Relevant bibliographies by topics / Neurodegenerative disease

Academic literature on the topic 'Neurodegenerative disease'

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Published: 4 June 2021
Last updated: 24 August 2024

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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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Dissertations / Theses on the topic "Neurodegenerative disease"

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Biro, Andrew J. "Specific aspects of neurodegenerative disease." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28919.

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This thesis is broken into four chapters. The first two chapters summarize two separate lines of investigation into the role of a putative neurotoxin in the pathogenesis of Huntington's Disease (HD). The third chapter outlines an investigation of the putative role of beta-N-methylamino-L-alanine (BMAA) in the pathogenesis of amyotrophic lateral sclerosis (ALS), while the final chapter details a post-mortem investigation of the contents of biogenic amines and amino acids in the brain of a man who died of a familial form of parkinsonism. Chapter I is a description of a chromatographic technique developed to isolate quinolinic acid (QA), an endogenous compound implicated in the pathogenesis of HD, from deproteinized human sera. A cation exchange column was used to selectively isolate QA, which was eluted with 10 mM HCl. The eluted fractions were analyzed by UV spectrometry to isolate and quantify QA. Once the fractions corresponding the elution of authentic QA were isolated, concentrated and the excess HCl removed, the fractions were added to growing fetal rat striatal explant cultures as an assay of neurotoxicity. Since HD involves the selective degeneration of GABAergic neurons in the striatum, the activity of glutamic acid decarboxylase, the final enzyme in the synthesis of GABA, was used to determine the viability of the cultures. Unfortunately, the method was confounded by the contamination of all effluents by compounds originating from the cation exchange resin, which were discovered to be neurotoxic to the striatal cultures, and as a result the investigation had to be abandoned. Chapter II describes an investigation designed to further characterize the nature of neurotoxicity observed in the sera obtained from patients with HD (Perry et al. 1987). Compounds with the capacity to selectively stimulate neurons at the N-methyl-D-aspartate (NMDA) receptor have been implicated in a variety of neurodegenerative disorders, including HD. Selective antagonists at the NMDA receptor have been shown to protect neurons from the degenerative effects of such "excitotoxins". The investigation described used MK-801, a potent noncompetitive NMDA antagonist, in an attempt to protect fetal rat striatal cultures from the neurodegenerative effects of the sera obtained from HD patients. The results obtained were equivocal. No evidence was obtained to support a role of the NMDA receptor in the mediation of the neurotoxicity, and in addition the neurodegenerative effects of HD sera were not reproduced in the present investigation. A variety of possible explanations for the apparent discrepancy are suggested. Chapter III describes an experiment intended to produce an animal model of ALS based on the observations by Spencer et al. 1987 that chronic oral administration of BMAA in monkeys produced the histological and behavioural characteristics of this disease. In the present investigation synthetic D,L-BMAA was given by gavage to mice over an eleven week period. Since BMAA is known to act at the NMDA receptor, a subset of the mice were also given MK-801 in an effort to protect them from any deleterious effects based on the action of BMAA at this receptor. The animals were sacrificed at the end of the experiment, and biochemical analyses were performed on the striata and cortices of the animals. In addition, neuropathological studies were performed on the spinal cords, basal ganglia and related structures. The results indicated no biochemical or neuropathological abnormality as a result of BMAA administration. Chapter IV describes a post-mortem investigation of a man who was a member of a well described pedigree which carries an autosomal dominant form of parkinsonism. The object of the investigation was to determine post-mortem levels of dopamine, noradrenaline, serotonin and their metabolites, in addition to amino acids in various regions of brain. Although conflicting evidence was obtained during life, neuropathological findings and the present neurochemical analyses confirm the degeneration of the nigrostriatal dopaminergic tract, characteristic of parkinsonism, in this man.
Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
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Sleven, Hannah. "Models of neurodegenerative mitochondrial disease." Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598048.

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Mitochondrial diseases affect the core energy generating pathways and can result in significant cognitive impairment and neurodegeneration. The mechanisms underlying the neurological and pathological consequences of mitochondrial disease are not understood and current treatment of mitochondrial diseases is limited in scope and efficacy. pyruvate dehydrogenase (PDH) and Complex I are key mitochondrial enzymes pivotal for cellular energy metabolism, and mutations in genes coding for PDH and Complex I proteins are common causes of mitochondrial disease. This thesis describes the use oftwo techniques, gene targeting, and RNA interference, to generate in vitro models of Complex I and PDH deficiency in pluripotent cell lines. Gene targeting of the ndufal gene was unsuccessful, however, a number of cell lines were isolated with significant reductions in PDH activity mediated by RNAi targeted against the Pdhal transcript. These cells lines were neurodifferentiated in vitro and used to characterise the developmental and degenerative consequences of PDH deficiency on neural cultures. The cultures were found to successfully differentiate into neural cells, but were developmentally abnormal with defective neuronal migration and neurite extension, and neuritic varicosities, an indication of neuritic degeneration in many neurological disease models. These features were activity-dependent with the most severe phenotype found in the cell line with the least residual PDH activity. These cultures were used to explore the nature of energy metabolism in PDH deficient neurons, and therapeutic strategies were successfully tested. This research has successfully established a reproducible and practical model to assess neurodegeneration in PDH deficiency, to test t reatments and to model theories of disease mechanisms. As such it provides promise for the improvement of the understanding of and treatment of disorders of brain energy metabolism in the future.
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Radakovic, Ratko. "Multidimensional apathy in neurodegenerative disease." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/25959.

