegenerative Erkrankungen wie z.B. PSP und CBD, deren dominantes pathophysiologisches Merkmal die Ansammlung von Tau-Proteinen im Gehirn sind, steht die Validierung der wissenschaftlich genutzten Tau-PET Tracer noch aus, aber erste Hinweise aus Studien mit Tau-PET Tracern der zweiten Generation sind vielversprechend. Diese zeigen, dass die räumliche Verteilung der Tracer-Anreicherung bei primären Tauopathien von dem räumlichen Verteilungsmuster bei der Alzheimer Demenz unterschieden werden kann.Dennoch fehlen aktuell wichtige Validierungsstudien, die in größeren Kohorten den direkten klinischen Nutzen der Tau-PET Bildgebung belegen. Auf der anderen Seite haben die bisherigen wissenschaftlichen Erkenntnisse, die durch die Tau-PET Bildgebung gewonnen wurden, bereits einen wesentlichen Beitrag zum Zusammenhang von Tau-Pathologie und Neurodegeneration geleistet.

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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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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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Guerreiro, Serge, Anne-Laure Privat, Laurence Bressac, and Damien Toulorge. "CD38 in Neurodegeneration and Neuroinflammation." Cells 9, no. 2 (February 18, 2020): 471. http://dx.doi.org/10.3390/cells9020471.

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Neurodegenerative diseases are characterized by neuronal degeneration as well as neuroinflammation. While CD38 is strongly expressed in brain cells including neurons, astrocytes as well as microglial cells, the role played by CD38 in neurodegeneration and neuroinflammation remains elusive. Yet, CD38 expression increases as a consequence of aging which is otherwise the primary risk associated with neurodegenerative diseases, and several experimental data demonstrated that CD38 knockout mice are protected from neurodegenerative and neuroinflammatory insults. Moreover, nicotinamide adenine dinucleotide, whose levels are tightly controlled by CD38, is a recognized and potent neuroprotective agent, and NAD supplementation was found to be beneficial against neurodegenerative diseases. The aims of this review are to summarize the physiological role played by CD38 in the brain, present the arguments indicating the involvement of CD38 in neurodegeneration and neuroinflammation, and to discuss these observations in light of CD38 complex biology.

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Batista, Carla Ribeiro Alvares, Giovanni Freitas Gomes, Eduardo Candelario-Jalil, Bernd L. Fiebich, and Antonio Carlos Pinheiro de Oliveira. "Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration." International Journal of Molecular Sciences 20, no. 9 (May 9, 2019): 2293. http://dx.doi.org/10.3390/ijms20092293.

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A large body of experimental evidence suggests that neuroinflammation is a key pathological event triggering and perpetuating the neurodegenerative process associated with many neurological diseases. Therefore, different stimuli, such as lipopolysaccharide (LPS), are used to model neuroinflammation associated with neurodegeneration. By acting at its receptors, LPS activates various intracellular molecules, which alter the expression of a plethora of inflammatory mediators. These factors, in turn, initiate or contribute to the development of neurodegenerative processes. Therefore, LPS is an important tool for the study of neuroinflammation associated with neurodegenerative diseases. However, the serotype, route of administration, and number of injections of this toxin induce varied pathological responses. Thus, here, we review the use of LPS in various models of neurodegeneration as well as discuss the neuroinflammatory mechanisms induced by this toxin that could underpin the pathological events linked to the neurodegenerative process.

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Werdann, Michelle, and Yong Zhang. "Circadian rhythm and neurodegenerative disorders." Brain Science Advances 6, no. 2 (June 2020): 71–80. http://dx.doi.org/10.26599/bsa.2020.9050006.

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The circadian clock controls daily rhythms in animal physiology, metabolism, and behavior, such as the sleep‐wake cycle. Disruption of circadian rhythms has been revealed in many diseases including neurodegenerative disorders. Interestingly, patients with many neurodegenerative diseases often show problems with circadian clocks even years before other symptoms develop. Here we review the recent studies identifying the association between circadian rhythms and several major neurodegenerative disorders. Early intervention of circadian rhythms may benefit the treatment of neurodegeneration.

