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Relevant bibliographies by topics / Molecular aspects of Amyotrophic lateral sclerosis

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Academic literature on the topic 'Molecular aspects of Amyotrophic lateral sclerosis'

Author: Grafiati

Published: 4 June 2021

Last updated: 28 July 2025

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Journal articles on the topic "Molecular aspects of Amyotrophic lateral sclerosis"

1

Dilliott, Allison A., Catherine M. Andary, Meaghan Stoltz, Andrey A. Petropavlovskiy, Sali M. K. Farhan, and Martin L. Duennwald. "DnaJC7 in Amyotrophic Lateral Sclerosis." International Journal of Molecular Sciences 23, no. 8 (2022): 4076. http://dx.doi.org/10.3390/ijms23084076.

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Protein misfolding is a common basis of many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). Misfolded proteins, such as TDP-43, FUS, Matrin3, and SOD1, mislocalize and form the hallmark cytoplasmic and nuclear inclusions in neurons of ALS patients. Cellular protein quality control prevents protein misfolding under normal conditions and, particularly, when cells experience protein folding stress due to the fact of increased levels of reactive oxygen species, genetic mutations, or aging. Molecular chaperones can prevent protein misfolding, refold misfolded proteins, or

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Strong, Michael J., and Ralph M. Garruto. "Chronic Aluminum-Induced Motor Neuron Degeneration: Clinical, Neuropathological and Molecular Biological Aspects." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 18, S3 (1991): 428–31. http://dx.doi.org/10.1017/s0317167100032601.

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ABSTRACT:The monthly intracisternal inoculation of young adult New Zealand white rabbits with low-dose (100 Μg) aluminum chloride induces aggregates of phosphorylated neurofilament that mimics the intraneuronal inclusions of amyotrophic lateral sclerosis. The chronic progressive myelopathy and topographically-specific motor neuron degeneration that occurs in the absence of suppressions of neurofilament messenger RNA levels in this model contrasts with the acute fulminant encephalomyelopathy and nonspecific gene suppressions that occur subsequent to high-dose (1000 Μg) aluminum chloride inocula

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Grunseich, Christopher, Aneesh Patankar, Joshua Amaya, et al. "Clinical and Molecular Aspects of Senataxin Mutations in Amyotrophic Lateral Sclerosis 4." Annals of Neurology 87, no. 4 (2020): 547–55. http://dx.doi.org/10.1002/ana.25681.

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Jankovic, Milena, Ivana Novakovic, Phepy Gamil Anwar Dawod, et al. "Current Concepts on Genetic Aspects of Mitochondrial Dysfunction in Amyotrophic Lateral Sclerosis." International Journal of Molecular Sciences 22, no. 18 (2021): 9832. http://dx.doi.org/10.3390/ijms22189832.

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Amyotrophic Lateral Sclerosis (ALS), neurodegenerative motor neuron disorder is characterized as multisystem disease with important contribution of genetic factors. The etiopahogenesis of ALS is not fully elucidate, but the dominant theory at present relates to RNA processing, as well as protein aggregation and miss-folding, oxidative stress, glutamate excitotoxicity, inflammation and epigenetic dysregulation. Additionally, as mitochondria plays a leading role in cellular homeostasis maintenance, a rising amount of evidence indicates mitochondrial dysfunction as a substantial contributor to di

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Bampton, Alexander, Lauren M. Gittings, Pietro Fratta, Tammaryn Lashley, and Ariana Gatt. "The role of hnRNPs in frontotemporal dementia and amyotrophic lateral sclerosis." Acta Neuropathologica 140, no. 5 (2020): 599–623. http://dx.doi.org/10.1007/s00401-020-02203-0.

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Abstract Dysregulated RNA metabolism is emerging as a crucially important mechanism underpinning the pathogenesis of frontotemporal dementia (FTD) and the clinically, genetically and pathologically overlapping disorder of amyotrophic lateral sclerosis (ALS). Heterogeneous nuclear ribonucleoproteins (hnRNPs) comprise a family of RNA-binding proteins with diverse, multi-functional roles across all aspects of mRNA processing. The role of these proteins in neurodegeneration is far from understood. Here, we review some of the unifying mechanisms by which hnRNPs have been directly or indirectly link

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Stangl, Michaela, Wolfgang Böcker, Vladimir Chubanov, et al. "Sarcopenia – Endocrinological and Neurological Aspects." Experimental and Clinical Endocrinology & Diabetes 6, no. 01 (2018): 8–22. http://dx.doi.org/10.1055/a-0672-1007.