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Apathy is characterised by a lack of motivation towards goal directed behaviour and is a symptom of various neurodegenerative diseases. There are various tools that can be used to assess apathy but a caveat of these is that they usually assess it as a unidimensional concept. Apathy has been recognised to have a multidimensional substructure. The Dimensional Apathy Scale is the only comprehensive measure designed to quantify neurobiologically-based subtypes, called Executive, Emotional and Initiation apathy. The first aim of this study was to explore multidimensional apathy, and its associations with demographic variables, in healthy, community dwelling adults. Secondly, multidimensional apathy was explored in neurodegenerative diseases, specifically Amyotrophic lateral sclerosis (ALS), Parkinson’s disease (PD) and Alzheimer’s disease (AD). For each disease group, the validity and reliability of both the self rated and carer rated DAS were also determined. Finally, the association between specific apathy subtype impairments and executive dysfunction was explored in ALS patients. Four hundred healthy community dwelling adults, eighty-three ALS patients (seventy-five carers), thirty-four PD patients (thirty carers) and forty-nine AD patients (eighty-nine carers) were recruited for the questionnaire study. In the healthy community dwelling adults, Executive apathy decreased with age, whereas Emotional increased with age. Gender differences were also shown with higher apathy in males on Emotional apathy. There were also employment differences, in that Executive apathy was higher in unemployed individuals compared to those who were employed. Emotional apathy showed difference in type of employment, where full time employed individuals were significantly more apathetic than those employed part time. These findings were taken into account in selecting the appropriate control samples to match our patient groups. In the patient groups, ALS patients were found to be significantly more impaired on the Initiation subscale when compared to controls. Furthermore, Initiation apathy was found to be the most frequent impairment above abnormality cut-off on the carer rated DAS. PD patients were significantly more impaired on Executive and Initiation apathy when compared to controls. These two subscales were most frequently above abnormality cut-off in the carer rated DAS. Finally, AD patients were significantly more impaired on all subscales when compared to controls and, on the carer rated DAS, global impairment over all subscales was most often reported as above abnormality cut-off. Additionally in AD, there was a significant disparity between carer and patient ratings on Executive and Initiation apathy, indicating patients’ impaired awareness. When comparing patient groups, there was a significant difference between carer rated apathy subtype impairments for each patient group. Validity and reliability of the DAS was found to be robust when compared to standard measures of apathy and depression. In the experimental study, a sample of ALS patients (and their carers) and healthy controls (and their informants) were recruited to complete a battery of neuropsychological tests, the DAS, other apathy and depression measures. ALS patients were impaired on tasks of executive functioning when compared to controls. Furthermore, apathy subtype deficits were associated with executive dysfunction in ALS. In conclusion, apathy is a multidimensional concept that manifests in different subtype profiles dependent on neurodegenerative disease. This has further implications for understanding and assessment of cognitive dysfunction and neuropsychiatric symptoms, such as apathy, in ALS and other neurodegenerative disease patient groups.
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Dury, R. J. "Understanding haemodynamics in neurodegenerative disease." Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/50380/.

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In this thesis, the haemodynamic, functional and structural changes in Alzheimer's Disease, Huntington's Disease and Multiple Sclerosis are assessed at 7T. Across all chapters, there is a focus on the use of Arterial Spin Labelling (ASL) to provide haemodynamic measures of perfusion (or cerebral blood flow) and transit time (TT) to provide a useful marker of disease. Arterial Spin Labelling (ASL) has the advantage that it is a non-invasive method to measure perfusion using magnetic resonance imaging (MRI). Clinically, perfusion is assessed using contrast-enhanced techniques which requires the intravenous administration of an exogenous gadolinium-based contrast agent, such as Prohance-TM and Gadovist-TM. Contrast-enhanced techniques typically provide higher SNR than ASL methods, however the non-invasive nature of ASL makes it a safe method suited for repeated measures in any subjects, including those with poor renal clearance. Additionally, gadolinium contrast agents have been shown to accumulate in neuronal tissue, and until the clinical significance of this is determined, contrast-enhanced scans should be performed with caution. In Chapter 5, arterial spin labelling is used to assess cerebral perfusion in a patient group with Alzheimer's Disease (AD) and compared with an age-matched healthy control group (HC). Functional MRI (fMRI) is used to assess functional connectivity within the default mode network (DMN) and measures compared between the AD and HC group. In addition, high resolution structural data is acquired to assess the effects of atrophy in AD. Results demonstrate a significant decrease in grey matter perfusion and a significant increase in grey matter transit time in the AD group compared the HC group. A trend showing a decrease in functional connectivity in the DMN was found in the AD group as compared to the HC group. As expected, significant grey matter loss and cortical thinning were observed in the AD group compared to the HC group. Secondly, haemodynamic and vascular changes in a Huntington's Disease (HD) patient group are assessed and compared with healthy age matched controls (HC). Phase contrast angiography is used to assess vessel density and vessel radius distributions between the two groups. Structural data was also acquired to assess grey matter volume and cortical thickness differences between the two groups. A significant reduction in perfusion was found in grey matter, putamen and the caudate in the HD group compared to the HC group. The ASL transit time was found to be significantly increased in the caudate and putamen in the HD group compared to the HC group. Phase contrast angiography data showed an increase in the frequency of smaller vessels (0.15-0.35mm) in the HD group compared to the HC group, whereas larger vessels appeared more frequently in the HC group. A significant reduction in grey matter volume was also observed in the HD group compared to the HC group, which manifested as thinning of the cortical ribbon. In the final study of this thesis, high spatial resolution arterial spin labelling is used to assess perfusion inside cortical lesions and compare with perfusion in surrounding normal appearing grey matter in a Multiple Sclerosis (MS) patient group. Grey matter perfusion as a function of distance from the cortical lesions was also assessed. It was found that cortical lesions have reduced perfusion compared to surrounding normal appearing grey matter. Perfusion increased and stabilised immediately outside of the cortical lesion itself, suggesting that the perfusion deficit observed is highly spatially localised.
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Vadnal, Jonathan. "Epigenetic Mechanisms in Neurodegenerative Disease." Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1353955013.