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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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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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Sferra, Antonella, Francesco Nicita, and Enrico Bertini. "Microtubule Dysfunction: A Common Feature of Neurodegenerative Diseases." International Journal of Molecular Sciences 21, no. 19 (October 5, 2020): 7354. http://dx.doi.org/10.3390/ijms21197354.

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Neurons are particularly susceptible to microtubule (MT) defects and deregulation of the MT cytoskeleton is considered to be a common insult during the pathogenesis of neurodegenerative disorders. Evidence that dysfunctions in the MT system have a direct role in neurodegeneration comes from findings that several forms of neurodegenerative diseases are associated with changes in genes encoding tubulins, the structural units of MTs, MT-associated proteins (MAPs), or additional factors such as MT modifying enzymes which modulating tubulin post-translational modifications (PTMs) regulate MT functions and dynamics. Efforts to use MT-targeting therapeutic agents for the treatment of neurodegenerative diseases are underway. Many of these agents have provided several benefits when tested on both in vitro and in vivo neurodegenerative model systems. Currently, the most frequently addressed therapeutic interventions include drugs that modulate MT stability or that target tubulin PTMs, such as tubulin acetylation. The purpose of this review is to provide an update on the relevance of MT dysfunctions to the process of neurodegeneration and briefly discuss advances in the use of MT-targeting drugs for the treatment of neurodegenerative disorders.

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Fiskum, Gary, Anne N. Murphy, and M. Flint Beal. "Mitochondria in Neurodegeneration: Acute Ischemia and Chronic Neurodegenerative Diseases." Journal of Cerebral Blood Flow & Metabolism 19, no. 4 (April 1999): 351–69. http://dx.doi.org/10.1097/00004647-199904000-00001.

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Clarke, G. "Inherited neurodegenerative diseases: the one-hit model of neurodegeneration." Human Molecular Genetics 10, no. 20 (October 1, 2001): 2269–75. http://dx.doi.org/10.1093/hmg/10.20.2269.

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Shukla, Varsha, Santosh K. Mishra, and Harish C. Pant. "Oxidative Stress in Neurodegeneration." Advances in Pharmacological Sciences 2011 (2011): 1–13. http://dx.doi.org/10.1155/2011/572634.

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It has been demonstrated that oxidative stress has a ubiquitous role in neurodegenerative diseases. Major source of oxidative stress due to reactive oxygen species (ROS) is related to mitochondria as an endogenous source. Although there is ample evidence from tissues of patients with neurodegenerative disorders of morphological, biochemical, and molecular abnormalities in mitochondria, it is still not very clear whether the oxidative stress itself contributes to the onset of neurodegeneration or it is part of the neurodegenerative process as secondary manifestation. This paper begins with an overview of how oxidative stress occurs, discussing various oxidants and antioxidants, and role of oxidative stress in diseases in general. It highlights the role of oxidative stress in neurodegenerative diseases like Alzheimer's, Parkinson's, and Huntington's diseases and amyotrophic lateral sclerosis. The last part of the paper describes the role of oxidative stress causing deregulation of cyclin-dependent kinase 5 (Cdk5) hyperactivity associated with neurodegeneration.

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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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Fiorito, Veronica, Deborah Chiabrando, and Emanuela Tolosano. "Mitochondrial Targeting in Neurodegeneration: A Heme Perspective." Pharmaceuticals 11, no. 3 (September 18, 2018): 87. http://dx.doi.org/10.3390/ph11030087.

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Mitochondrial dysfunction has achieved an increasing interest in the field of neurodegeneration as a pathological hallmark for different disorders. The impact of mitochondria is related to a variety of mechanisms and several of them can co-exist in the same disease. The central role of mitochondria in neurodegenerative disorders has stimulated studies intended to implement therapeutic protocols based on the targeting of the distinct mitochondrial processes. The review summarizes the most relevant mechanisms by which mitochondria contribute to neurodegeneration, encompassing therapeutic approaches. Moreover, a new perspective is proposed based on the heme impact on neurodegeneration. The heme metabolism plays a central role in mitochondrial functions, and several evidences indicate that alterations of the heme metabolism are associated with neurodegenerative disorders. By reporting the body of knowledge on this topic, the review intends to stimulate future studies on the role of heme metabolism in neurodegeneration, envisioning innovative strategies in the struggle against 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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Yaribeygi, Habib, Yunes Panahi, Behjat Javadi, and Amirhossein Sahebkar. "The Underlying Role of Oxidative Stress in Neurodegeneration: A Mechanistic Review." CNS & Neurological Disorders - Drug Targets 17, no. 3 (June 19, 2018): 207–15. http://dx.doi.org/10.2174/1871527317666180425122557.