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AbstractSarcopenia in geriatric patients is often associated with or even caused by changes of the endocrine and nervous system. The multifactorial pathogenesis of sarcopenia and additional multimorbidity in geriatric patients makes it difficult to study distinct pathogenic pathways leading to sarcopenia. Patients suffering from diabetes, Cushing’s syndrome, chronic kidney disease, Klinefelter’s syndrome or motor neuron diseases, such as amyotrophic lateral sclerosis for example are known to have impaired muscle property and reduced physical performance. These patients are typically younger an

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De Giorgio, Francesca, Cheryl Maduro, Elizabeth M. C. Fisher, and Abraham Acevedo-Arozena. "Transgenic and physiological mouse models give insights into different aspects of amyotrophic lateral sclerosis." Disease Models & Mechanisms 12, no. 1 (2019): dmm037424. http://dx.doi.org/10.1242/dmm.037424.

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Cho, HaEun, and Surabhi Shukla. "Role of Edaravone as a Treatment Option for Patients with Amyotrophic Lateral Sclerosis." Pharmaceuticals 14, no. 1 (2020): 29. http://dx.doi.org/10.3390/ph14010029.

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Amyotrophic Lateral Sclerosis (ALS), also known as Lou Gehrig’s disease, is a progressive and fatal neurodegenerative disease that leads to a loss of muscle control due to nerve cells being affected in the brain and spinal cord. Some of the common clinical presentations of ALS include weakness of muscles, changes in behavior, dysfunction in speech, and cognitive difficulties. The cause of ALS is uncertain, but through several studies, it is known that mutations in SOD1 or C9orf72 genes could play a role as a factor of ALS. In addition, studies indicate that an excessive amount of free radicals

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Tzeplaeff, Laura, Alexandra V. Jürs, Camilla Wohnrade, and Antonia F. Demleitner. "Unraveling the Heterogeneity of ALS—A Call to Redefine Patient Stratification for Better Outcomes in Clinical Trials." Cells 13, no. 5 (2024): 452. http://dx.doi.org/10.3390/cells13050452.

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Despite tremendous efforts in basic research and a growing number of clinical trials aiming to find effective treatments, amyotrophic lateral sclerosis (ALS) remains an incurable disease. One possible reason for the lack of effective causative treatment options is that ALS may not be a single disease entity but rather may represent a clinical syndrome, with diverse genetic and molecular causes, histopathological alterations, and subsequent clinical presentations contributing to its complexity and variability among individuals. Defining a way to subcluster ALS patients is becoming a central end

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Wright, Gareth S. A. "Molecular and pharmacological chaperones for SOD1." Biochemical Society Transactions 48, no. 4 (2020): 1795–806. http://dx.doi.org/10.1042/bst20200318.

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The efficacy of superoxide dismutase-1 (SOD1) folding impacts neuronal loss in motor system neurodegenerative diseases. Mutations can prevent SOD1 post-translational processing leading to misfolding and cytoplasmic aggregation in familial amyotrophic lateral sclerosis (ALS). Evidence of immature, wild-type SOD1 misfolding has also been observed in sporadic ALS, non-SOD1 familial ALS and Parkinson's disease. The copper chaperone for SOD1 (hCCS) is a dedicated and specific chaperone that assists SOD1 folding and maturation to produce the active enzyme. Misfolded or misfolding prone SOD1 also int

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Dissertations / Theses on the topic "Molecular aspects of Amyotrophic lateral sclerosis"

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Flowers, Joanna Mary. "Molecular studies in amyotrophic lateral sclerosis." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.397027.

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Skinner, Thomas. "Molecular and neurological effects of fenretinide on Amyotrophic Lateral Sclerosis." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=32585.