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Gu, Mei. "Mitochondrial function in Parkinson's disease and other neurodegenerative diseases." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.322371.

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Franco, Iborra Sandra. "Mitochondrial quality control in neurodegenerative diseases: focus on Parkinson’s disease and Huntington’s disease." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/565668.

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Darrerament s’han produït avanços importants que han contribuït al coneixement dels mecanismes de disfunció cel·lular i mort en la malaltia de Parkinson (MP) i en la malaltia de Huntington (MH). Ambdues malalties són trastorns del moviment que es caracteritzen per la pèrdua específica de neurones dels ganglis basals, les neurones dopaminèrgiques de la substància nigra (SN), en el cas de la MP i les neurones espinoses de l’estriat, en el cas de la MH. Malgrat les diferències, ambdues comparteixen processos patològics comuns com la presència de proteïnes malplegades, l’estrés oxidatiu i disfunció mitocondrial. La mitocòndria és la font d’energia principal en les cèl·lules eucariotes, però també és un orgànul dinàmic relacionat amb una gran quantitat de processos cel·lulars. La disrupció de la homeòstasis mitocondrial i la subseqüent disfunció mitocondrial juguen un paper important en la patofisiologia de les malalties neurodegeneratives. El manteniment de la integritat mitocondrial a través de diferents mecanismes de control és crític per a la superviviència neuronal. Aquesta tesi es centra en l’estudi dels mecanismes de control de qualitat mitocondrial en la MP i la MH, per tal d’entendre millor els mecanismes que duen a la mort cel·lular. En el primer capítol, he estudiat el transport de proteïnes a la mitocòndria en models in vitro i in vivo de la MP. In vitro, la inhibició del complexe I produeix una alteració del transport de proteïnes a la mitocòndria així com una disminució dels nivells de proteïnes OXPHOS, acumulació de proteïnes agregades i disminució dels nivells de chaperones mitocondrials. Per tal de restablir el transport de proteïnes mitocondrials es van sobreexpressar dos components clau del sistema de translocases: la translocasa de la membrana externa 20 (TOM20) i la translocasa de la membrana interna 23 (TIM23). La sobreexpressió in vitro de TOM20 i TIM23 va restaurar el transport de proteïnes mitocondrials i va alleugerar la disfunció mitocondrial i la mort cel·lular. La inhibició del complexe I en ratolins també dóna lloc a una alteració del transport de proteïnes mitocondrials i produeix neurodegeneració del sistema dopaminèrgic. La sobreexpressió de TIM23 va restaurar parcialment el transport de proteïnes i va protegir lleugerament les neurones dopaminèrgiques de la SN. En canvi, la sobreexpressió de TOM20 va ser incapaç de millorar el transport de proteïnes mitocondrials i, fins i tot, va exacerbar la mort cel·lular. Aquests resultats posen de relleu el paper de la disfunció del transport de proteïnes mitocondrials, en particular de dos dels seus components, en la patogènesis de la MP i suggereixen la necessitat de futurs estudis es centrin en altres elements d’aquest sistema. En el segon capítol, he estudiat el paper de la proteïna huntingtina en la mitofàgia i com la seva mutació, que dóna lloc a una expansió de glutamines, pot afectar a aquesta funció. Per a tal fi, he treballat en un model in vitro de cèl·lules estriatals ST-Q7 (control) i ST-Q111 (mutant). En condicions fisiològiques, la mitofàgia induïda no es troba mitjançada pel reclutament de parkin als mitocondris despolaritzats. La huntingtina mutada afecta la mitofàgia induïda a través de l’alteració de la seva funció de scaffold en diferents passos del procés de mitofàgia: (i) activació d’ULK1 a través de l’alliberament de mTORC1, (ii) formació del complexe Beclin 1-Vps15,(iii) interacció dels adaptadors de mitofàgia OPTN i NDP52 amb huntingtina i, (iv) amb LC3. Com a resultat, els mitocondris de les cèl·lules ST-Q111 estan més danyats i tenen una respiració mitocondrial deficient. Aquests resultats demostren la presència d’una alteració en la mitofàgia com un mecanisme lligat a la MH. En conclusió, el descobriment de noves dianes mitocondrials en la MP i MH emfatitza el paper important que juga el control de qualitat mitocondrial en la neurodegeneració.
In the past years, several important advances have expanded our understanding of the pathways that lead to cell dysfunction and death in Parkinson’s disease (PD) and Huntington’s disease (HD). Both diseases are movement disorders characterized by the loss of a specific subset of neurons within the basal ganglia, dopaminergic neurons in the substantia nigra pars compacta (SNpc), in the case of PD, and medium spiny neurons in the striatum, in the case of HD,. Despite distinct clinical and pathological features, these two neurodegenerative disorders share critical underlying pathogenic mechanisms such as the presence of misfolded and/or aggregated proteins, oxidative stress and mitochondrial anomalies. Mitochondria are the prime energy source in most eukaryotic cells, but these highly dynamic organelles are also involved in a multitude of cellular events. Disruption of mitochondrial homeostasis and the subsequent mitochondrial dysfunction plays a key role in the pathophysiology of neurodegenerative diseases. Therefore, maintenance of mitochondrial integrity through different surveillance mechanisms is critical for neuronal survival. In this thesis I have studied in depth some mitochondrial quality control mechanisms in the context of PD and HD, in order to broaden the knowledge about the pathomechanisms leading to cell death. In the first chapter I have studied mitochondrial protein import in in vitro and in vivo models of PD. In vitro, complex I inhibition, a characteristic pathological hallmark in PD, impaired mitochondrial protein import. This was associated with OXPHOS protein downregulation, accumulation of aggregated proteins inside mitochondria and downregulation of mitochondrial chaperones. Therefore, we aimed to reestablish the mitochondrial protein import by overexpressing two key components of the system: translocase of the outer membrane 20 (TOM20) and translocase of the inner membrane 23 (TIM23). Overexpression of TOM20 and TIM23 in vitro restored protein import into mitochondria and ameliorated mitochondrial dysfunction and cell death. Complex I inhibition also impaired mitochondrial protein import and led to dopaminergic neurodegeneration in vivo. Overexpression of TIM23 partially rescued protein import into mitochondria and slightly protected dopaminergic neurons in the SNpc. On the contrary, TOM20 overexpression did not rescue protein import into mitochondria and exacerbated neurodegeneration in both SNpc and striatum. These results highlight mitochondrial protein import dysfunction and the distinct role of two of their components in the pathogenesis of PD and suggest the need for future studies to target other elements in the system. In the second chapter, I have studied the role of huntingtin in mitophagy and how the polyglutamine expansion present in mutant huntingtin can affect its function. For such, I worked with differentiated striatal ST-Q7 (as control) and ST-Q111 (as mutant) cells, expressing full length huntingtin. In these conditions, induced mitophagy was not mediated by Parkin recruitment into depolarized mitochondria. Mutant huntingtin impaired induced mitophagy by altering wildtype huntingtin scaffolding activity at different steps of mitophagy process: (i) ULK1 activation through its release from the mTORC1, (ii) Beclin1-Vps15 complex formation, (iii) interaction of the mitophagy adapters OPTN and NDP52 with huntingtin and (iv) with LC3. As a result, mitochondria from ST-Q111 cells exhibited increased damage and altered mitochondrial respiration. These results uncover impaired mitophagy as a potential pathological mechanism linked with HD. In conclusion, we have discovered new mitochondrial targets for PD and HD emphasizing the important role that mitochondrial quality control plays in neurodegeneration
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Ryan, Philip. "An Investigation Into Novel Molecular Strategies Targeting Neurodegenerative Diseases." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/395102.