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Background: Neurodegeneration is a condition in which progressive loss of function and structure of neurons occurs. Several lines of evidence suggest that oxidative stress has a central role in neurodegenerative diseases. Objective: The aim was to survey molecular mechanisms underlying the involvement of oxidative stress in developing different neurodegenerative diseases. Methods: Original and review articles were retrieved through a PubMed and Google scholar search (from 1989 to 2015) using the following key words: “oxidative stress”, “nerve degeneration” and “neurodegenerative diseases”. Results: A comprehensive analysis of the obtained articles confirmed strong involvement of oxidative stress in the pathophysiology of neurodegenerative diseases through a variety of mechanisms including induction of oxidation of nucleic acids, proteins and lipids, formation of advanced glycation end products, mitochondrial dysfunction, glial cell activation, amyloid β deposition and plaque formation, apoptosis, cytokine production and inflammatory responses, and proteasome dysfunction. Conclusion: Regarding the pivotal role of oxidative stress in neurodegeneration, modulation of free radical production or alleviating their harmful effects can be considered as a potential therapeutic strategy for preventing and controlling neurodegenerative diseases. Accordingly; boosting endogenous antioxidant capacity besides providing exogenous sources of antioxidants merits future research in order to discover new therapeutic agents.

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Sheikh, Saba, Safia, Ejazul Haque, and Snober S. Mir. "Neurodegenerative Diseases: Multifactorial Conformational Diseases and Their Therapeutic Interventions." Journal of Neurodegenerative Diseases 2013 (December 30, 2013): 1–8. http://dx.doi.org/10.1155/2013/563481.

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Neurodegenerative diseases are multifactorial debilitating disorders of the nervous system that affect approximately 30 millionindividuals worldwide. Neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s, and amyotrophic lateral sclerosis diseases are the consequence of misfolding and dysfunctional trafficking of proteins. Beside that, mitochondrial dysfunction, oxidative stress, and/or environmental factors strongly associated with age have also been implicated in causing neurodegeneration. After years of intensive research, considerable evidence has accumulated that demonstrates an important role of these factors in the etiology of common neurodegenerative diseases. Despite the extensive efforts that have attempted to define the molecular mechanisms underlying neurodegeneration, many aspects of these pathologies remain elusive. However, in order to explore the therapeutic interventions directed towards treatment of neurodegenerative diseases, neuroscientists are now fully exploiting the data obtained from studies of these basic mechanisms that have gone awry. The novelty of these mechanisms represents a challenge to the identification of viable drug targets and biomarkers for early diagnosis of the diseases. In this paper, we are reviewing various aspects associated with the disease and the recent trends that may have an application for the treatment of the neurodegenerative disorders.

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Mitra, Sarmistha, Raju Dash, Yeasmin Akter Munni, Nusrat Jahan Selsi, Nasrin Akter, Md Nazim Uddin, Kishor Mazumder, and Il Soo Moon. "Natural Products Targeting Hsp90 for a Concurrent Strategy in Glioblastoma and Neurodegeneration." Metabolites 12, no. 11 (November 21, 2022): 1153. http://dx.doi.org/10.3390/metabo12111153.

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Glioblastoma multiforme (GBM) is one of the most common aggressive, resistant, and invasive primary brain tumors that share neurodegenerative actions, resembling many neurodegenerative diseases. Although multiple conventional approaches, including chemoradiation, are more frequent in GBM therapy, these approaches are ineffective in extending the mean survival rate and are associated with various side effects, including neurodegeneration. This review proposes an alternative strategy for managing GBM and neurodegeneration by targeting heat shock protein 90 (Hsp90). Hsp90 is a well-known molecular chaperone that plays essential roles in maintaining and stabilizing protein folding to degradation in protein homeostasis and modulates signaling in cancer and neurodegeneration by regulating many client protein substrates. The therapeutic benefits of Hsp90 inhibition are well-known for several malignancies, and recent evidence highlights that Hsp90 inhibitors potentially inhibit the aggressiveness of GBM, increasing the sensitivity of conventional treatment and providing neuroprotection in various neurodegenerative diseases. Herein, the overview of Hsp90 modulation in GBM and neurodegeneration progress has been discussed with a summary of recent outcomes on Hsp90 inhibition in various GBM models and neurodegeneration. Particular emphasis is also given to natural Hsp90 inhibitors that have been evidenced to show dual protection in both GBM and neurodegeneration.