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Amyotrophic Lateral Sclerosis (ALS) is the most common adult motor neuron disease. Currently there is only one modestly beneficial pharmacological treatment, Riluzole, approved by the FDA. It has been documented that polyunsaturated fatty acid (PUFA) concentrations can affect the progression of neurodegenerative conditions however most interventions rely on nutritional supplementation and have limited long-term effectiveness. This thesis describes experiments using fenretinide, a synthetic retinoid capabl

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Mustill, W. "The role of the molecular chaperone HSJ1 in amyotrophic lateral sclerosis." Thesis, University College London (University of London), 2010. http://discovery.ucl.ac.uk/791950/.

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Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterised by the selective death of motor neurons. Mutations in the SOD1 gene lead to protein misfolding and cause a dominant familial form of ALS (fALS). The accumulation of misfolded proteins in proteinaceous inclusions is a prominent pathological feature in ALS and other related neurological diseases such as Alzheimer’s disease, Huntington’s disease and Parkinson’s disease. The degradation of misfolded proteins by the proteasome involves the cooperation of molecular chaperones and ubiquitin chain recognition

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Andrés, Benito Pol. "Novel molecular alterations in amyotrophic lateral sclerosis and frontotemporal lobar degeneration spectrum." Doctoral thesis, Universitat de Barcelona, 2019. http://hdl.handle.net/10803/668320.

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Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are clinically distinct neurodegenerative diseases that are connected by genetic and pathological overlap. ALS patients present with muscle weakness and spasticity associated with degeneration of motor neurons in the motor cortex, brainstem, and spinal cord that ultimately leads to death. In contrast, patients with FTLD display cognitive dysfunction associated with degeneration of neurons in the frontal and temporal lobes of the brain. Despite being clinically distinct, 15% of individuals presenting FTLD also have

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Manser, Charlotte. "Extracellular Vesicles and the Quest for Molecular Biomarkers for Amyotrophic Lateral Sclerosis." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40949.

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Amyotrophic lateral sclerosis is a relentlessly progressive and fatal neuromuscular disease with no effective biomarkers, treatments or cure. In the early stages of ALS, it can be difficult to provide a diagnosis as patients do not meet diagnostic criteria until they become symptomatic, a sign of neuron degeneration. Early detection is therefore crucial to provide access to therapeutics prior to significant neuron loss. Extracellular vesicles are an ideal source of biomarkers as they contain a mix of proteins and nucleic acids reflective of the physiological state and are released from all cel

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Di, Scala Franck. "Analysis of skeletal muscle in amyotrophic lateral sclerosis : Etiological, diagnostic and therapeutic aspects." Université Louis Pasteur (Strasbourg) (1971-2008), 2005. http://www.theses.fr/2005STR13188.

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La Sclérose Latérale Amyotrophique (SLA) est une maladie neurodégénérative caractérisée par une atteinte des neurones moteurs et une paralysie progressive des muscles du squelette. Tandis que le muscle est un tissu assez peu étudié, de nombreux travaux font de lui une cible prometteuse dans la recherche sur la maladie. L'objectif de ce travail de thèse était d'explorer les modifications d'expression génétique dans le muscle squelettique affecté par la SLA en conduisant deux approches indépendantes. Dans un premier temps, nos études d'expression génique ont ciblé la protéine Nogo-A et l'isoform

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Pek, Sim Ruth Chia. "Investigation of molecular pathogenesis of amyotrophic lateral sclerosis and mouse models of neurodegeneration." Thesis, University College London (University of London), 2008. http://discovery.ucl.ac.uk/1444143/.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting motor neurons causing a progressive fatal loss of motor function. Superoxide dismutase 1 (SOD1) was the first gene in which mutations were found to be causative in some familial ALS cases. To date, more than 140 genetic variants, with good evidence for pathogenicity in around 30 of these, have been identified in SOD1 to be causative in ALS. Although we now know that mutations in SOD1 cause the protein to acquire some unknown toxic function(s), the mechanism that leads to disease is unknown. The work presented in this

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Balendra, Rubika. "Molecular mechanisms and therapeutic strategies in C9orf72 amyotrophic lateral sclerosis and frontotemporal dementia." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10040362/.