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Neurodegenerative diseases are characterised by the progressive loss of neuron function and structure. The most prevalent neurodegenerative diseases are hypothesized to be due to the misfolding and accumulation of specific proteins in the brain. Alzheimer’s disease (AD) is suspected to result from the aggregation of amyloid-β (Aβ) or tau proteins, Parkinson’s disease (PD) from the aggregation of α-synuclein (α-syn), and so on for numerous other diseases including Huntington’s disease, amyotrophic lateral sclerosis, and Creutzfeldt-Jakob disease. There are no curative therapies for any of these fatal diseases, only palliative care is available in some cases currently. Research is currently focussed on modulating the aggregation processes common amongst the diseases. Various projects are dedicated to targeting the protein monomers, or small oligomeric assemblies, present at the early stages toward therapy. Modern strategies to target these proteins involve the use of peptide-based agents, effective at selectively binding the proteins through engaging with multiple sites along the protein sequences; and multitarget directed ligands (MTDL), which engage with multiple pathological factors to produce an overall beneficial effect. Here we set out to investigate various novel chemical scaffolds that we envisaged may prove effective at inhibiting protein aggregation mechanisms in the hopes of identifying new strategies and promising leads. Following review of the literature, compound scaffolds were designed based on existing data and then synthetic chemistry was employed to construct panels of candidate inhibitors. The compounds synthesised were then screened against protein aggregation including Aβ, α-syn and prion formation. Chapter 2 describes the development of a novel strategy to construct selective glycopeptide-based inhibitors of protein aggregation. This strategy employs the peptide sequences that are reported to recognise the target proteins in their monomeric or oligomeric state and then hinder their aggregation via a disruptive glycoside unit. This component of the project led to the identification of an inhibitor of α-syn aggregation and provided proof-of-concept for the design. The rationale was also used for the construction of Aβ and tau-targeted inhibitors, however evaluation of their effectiveness is ongoing. Chapter 3 describes the use of the quinazoline scaffold to construct MTDLs designed to be capable of modulating the aggregation of α-syn and the formation of prion proteins. This component of the project led to the identification of a panel of highly potent inhibitors of prion formation in yeast, which are undergoing further evaluation currently, as well as a number of leads that are effective α-syn aggregation inhibitors. Chapter 4 describes investigation into α-syn oligomerisation modulating analogues of anle138b, a promising candidate undergoing preclinical development. The compounds designed and synthesised were found to be as effective as inhibiting α-syn aggregation in vitro as the preclinical candidate. Chapter 5 describes attempts at investigating the thiazolone scaffold for use in the design of MTDLs targeting protein aggregation. Unfortunately, this objective of the project was hampered by challenging syntheses and unfavourable solubility profiles, discouraging further commitment to the component of the project. In summary, a number of novel molecular scaffolds were designed, synthesised and found to be effective modulators of protein aggregation implicated in multiple neurodegenerative diseases. This project has culminated in the identification of promising leads against pathological targets for PD, prionopathy, and AD therapy, as well as contributing to the knowledgebase to stimulate future research efforts.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Pharmacy and Pharmac
Griffith Health
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Blundell, James Michael. "Cognitive assessment of paediatric neurodegenerative disease." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/6042/.