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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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Cachán-Vega, Cristina, Ignacio Vega-Naredo, Yaiza Potes, Juan Carlos Bermejo-Millo, Adrian Rubio-González, Claudia García-González, Eduardo Antuña, et al. "Chronic Treatment with Melatonin Improves Hippocampal Neurogenesis in the Aged Brain and Under Neurodegeneration." Molecules 27, no. 17 (August 29, 2022): 5543. http://dx.doi.org/10.3390/molecules27175543.

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Adult hippocampal neurogenesis is altered during aging and under different neuropsychiatric and neurodegenerative diseases. Melatonin shows neurogenic and neuroprotective properties during aging and neuropathological conditions. In this study, we evaluated the effects of chronic treatment with melatonin on different markers of neurodegeneration and hippocampal neurogenesis using immunohistochemistry in the aged and neurodegenerative brains of SAMP8 mice, which is an animal model of accelerated senescence that mimics aging-related Alzheimer’s pathology. Neurodegenerative processes observed in the brains of aged SAMP8 mice at 10 months of age include the presence of damaged neurons, disorganization in the layers of the brain cortex, alterations in neural processes and the length of neuronal prolongations and β-amyloid accumulation in the cortex and hippocampus. This neurodegeneration may be associated with neurogenic responses in the hippocampal dentate gyrus of these mice, since we observed a neurogenic niche of neural stem and progenitor/precursors cells in the hippocampus of SAMP8 mice. However, hippocampal neurogenesis seems to be compromised due to alterations in the cell survival, migration and/or neuronal maturation of neural precursor cells due to the neurodegeneration levels in these mice. Chronic treatment with melatonin for 9 months decreased these neurodegenerative processes and the neurodegeneration-induced neurogenic response. Noticeably, melatonin also induced recovery in the functionality of adult hippocampal neurogenesis in aged SAMP8 mice.

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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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Li, Kelu, Zichao Chen, Yonggang Zhang, and Xinglong Yang. "Applications of iTRAQ and TMT Labeling Techniques to the Study of Neurodegenerative Diseases." Current Protein & Peptide Science 21, no. 12 (December 31, 2020): 1202–17. http://dx.doi.org/10.2174/1389203721666201103085704.

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: Neurodegenerative diseases are caused by progressive lesions or loss of specific nerve cells, which endanger human health. However, the mechanism by which neurodegeneration manifests remains unclear. Proteomics can shed light on this question as well as help establish diagnostic standards and discover new drug targets. The power of proteomics for understanding neurodegenerative diseases has increased substantially with the application of iTRAQ and TMT labeling techniques. This review focuses on progress in these labeling techniques and their applications in neurodegeneration research.

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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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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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Jantas, Danuta, and Władysław Lasoń. "Preclinical Evidence for the Interplay between Oxidative Stress and RIP1-Dependent Cell Death in Neurodegeneration: State of the Art and Possible Therapeutic Implications." Antioxidants 10, no. 10 (September 24, 2021): 1518. http://dx.doi.org/10.3390/antiox10101518.