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Background A hexanucleotide expansion in C9orf72 is a common cause of the fatal neurodegenerative disorders amyotrophic lateral sclerosis and frontotemporal dementia. We have found evidence in a Drosophila model that neurotoxicity is mediated by dipeptide repeat (DPR) proteins generated by repeat-associated non-ATG translation. Here we aimed to evaluate in models of amyotrophic lateral sclerosis and frontotemporal dementia caused by the C9orf72 mutation (C9FTD/ALS) whether DPR proteins cause nucleolar dysfunction and whether small molecules that bind C9orf72 G-quadruplex repeat RNA reduce dise

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Sama, Reddy Ranjith Kumar. "FUS/TLS in Stress Response - Implications for Amyotrophic Lateral Sclerosis: A Dissertation." eScholarship@UMMS, 2014. http://escholarship.umassmed.edu/gsbs_diss/704.

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Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease is a fatal neurodegenerative disease. ALS is typically adult onset and is characterized by rapidly progressive loss of both upper and lower motor neurons that leads to death usually within 3-5 years. About 90% of all the cases are sporadic with no family history while the remaining 10% are familial cases with mutations in several genes including SOD1, FUS/TLS, TDP43 and C9ORF72. FUS/TLS (Fused in Sarcoma/Translocated in Liposarcoma or FUS) is an RNA/DNA binding protein that is involved in multiple cellular functions includ

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Bennett, Steven Prescott. "Molecular Intervention in Mouse Models of Amyotrophic Lateral Sclerosis and Alzheimer’s Disease – Neuropathology and Behavior." Scholar Commons, 2009. http://scholarcommons.usf.edu/etd/3694.

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Neurodegeneration describes the progressive loss of structure and function of neurons, leading ultimately to cell and organism death. Although the initiating factors of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, Huntington’s, and Amyotrophic Lateral Sclerosis may be different, they share common pathophysiologies. Proteinopathies, as these diseases are now termed, are characterized by atypical deposits of proteins, often due to misfolding. Associated with these deposits are dysfunctional mitochondria, oxidative stress, disrupted axonal transport, inflammation, and apoptotic ce

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Books on the topic "Molecular aspects of Amyotrophic lateral sclerosis"

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International, Congress on Therapeutic Psychological and Research Aspects of Amyotrophic Lateral Sclerosis (1985 Varese Italy). Amyotrophic lateral sclerosis: Therapeutic, psychological, and research aspects. Plenum Press, 1987.

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2

Judy, Oliver, Findlay Ted, Schudy Patricia, and Keith Worthington ALS Society (Prairie Village, Kan.), eds. In sunshine and in shadow. Keith Worthington ALS Society, 1986.

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3

Spencer, Michael. I watch and I cry: A brain in a chair : the face of Lou Geherig's disease. Doubleday, 2013.

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1958-, Albom Mitch, ed. Mitch Albom's Tuesdays with Morrie. Dramatists Play Service, 2008.

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Simmons, Philip E. Learning to fall: The blessings of an imperfect life. Bantam Books, 2003.

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Vais, Chris J. For words: A journal of hope and healing. Published by Susan McLeod, 2003.

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Albom, Mitch. Velichaĭshiĭ urok zhizni, ili Vtorniki s Morri. Izd-vo "AST", 2010.

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Albom, Mitch. Tuesdays with Morrie: An old man, a young man and life's greatest lesson. Random House Large Print, 2007.

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Albom, Mitch. Sihʹshanbihʹhā ba Murī: [sihʹshanbihā-yi bih yād māndani]. 2-ге вид. Intishārāt-i Jayhūn, 2005.

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Albom, Mitch. Tuesdays with Morrie: An old man, a young man, and life's greatest lesson. Wheeler, 1997.

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Book chapters on the topic "Molecular aspects of Amyotrophic lateral sclerosis"

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Scharnagl, Hubert, Winfried März, Markus Böhm, et al. "Amyotrophic Lateral Sclerosis." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_98.

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2

Ferro, F. M., G. Riefolo, D. A. Nesci, and S. Mazza. "Psychodynamic Aspects in Patients with Amyotrophic Lateral Sclerosis (ALS)." In Amyotrophic Lateral Sclerosis. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5302-7_46.