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Inherited metabolic diseases (IMD’s) are a large class of heterogeneous genetic disorders caused by dysfunction within a single pathway of intermediary metabolism. In many of these diseases, the dysfunction of metabolic enzymes leads to the accumulation of toxic metabolites which disrupts the normal development of the central nervous system. With the advent of treatments that positively influence neuropsychological outcomes, there is a need for sensitive and objective neuropsychological measures that allow patients to be systematically tracked in order to understand the efficacy of existing treatments. In this thesis, a neuropsychological test battery consisting of attention, language and oculomotor measures was developed to accurately describe individual and developmental differences between IMD patients and healthy developing controls. The functioning of five diseases was examined: Morquio syndrome (\(N\) = 12), Hurler syndrome (\(N\) = 3), Maroteux-Lamy syndrome (\(N\) = 2), Tyrosinemia type I (\(N\) = 13) and Tyrosinemia type III (\(N\) = 5). Findings indicated that disease effects were not homogeneous across tasks, and that performance on the same tasks was not uniform across diseases. The obtained data offers a promising basis for understanding how biological factors influence the severity and timecourse of developmental effects in future research.
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STOCCORO, ANDREA. "Mitoepigenetics investigations in neurodegenerative diseases." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1072183.

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Neurodegenerative diseases (NDs) represent a group of disorders characterized by the progressive neuronal loss in specific areas of the central nervous system. NDs are incurable and often fatal shortly after diagnosis. The global prevalence of these disorders is dramatically increasing worldwide as populations age and life expectancies increase. The identification of valuable biomarkers for an early diagnosis is of outmost importance as it would promote early interventions able to prevent or delay as much as possible the onset of the disease. Despite their high heterogeneity and the differences in their primary etiologies, NDs share many common aspects in relation to their clinical, biochemical, and pathological features and multiple lines of evidence suggest that mitochondrial dysfunction is involved in the pathogenesis of many NDs, especially Alzheimer´s disease (AD), Parkinson´s disease (PD) and amyotrophic lateral sclerosis (ALS). To date, several papers showed that aberrant epigenetic mechanisms in the nuclear DNA may be involved in the onset and development of NDs, and several studies have found altered gene methylation levels in both post-mortem brain specimens and peripheral tissues from patients with these diseases. In recent years growing evidence for a potential role of altered mitochondrial DNA (mtDNA) methylation and hydroxymethylation in several diseases has emerged. Although mitochondrial impairment is a classical feature of neurodegeneration, little attention has been given until now to the role of the mitochondrial epigenome itself in NDs. Particularly, studies performed so far have investigated mtDNA methylation in animal models of ALS, and in brain tissue of patients with AD, PD and ALS. However, potential mtDNA methylation alterations in peripheral tissues of NDs patients have not been investigated in those studies. The main aim of the work presented in the current thesis was to investigate the presence of mitoepigenetic signatures in peripheral blood of patients with AD (Study 1), ALS (Study 2) and PD (Study 3). DNA methylation analysis of the mitochondrial D-loop region, which regulates mitochondrial transcription and replication, was performed by means of Methylation Sensitive-High Resolution Melting and Pyrosequencing techniques. In study 1 D-loop methylation levels were analyzed in people affected by AD with different clinical dementia impairment degrees and results suggest that mtDNA methylation could vary with the stage of the disease. In study 2 D-loop methylation levels were analyzed in ALS patients with mutations in SOD1, TARDBP, FUS or C9ORF72 genes, and in their relatives, and results showed that mtDNA methylation levels were decreased in ALS tissues, partcularly in carriers of SOD1 mutations. In study 3 higher Dloop methylation levels, although not statistically significant, were detected in peripheral blood from PD patients. Results presented in the current thesis indicate a potential involvement for impaired mtDNA methylation in NDs, which is detectable in peripheral blood suggesting that this field of research deserves to be further studied. Moreover, current results suggest that mtDNA methylation could be sensitive to different disease stages and dementia levels, thus adding a new layer of interest in the search for peripheral mitoepigenetic biomarkers for neurodegeneration. Given the pivotal role of mitochondrial dysfunction and of epigenetic mechanisms in neurodegeneration, the field of mitoepigenetics in neurodegenerative diseases is a timely and attractive recent area of investigation, where preliminary results really seem encouraging, but more research is warranted to clarify the connections between epigenetic changes occurring in the mitochondrial genome, mitochondrial DNA dynamics, and the neurodegenerative process.
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Books on the topic "Neurodegenerative disease"

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W, Langston J., and Young Anne B. 1947-, eds. Neurotoxins and neurodegenerative disease. New York, N.Y: New York Academy of Sciences, 1992.