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Neurodegenerative diseases are the most frequent chronic, age-associated neurological pathologies having a major impact on the patient’s quality of life. Despite a heavy medical, social and economic burden they pose, no causative treatment is available for these diseases. Among the important pathogenic factors contributing to neuronal loss during neurodegeneration is elevated oxidative stress resulting from a disturbed balance between endogenous prooxidant and antioxidant systems. For many years, it was thought that increased oxidative stress was a cause of neuronal cell death executed via an apoptotic mechanism. However, in recent years it has been postulated that rather programmed necrosis (necroptosis) is the key form of neuronal death in the course of neurodegenerative diseases. Such assumption was supported by biochemical and morphological features of the dying cells as well as by the fact that various necroptosis inhibitors were neuroprotective in cellular and animal models of neurodegenerative diseases. In this review, we discuss the relationship between oxidative stress and RIP1-dependent necroptosis and apoptosis in the context of the pathomechanism of neurodegenerative disorders. Based on the published data mainly from cellular models of neurodegeneration linking oxidative stress and necroptosis, we postulate that administration of multipotential neuroprotectants with antioxidant and antinecroptotic properties may constitute an efficient pharmacotherapeutic strategy for the treatment of neurodegenerative diseases.

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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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Paudel, Yam Nath, Efthalia Angelopoulou, Christina Piperi, Iekhsan Othman, and Mohd Farooq Shaikh. "Revisiting the Impact of Neurodegenerative Proteins in Epilepsy: Focus on Alpha-Synuclein, Beta-Amyloid, and Tau." Biology 9, no. 6 (June 12, 2020): 122. http://dx.doi.org/10.3390/biology9060122.

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Lack of disease-modifying therapy against epileptogenesis reflects the complexity of the disease pathogenesis as well as the high demand to explore novel treatment strategies. In the pursuit of developing new therapeutic strategies against epileptogenesis, neurodegenerative proteins have recently gained increased attention. Owing to the fact that neurodegenerative disease and epileptogenesis possibly share a common underlying mechanism, targeting neurodegenerative proteins against epileptogenesis might represent a promising therapeutic approach. Herein, we review the association of neurodegenerative proteins, such as α-synuclein, amyloid-beta (Aβ), and tau protein, with epilepsy. Providing insight into the α-synuclein, Aβ and tau protein-mediated neurodegeneration mechanisms, and their implication in epileptogenesis will pave the way towards the development of new agents and treatment strategies.

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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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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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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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Petrova, Teodora, Camila Orellana, Vesna Jelic, Anne-Rita Oeksengaard, Jon Snaedal, Peter Høgh, Birgitte Bo Andersen, et al. "Cholinergic dysfunction, neurodegeneration, and amyloid-beta pathology in neurodegenerative diseases." Psychiatry Research: Neuroimaging 302 (August 2020): 111099. http://dx.doi.org/10.1016/j.pscychresns.2020.111099.

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Dhib-Jalbut, Suhayl, Douglas L. Arnold, Don W. Cleveland, Mark Fisher, Robert M. Friedlander, M. Maral Mouradian, Serge Przedborski, Bruce D. Trapp, Tony Wyss-Coray, and V. Wee Yong. "Neurodegeneration and neuroprotection in multiple sclerosis and other neurodegenerative diseases." Journal of Neuroimmunology 176, no. 1-2 (July 2006): 198–215. http://dx.doi.org/10.1016/j.jneuroim.2006.03.027.

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Cannon, Jason R., and J. Timothy Greenamyre. "The Role of Environmental Exposures in Neurodegeneration and Neurodegenerative Diseases." Toxicological Sciences 124, no. 2 (September 13, 2011): 225–50. http://dx.doi.org/10.1093/toxsci/kfr239.

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Martínez-Iglesias, Olaia, Vinogran Naidoo, Natalia Cacabelos, and Ramón Cacabelos. "Epigenetic Biomarkers as Diagnostic Tools for Neurodegenerative Disorders." International Journal of Molecular Sciences 23, no. 1 (December 21, 2021): 13. http://dx.doi.org/10.3390/ijms23010013.

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Epigenetics is the study of heritable changes in gene expression that occur without alterations to the DNA sequence, linking the genome to its surroundings. The accumulation of epigenetic alterations over the lifespan may contribute to neurodegeneration. The aim of the present study was to identify epigenetic biomarkers for improving diagnostic efficacy in patients with neurodegenerative diseases. We analyzed global DNA methylation, chromatin remodeling/histone modifications, sirtuin (SIRT) expression and activity, and the expression of several important neurodegeneration-related genes. DNA methylation, SIRT expression and activity and neuregulin 1 (NRG1), microtubule-associated protein tau (MAPT) and brain-derived neurotrophic factor (BDNF) expression were reduced in buffy coat samples from patients with neurodegenerative disorders. Our data suggest that these epigenetic biomarkers may be useful in clinical practical for the diagnosis, surveillance, and prognosis of disease activity in patients with neurodegenerative diseases.