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Stoothoff, William H., and Bradley T. Hyman. "From genetic defects to molecular pathogenesis of memory and movement disorders." In Amyotrophic Lateral Sclerosis, 2nd ed. CRC Press, 2021. http://dx.doi.org/10.1201/9781003076445-14.

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Wills, Anne-Marie A., and Robert H. Brown. "Amyotrophic lateral sclerosis and neurodegeneration: possible insights from the molecular biology of aging." In Amyotrophic Lateral Sclerosis, 2nd ed. CRC Press, 2021. http://dx.doi.org/10.1201/9781003076445-18.

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Strong, Michael J., Tibor Hortobágyi, Koichi Okamoto, and Shinsuke Kato. "Amyotrophic Lateral Sclerosis, Primary Lateral Sclerosis and Spinal Muscular Atrophy." In Neurodegeneration: The Molecular Pathology of Dementia and Movement Disorders. Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444341256.ch44.

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Cudkowicz, Meret E., and Robert H. Brown. "Amyotrophic Lateral Sclerosis and Related Motor Neuron Diseases." In Principles of Molecular Medicine. Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-726-0_99.

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Brown, Robert H. "Amyotrophic Lateral Sclerosis and Related Motor Neuron Disorders." In Principles of Molecular Medicine. Humana Press, 2006. http://dx.doi.org/10.1007/978-1-59259-963-9_115.

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Aquilonius, S. M., and P. G. Gillberg. "Aspects of Cholinergic Function in Amyotrophic Lateral Sclerosis." In Neurobiology of Acetylcholine. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5266-2_29.

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Filippini, Tommaso, Bernhard Michalke, Jessica Mandrioli, Aristidis M. Tsatsakis, Jennifer Weuve, and Marco Vinceti. "Selenium Neurotoxicity and Amyotrophic Lateral Sclerosis: An Epidemiologic Perspective." In Molecular and Integrative Toxicology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-95390-8_12.

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Upadhyay, Arun, Ayeman Amanullah, Vibhuti Joshi, Ribhav Mishra, and Amit Mishra. "Molecular and Cellular Insights: Neuroinflammation and Amyotrophic Lateral Sclerosis." In Inflammation: the Common Link in Brain Pathologies. Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-1711-7_8.

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Conference papers on the topic "Molecular aspects of Amyotrophic lateral sclerosis"

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Pellegrino, Giulia Michela, Giuseppe Francesco Sferrazza Papa, Dinas Aleksonis, et al. "Late Breaking Abstract - Measurement of Vital Capacity in Amyotrophic Lateral Sclerosis: Methodological Aspects." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa1361.

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Costa, Maria Alice Dias da, Danielle Antoniazzi Costa Sousa, Igor Roque de Paula, Marcela Ferreira de Andrade Rangel, and Mariana Asmar Alencar. "Fatigue presence in amiotrophic lateral sclerosis and related clinical and functional aspects." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.481.

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Background: Some symptoms are reported in Amyotrophic Lateral Sclerosis (ALS), such as fatigue, which, despite having an impact on the individual, is still poorly investigated, seeming to have a multifactorial cause and manifesting itself as tiredness. Therefore, it is necessary to investigate this symptom and check the factors associated with this condition. Objective: To investigate the presence of ALS fatigue and the correlated clinical and functional factors. Objectives: 65 people with ALS attended at the Neuromuscular Diseases Clinic of HC / UFMG participated. Demographic, clinical, funct

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Sousa, Danielle Antoniazzi Kirscht Auermann D'Allembert Costa, Julia Magalhães Waybe Gonçalves, Marcela Ferreira de Andrade Rangel, Igor Roque de Paula, and Mariana Asmar Alencar. "Pain and dysfunction in amiotrophic side sclerosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.051.

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Background: Amyotrophic Lateral Sclerosis (ALS) is a progressive disease characterized by degenerative symptoms of motor neurons. Pain has been described as a frequent symptom and is associated with a negative impact on the life of the person with ALS, however it is often neglected in clinical practice. There is a need for a better understanding of its characteristics and its relationship with the clinical and functional aspects of ALS. Objective: To investigate the occurrence and characteristics of pain in individuals with sporadic ALS and to verify the association between pain and clinical,

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