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Avila, Jesus, Jose J. Lucas, and Felix Hernandez, eds. Animal Models for Neurodegenerative Disease. Cambridge: Royal Society of Chemistry, 2011. http://dx.doi.org/10.1039/9781849732758.

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Saghir, Atif N. Free radicals in neurodegenerative disease. Birmingham: University of Birmingham, 1996.

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1952-, Marwah J., and Teitelbaum Herman, eds. Advances in neurodegenerative disorders. Scottsdale, Ariz: Prominent Press, 1998.

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Board, National Radiological Protection, ed. ELF electromagnetic fields and neurodegenerative disease. Didcot: NRPB, 2001.

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Singh, Sarika, and Neeraj Joshi, eds. Pathology, Prevention and Therapeutics of Neurodegenerative Disease. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-0944-1.

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Mauro, Fasano, ed. The proteomic approach in neurodegenerative disease research. Trivandrum, Kerala, India: Research Signpost, 2007.

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Mauro, Fasano, ed. The proteomic approach in neurodegenerative disease research. Trivandrum, Kerala, India: Research Signpost, 2007.

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Selkoe, Dennis J., and Yves Christen, eds. Immunization Against Alzheimer’s Disease and Other Neurodegenerative Disorders. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59332-1.

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von, Bernhardi Rommy, and Inestrosa Nibaldo C, eds. Neurodegenerative diseases: From molecular concepts to therapeutic targets. New York: Nova Biomedical Books, 2008.

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Book chapters on the topic "Neurodegenerative disease"

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Clausen, Torben, José Luis Trejo, Mark P. Mattson, Alexis M. Stranahan, Joanna Erion, Rosa Maria Bruno, Stefano Taddei, and Melinda M. Manore. "Neurodegenerative Disease." In Encyclopedia of Exercise Medicine in Health and Disease, 637–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_145.

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Meyer, Michael Andrew. "Neurodegenerative Diseases." In Neurologic Disease, 161–75. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39581-4_8.

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Gallagher, Damien, Robert F. Coen, and Brian A. Lawlor. "Alzheimer’s Disease." In Neurodegenerative Disorders, 57–74. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23309-3_4.

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Olszewska, Diana A., Stanley Fahn, Richard A. Walsh, and Tim Lynch. "Parkinson’s Disease." In Neurodegenerative Disorders, 85–115. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23309-3_6.

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Burke, Tom, Colin P. Doherty, Walter Koroshetz, and Niall Pender. "Huntington’s Disease." In Neurodegenerative Disorders, 167–79. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-23309-3_9.

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Gallagher, Damien J., Aine Ní Mhaolaín, Reisa A. Sperling, and Brian A. Lawlor. "Alzheimer’s Disease." In Neurodegenerative Disorders, 43–64. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84996-011-3_3.

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Walsh, Richard A., Timothy Lynch, and Stanley Fahn. "Parkinson’s Disease." In Neurodegenerative Disorders, 77–114. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84996-011-3_5.

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Pender, Niall P., and Walter J. Koroshetz. "Huntington’s Disease." In Neurodegenerative Disorders, 167–79. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84996-011-3_8.

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Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Neurodegenerative Diseases: Parkinson Disease." In Imaging Brain Diseases, 1001–20. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_37.

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Weis, Serge, Michael Sonnberger, Andreas Dunzinger, Eva Voglmayr, Martin Aichholzer, Raimund Kleiser, and Peter Strasser. "Neurodegenerative Diseases: Huntington Disease." In Imaging Brain Diseases, 1059–68. Vienna: Springer Vienna, 2019. http://dx.doi.org/10.1007/978-3-7091-1544-2_40.

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Conference papers on the topic "Neurodegenerative disease"

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Vidya, J., and Vamsidhar Yendapalli. "Comparative Analysis of Neurodegenerative disease detection using Artificial Intelligence." In 2024 International Conference on Knowledge Engineering and Communication Systems (ICKECS), 1–6. IEEE, 2024. http://dx.doi.org/10.1109/ickecs61492.2024.10616608.

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Faria, Gustavo Hugo de Souza. "The impact of epigenetics on the development of neurodegenerative diseases." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.654.

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Introduction: Neurodegenerative diseases affect thousands of people in Brazil and have been increasing in frequency with the aging population. However, little is known about the molecular mechanisms and biomarkers of these diseases, which leads to a medical approach based on symptomatic and unresolving characteristics. Epigenetics, including DNA methylation, histone modifications, and changes in regulatory RNAs, emerges as a tool for prevention of neurodegenerative diseases. Objectives: To review studies that discuss the role of epigenetics in the development of neurodegenerative diseases. Methodology: This study involved an integrative review of papers published from 2016 to 2021 by searching PubMed and Scopus. Results: The studies showed that there is evidence that epigenetic mechanisms interfere with the development of major neurodegenerative diseases. Huntington’s disease presents an altered gene from birth, but transcriptional dysregulation is characteristic of the pathology that may be correlated to the age of disease onset in the cortex. In Parkinson’s disease dysregulation of expression of a specific protein is believed to play a central role in the disease and occurs through aberrant methylation that controls activation or suppression. In relation to Alzheimer’s disease, it has been found that deregulated DNA methylation and demethylation is linked to the onset and progression of the disease. In addition, these epigenetic factors are interfered with by diet, aging, and exercise. Conclusions: Investment in epigenetic studies is needed to understand possible markers of neurodegenerative diseases, for early diagnosis and the formation of epidrugs with the ability to treat.
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Sordillo, Laura A., Peter P. Sordillo, Lin Zhang, and Robert R. Alfano. "Tryptophan and kynurenines in neurodegenerative disease." In Bio-Optics: Design and Application. Washington, D.C.: OSA, 2019. http://dx.doi.org/10.1364/boda.2019.jt4a.8.