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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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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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Zheng, Xiang-Yu, Hong-Liang Zhang, Qi Luo, and Jie Zhu. "Kainic Acid-Induced Neurodegenerative Model: Potentials and Limitations." Journal of Biomedicine and Biotechnology 2011 (2011): 1–10. http://dx.doi.org/10.1155/2011/457079.

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Excitotoxicity is considered to be an important mechanism involved in various neurodegenerative diseases in the central nervous system (CNS) such as Alzheimer's disease (AD). However, the mechanism by which excitotoxicity is implicated in neurodegenerative disorders remains unclear. Kainic acid (KA) is an epileptogenic and neuroexcitotoxic agent by acting on specific kainate receptors (KARs) in the CNS. KA has been extensively used as a specific agonist for ionotrophic glutamate receptors (iGluRs), for example, KARs, to mimic glutamate excitotoxicity in neurodegenerative models as well as to distinguish other iGluRs such asα-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors and N-methyl-D-aspartate receptors. Given the current knowledge of excitotoxicity in neurodegeneration, interventions targeted at modulating excitotoxicity are promising in terms of dealing with neurodegenerative disorders. This paper summarizes the up-to-date knowledge of neurodegenerative studies based on KA-induced animal model, with emphasis on its potentials and limitations.

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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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Kukucka, Jessica, Tessa Wyllie, Justin Read, Lauren Mahoney, and Cenk Suphioglu. "Human neuronal cells: epigenetic aspects." BioMolecular Concepts 4, no. 4 (August 1, 2013): 319–33. http://dx.doi.org/10.1515/bmc-2012-0053.

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AbstractHistone acetyltransferases (HATs) and histone deacetylases (HDACs) promote histone posttranslational modifications, which lead to an epigenetic alteration in gene expression. Aberrant regulation of HATs and HDACs in neuronal cells results in pathological consequences such as neurodegeneration. Alzheimer’s disease is the most common neurodegenerative disease of the brain, which has devastating effects on patients and loved ones. The use of pan-HDAC inhibitors has shown great therapeutic promise in ameliorating neurodegenerative ailments. Recent evidence has emerged suggesting that certain deacetylases mediate neurotoxicity, whereas others provide neuroprotection. Therefore, the inhibition of certain isoforms to alleviate neurodegenerative manifestations has now become the focus of studies. In this review, we aimed to discuss and summarize some of the most recent and promising findings of HAT and HDAC functions in neurodegenerative diseases.

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Bond, Sarah, Claudia Lopez-Lloreda, Patrick J. Gannon, Cagla Akay-Espinoza, and Kelly L. Jordan-Sciutto. "The Integrated Stress Response and Phosphorylated Eukaryotic Initiation Factor 2α in Neurodegeneration." Journal of Neuropathology & Experimental Neurology 79, no. 2 (January 8, 2020): 123–43. http://dx.doi.org/10.1093/jnen/nlz129.

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Abstract The proposed molecular mechanisms underlying neurodegenerative pathogenesis are varied, precluding the development of effective therapies for these increasingly prevalent disorders. One of the most consistent observations across neurodegenerative diseases is the phosphorylation of eukaryotic initiation factor 2α (eIF2α). eIF2α is a translation initiation factor, involved in cap-dependent protein translation, which when phosphorylated causes global translation attenuation. eIF2α phosphorylation is mediated by 4 kinases, which, together with their downstream signaling cascades, constitute the integrated stress response (ISR). While the ISR is activated by stresses commonly observed in neurodegeneration, such as oxidative stress, endoplasmic reticulum stress, and inflammation, it is a canonically adaptive signaling cascade. However, chronic activation of the ISR can contribute to neurodegenerative phenotypes such as neuronal death, memory impairments, and protein aggregation via apoptotic induction and other maladaptive outcomes downstream of phospho-eIF2α-mediated translation inhibition, including neuroinflammation and altered amyloidogenic processing, plausibly in a feed-forward manner. This review examines evidence that dysregulated eIF2a phosphorylation acts as a driver of neurodegeneration, including a survey of observations of ISR signaling in human disease, inspection of the overlap between ISR signaling and neurodegenerative phenomenon, and assessment of recent encouraging findings ameliorating neurodegeneration using developing pharmacological agents which target the ISR. In doing so, gaps in the field, including crosstalk of the ISR kinases and consideration of ISR signaling in nonneuronal central nervous system cell types, are highlighted.

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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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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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Mancino, Raffaele, Massimo Cesareo, Alessio Martucci, Emiliano Di Carlo, Elena Ciuffoletti, Clarissa Giannini, Luigi Antonio Morrone, Carlo Nucci, and Francesco Garaci. "Neurodegenerative Process Linking the Eye and the Brain." Current Medicinal Chemistry 26, no. 20 (September 13, 2019): 3754–63. http://dx.doi.org/10.2174/0929867325666180307114332.

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Recent literature agrees that neurodegenerative processes involve both the retina and the central nervous system, which are two strictly related anatomical structures. However, the causal mechanisms of this dual involvement are still uncertain. To date, anterograde transsynaptic neurodegeneration, triggered by retinal ganglion cells’ death, and retrograde transsynaptic neurodegeneration, induced by neurodegenerative processes of the central nervous system, has been considered the major possible causal mechanisms. The development of novel neuroimaging techniques has recently supported both the study of the central stations of the visual pathway as well as the study of the retina which is possibly an open window to the central nervous system.

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Mandik, Frida, and Melissa Vos. "Neurodegenerative Disorders: Spotlight on Sphingolipids." International Journal of Molecular Sciences 22, no. 21 (November 5, 2021): 11998. http://dx.doi.org/10.3390/ijms222111998.

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Neurodegenerative diseases are incurable diseases of the nervous system that lead to a progressive loss of brain areas and neuronal subtypes, which is associated with an increase in symptoms that can be linked to the affected brain areas. The key findings that appear in many neurodegenerative diseases are deposits of proteins and the damage of mitochondria, which mainly affect energy production and mitophagy. Several causative gene mutations have been identified in various neurodegenerative diseases; however, a large proportion are considered sporadic. In the last decade, studies linking lipids, and in particular sphingolipids, to neurodegenerative diseases have shown the importance of these sphingolipids in the underlying pathogenesis. Sphingolipids are bioactive lipids consisting of a sphingoid base linked to a fatty acid and a hydrophilic head group. They are involved in various cellular processes, such as cell growth, apoptosis, and autophagy, and are an essential component of the brain. In this review, we will cover key findings that demonstrate the relevance of sphingolipids in neurodegenerative diseases and will focus on neurodegeneration with brain iron accumulation and Parkinson’s disease.

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Bhatia-Dey, Naina, and Thomas Heinbockel. "The Olfactory System as Marker of Neurodegeneration in Aging, Neurological and Neuropsychiatric Disorders." International Journal of Environmental Research and Public Health 18, no. 13 (June 29, 2021): 6976. http://dx.doi.org/10.3390/ijerph18136976.

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Research studies that focus on understanding the onset of neurodegenerative pathology and therapeutic interventions to inhibit its causative factors, have shown a crucial role of olfactory bulb neurons as they transmit and propagate nerve impulses to higher cortical and limbic structures. In rodent models, removal of the olfactory bulb results in pathology of the frontal cortex that shows striking similarity with frontal cortex features of patients diagnosed with neurodegenerative disorders. Widely different approaches involving behavioral symptom analysis, histopathological and molecular alterations, genetic and environmental influences, along with age-related alterations in cellular pathways, indicate a strong correlation of olfactory dysfunction and neurodegeneration. Indeed, declining olfactory acuity and olfactory deficits emerge either as the very first symptoms or as prodromal symptoms of progressing neurodegeneration of classical conditions. Olfactory dysfunction has been associated with most neurodegenerative, neuropsychiatric, and communication disorders. Evidence revealing the dual molecular function of the olfactory receptor neurons at dendritic and axonal ends indicates the significance of olfactory processing pathways that come under environmental pressure right from the onset. Here, we review findings that olfactory bulb neuronal processing serves as a marker of neuropsychiatric and neurodegenerative disorders.

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Journal articles on the topic 'Neurodegenerative'

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