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Zhu, Xiangyun. "Role of MRI in neurodegenerative disease." In Radiopaedia 2023. Radiopaedia.org, 2023. http://dx.doi.org/10.53347/rposter-1636.

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Rezende, Maria Clara Lopes, Maria Luiza Franco de Oliveira, Júlia Campos Fabri, Maria Júlia Filgueiras Granato, Mariana Vanon Moreira, and Leandro Vespoli Campos. "Neuroprotective Effects of Creatine Supplementation in Neurodegenerative Diseases." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.234.

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Introduction: Creatine is important in providing energy for the resynthesis of adenosine triphosphate (ATP) and in the deposition of intracellular energy, being present mainly in muscle fibers and in the brain. Supplementation with exogenous creatine can be used in neurodegenerative disorders that are related to bioenergetic deficits in the etiology and progression of the disease. Objective: Highlight the neuroprotective mechanisms of creatine supplementation in neurodegenerative diseases. Methods: In April 2021, a search was carried out on MEDLINE, with the descriptors: “Creatine” and “Neuroprotection”; and its variations, obtained in MeSH. Studies published in the last five years were included. Results: Of the 122 articles found, four were used in this work. They concluded that creatine supplementation contributes to brain bioenergetics by increasing phosphocreatine deposits, restoring mitochondrial functions and decreasing susceptibility to apoptosis. In addition, creatine intake shortly after the diagnosis of Huntington’s and Parkinson’s Diseases can be used as a complementary therapy, because improve performance in tasks of memory and intelligence. Finally, it buffers cellular concentrations of ATP, being a possible therapeutic strategy to delay or stop neurodegeneration diseases. Conclusion: Creatine promote important neuroprotective effect, but further studies on the subject are needed.
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Bogdanović, Nenad, and Vladimira Vuletić. "Alzheimer disease and Alzheimer-like dementias." In Rijeka Forum on Neurodegenerative Diseases (2 ; 2018 ; Rijeka). Hrvatska akademija znanosti i umjetnosti, 2019. http://dx.doi.org/10.21857/m16wjc6j79.

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Vuletić, Vladimira, and Nenad Bogdanović. "Dementia with Lewy bodies and Parkinson’s disease dementia." In Rijeka Forum on Neurodegenerative Diseases (2 ; 2018 ; Rijeka). Hrvatska akademija znanosti i umjetnosti, 2019. http://dx.doi.org/10.21857/m8vqrtzwv9.

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Xavier, Lais de Paiva, Gabriella de Andrade Moreira, Luana Maria Amaral Cherain, Lucas Ferreira Flávio Souza, Tânia Maria da Silva Novaretti, and Valdeci de Oliveira Santos Rigolin. "Preliminary study on the number of deaths from neurodegenerative diseases in former Brazilian soccer players." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.212.

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Background: Neurodegenerative diseases have been reported in contact sports athletes. However, soccer has not been well characterized. Concerns were raised about the risk of neurodegenerative diseases being related to professional players in this sport. Objectives: To compare mortality from neurodegenerative diseases among Brazilian soccer players with the general population of the country. Methods: We conducted a retrospective cohort study. Causes of death were obtained from Brazilian teams’ databases and online content/public domain. Results: Among 1331 soccer players, 400 died. Acute Myocardial Infarction and Neoplasms were the highest causes of death, 58 and 53, respectively. We obtained a total of 35 deaths caused by neurodegenerative diseases. Alzheimer’s disease (18 deaths) and Stroke (14 deaths) were the most prevalent causes. These results are similar to the causes most found in the general population of Brazil: ischemic heart disease, cerebrovascular disease, airway infections and Alzheimer’s, in that order. This research had the following aspects as a limitation: the sources used were laymen, so the causes of death were not presented in a technical way in some moments; furthermore, the sampling space, still reduced, presented itself as another limitation. Conclusion: Preliminary results showed no correlation between soccer in Brazil and the higher occurrence of neurodegenerative diseases. The data sources and the sample space that were used may have contributed to such conclusions. These observations need to be confirmed on a larger scale with the prolongation of the study.
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Lei, Haijun, Yujia Zhao, Yuting Wen, and Baiying Lei. "Adaptive Sparse Learning for Neurodegenerative Disease Classification." In 2017 IEEE International Symposium on Multimedia (ISM). IEEE, 2017. http://dx.doi.org/10.1109/ism.2017.51.

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Lima, Aline Fonseca, Ana Luiza Almeida Carneiro, Bruna Torres Homem Fonseca, Alessandra Augusta Barroso Penna e. Costa, Fernanda Veiga Góes, Marcela Rodriguez de Freitas, Talys Jason Pinheiro, Tania Regina Dias Saad Salles, and Ludimila Marins de Almeida Moura. "Neurodegenerative disease caused by the TRAPPC4 gene." In SBN Conference 2022. Thieme Revinter Publicações Ltda., 2023. http://dx.doi.org/10.1055/s-0043-1774598.

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Reports on the topic "Neurodegenerative disease"

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Li, Jiawang, Xiangyun Chen, Hongrui Zhang, Wei Ding, Danni Chen, Ning Liang, Haiying Tong, Zhenhong Liu, and Zhen Yang. A Systematic Review of the Capsaicin and other TRPV1 agonists effects on three neurodegenerative diseases: Alzheimer's disease, Parkinson's disease and Ischemic Stroke. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2024. http://dx.doi.org/10.37766/inplasy2024.4.0115.

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Dao, Kimberly. Relationship Between The Gut-Brain Axis, Parkinson's Disease, and Use of Canines as Animal Models in Neurodegenerative Disease Research. Ames (Iowa): Iowa State University, January 2019. http://dx.doi.org/10.31274/cc-20240624-1212.

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Millhorn, David E. Signal Transduction and Gene Regulation During Hypoxic Stress: A Potential Role in Neurodegenerative Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2001. http://dx.doi.org/10.21236/ada397765.

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Millhorn, David E. Signal Transduction and Gene Regulation During Hypoxia Stress: A Potential Role in Neurodegenerative Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada416979.

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Millhorn, David E. Signal Transduction and Gene Regulation During Hypoxic Stress: A Potential Role in Neurodegenerative Disease. Fort Belvoir, VA: Defense Technical Information Center, August 2000. http://dx.doi.org/10.21236/ada383039.

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Ramos, Lauren. Therapeutic potential of cannabinoids in the management of Alzheimer's Disease and other neurodegenerative conditions. Ames (Iowa): Iowa State University, January 2019. http://dx.doi.org/10.31274/cc-20240624-1505.

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Santos, Ana Lúcia Yaeko da Silva, Deyse Mayara Rodrigues Caron, Livia Shirahige, and Abrahão Fontes Baptista. Alterations in Corticomotor Excitability in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0078.

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Review question / Objective: To systematically evaluate the utility of TMS to follow up on ALS patients using neurophysiological metrics and to quantify corticomotor excitability compared to sham controls or other neuromuscular diseases. Condition being studied: Amyotrophic Lateral Sclerosis (ALS) is the third most common neurodegenerative disease (BRUNET et al., 2020). The condition is characterized by progressive muscle atrophy due to upper and lower motor neuron death (GOETZ, 2000).
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Liu, Yangjun, Wei Xie, Zbigniew Ossowski, Juan Li, Juan Yang, Yiming Luo, Xia Wu, and Liying Liu. Physical activity, abdominal obesity and inflammatory response in the elderly: a systematic review and meta-analysis of randomized-controlled trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2023. http://dx.doi.org/10.37766/inplasy2023.3.0051.

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Review question / Objective: The purpose of this study was to explore the effects of physical activity (i.e., type of exercise, FITT criteria, control group, other interventions) on abdominal obesity and inflammatory response in elderly? The study method was a randomized controlled trial. Condition being studied: An increasing number of studies have demonstrated that chronic inflammation is closely associated with the initiation and progression of a broad range of age-related diseases, such as cardiovascular disease, cancer, diabetes, Alzheimer’s disease, and other neurodegenerative diseases and is an independent risk factor for mortality in healthy adults. Moreover, there is strong evidence that the development of age-related diseases is linked to low-grade elevation of circulating inflammatory mediators. Therefore, future interventional researches should focus on preserving overall homeostatic balance and controlling inflammatory status in the aging patient.
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Fu, Chengwei, Ziqiang Xia, Menghan Feng, Zhicheng Zhou, and Bo Liu. Comparative efficacy of noninvasive brain stimulation for the treatment of Parkinson disease: a systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, March 2022. http://dx.doi.org/10.37766/inplasy2022.3.0151.

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Review question / Objective: A variety of noninvasive brain stimulation have been applied in patients with Parkinson disease, but it is still controversial which is the best. Condition being studied: Parkinson disease(PD) is a highly prevalent neurodegenerative disease characterized by tremor, bradykinesia, rigidity. Currently, a series of noninvasive brain stimulation(NIBS) have been developed for PD. Some meta-analysis has proved the efficacy of NIBS. However, it is still unclear which NIBS is best. Therefore, we will conduct the problem by network meta-analysis.
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Andrades, Oscar, David Ulloa, Dario Martinez, Francisco Guede, Gustava Muñoz, Luis Javier Chirosa, and Amador García. Effect of the manipulation of the variables that configure the stimulus of strength training on motor symptoms in people with Parkinson's disease: A Systematic Review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0079.

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Review question / Objective: To analyze the evidence on studies that have manipulated the variables that make up the strength training stimulus and its effects on motor symptoms in people with Parkinson's disease. Condition being studied: Parkinson's is a multisystemic neurodegenerative disease that affects the central nervous system and is caused by a loss of dopaminergic neurons in the compact part of the substantia nigra of the basal ganglia of the midbrain. People with Parkinson's disease (PEP) have non-motor and motor clinical symptoms. Classic motor symptoms are rest tremor, joint stiffness, bradykinesia, decreased balance, gait disturbances (speed, temporality, spatiality, support, and freezing) and decreased functional performance.
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