Relevant bibliographies by topics / Creutzfeldt-Jakob disease; Alzheimers; Causative

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters

Academic literature on the topic 'Creutzfeldt-Jakob disease; Alzheimers; Causative'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Creutzfeldt-Jakob disease; Alzheimers; Causative"

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Carlson, George A., and Stanley B. Prusiner. "How an Infection of Sheep Revealed Prion Mechanisms in Alzheimer’s Disease and Other Neurodegenerative Disorders." International Journal of Molecular Sciences 22, no. 9 (May 4, 2021): 4861. http://dx.doi.org/10.3390/ijms22094861.

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Although it is not yet universally accepted that all neurodegenerative diseases (NDs) are prion disorders, there is little disagreement that Alzheimer’s disease (AD), Parkinson’s disease, frontotemporal dementia (FTD), and other NDs are a consequence of protein misfolding, aggregation, and spread. This widely accepted perspective arose from the prion hypothesis, which resulted from investigations on scrapie, a common transmissible disease of sheep and goats. The prion hypothesis argued that the causative infectious agent of scrapie was a novel proteinaceous pathogen devoid of functional nucleic acids and distinct from viruses, viroids, and bacteria. At the time, it seemed impossible that an infectious agent like the one causing scrapie could replicate and exist as diverse microbiological strains without nucleic acids. However, aggregates of a misfolded host-encoded protein, designated the prion protein (PrP), were shown to be the cause of scrapie as well as Creutzfeldt–Jakob disease (CJD) and Gerstmann–Sträussler–Scheinker syndrome (GSS), which are similar NDs in humans. This review discusses historical research on diseases caused by PrP misfolding, emphasizing principles of pathogenesis that were later found to be core features of other NDs. For example, the discovery that familial prion diseases can be caused by mutations in PrP was important for understanding prion replication and disease susceptibility not only for rare PrP diseases but also for far more common NDs involving other proteins. We compare diseases caused by misfolding and aggregation of APP-derived Aβ peptides, tau, and α-synuclein with PrP prion disorders and argue for the classification of NDs caused by misfolding of these proteins as prion diseases. Deciphering the molecular pathogenesis of NDs as prion-mediated has provided new approaches for finding therapies for these intractable, invariably fatal disorders and has revolutionized the field.
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Tateishi, Jun, Tetsuyuki Kitamoto, Gen Ishikawa, and Sei-ichi Manabe. "Removal of causative agent of Creutzfeldt-Jakob disease(CJD) through membrane filtration method." membrane 18, no. 6 (1993): 357–62. http://dx.doi.org/10.5360/membrane.18.357.

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O’Rourke, K. I., T. E. Besser, M. W. Miller, T. F. Cline, T. R. Spraker, A. L. Jenny, M. A. Wild, G. L. Zebarth, and E. S. Williams. "PrP genotypes of captive and free-ranging Rocky Mountain elk (Cervus elaphus nelsoni) with chronic wasting disease." Journal of General Virology 80, no. 10 (October 1, 1999): 2765–679. http://dx.doi.org/10.1099/0022-1317-80-10-2765.

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The PrP gene encodes the putative causative agent of the transmissible spongiform encephalopathies (TSEs), a heterogeneous group of fatal, neurodegenerative disorders including human Creutzfeldt–Jakob disease, bovine spongiform encephalopathy, ovine scrapie and chronic wasting disease (CWD) of North American deer and elk. Polymorphisms in the PrP gene are associated with variations in relative susceptibility, pathological lesion patterns, incubation times and clinical course of TSEs of humans, mice and sheep. Sequence analysis of the PrP gene from Rocky Mountain elk showed only one amino acid change (Met to Leu at cervid codon 132). Homozygosity for Met at the corresponding polymorphic site (Met to Val) in humans (human codon 129) predisposes exposed individuals to some forms of Creutzfeldt–Jakob disease. In this study, Rocky Mountain elk homozygous for PrP codon 132 Met were over-represented in both free- ranging and farm-raised CWD-affected elk when compared to unaffected control groups.
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CHINO, Fumitoshi, and Tokitada OHKAWA. "GROWTH AND SPREAD OF CAUSATIVE AGENT OF CREUTZFELDT-JAKOB DISEASE IN INTRAPERITONEALLY INFECTED MICE." Japanese Journal of Medical Science and Biology 43, no. 6 (1990): 197–208. http://dx.doi.org/10.7883/yoken1952.43.197.

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Sowemimo-Coker, S. O. "Making blood safe: A filtration technology for removing infectious prions from red-cell concentrates." Biochemist 27, no. 4 (August 1, 2005): 29–32. http://dx.doi.org/10.1042/bio02704029.

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Prion diseases (TSEs, transmissible spongiform encephalopathies) are fatal neurodegenerative diseases that affect both humans and animals, including scrapie in sheep, BSE (bovine spongiform encephalopathy) in cattle and CJD (Creutzfeldt–Jakob disease) and its variant (vCJD) in humans. The recent occurrences of probable cases of transmission of vCJD through blood transfusion raises concerns about the safety of the blood supply and the possibility of transmission of the causative agent by blood transfusion from asymptomatic infected individuals.
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Weiss, Robin A. "The Leeuwenhoek Lecture 2001. Animal origins of human infectious disease." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1410 (June 29, 2001): 957–77. http://dx.doi.org/10.1098/rstb.2001.0838.

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Since time immemorial animals have been a major source of human infectious disease. Certain infections like rabies are recognized as zoonoses caused in each case by direct animal–to–human transmission. Others like measles became independently sustained with the human population so that the causative virus has diverged from its animal progenitor. Recent examples of direct zoonoses are variant Creutzfeldt–Jakob disease arising from bovine spongiform encephalopathy, and the H5N1 avian influenza outbreak in Hong Kong. Epidemics of recent animal origin are the 1918–1919 influenza pandemic, and acquired immune deficiency syndrome caused by human immunodeficiency virus (HIV). Some retroviruses jump into and out of the chromosomal DNA of the host germline, so that they oscillate between being inherited Mendelian traits or infectious agents in different species. Will new procedures like animal–to–human transplants unleash further infections? Do microbes become more virulent upon cross–species transfer? Are animal microbes a threat as biological weapons? Will the vast reservoir of immunodeficient hosts due to the HIV pandemic provide conditions permissive for sporadic zoonoses to take off as human–tohuman transmissible diseases? Do human infections now pose a threat to endangered primates? These questions are addressed in this lecture.
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E. Miller, Sara, and David N. Howell. "Emerging Pathogens: Something Old, Something New." Microscopy and Microanalysis 7, S2 (August 2001): 164–65. http://dx.doi.org/10.1017/s1431927600026891.

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Infectious diseases are the leading cause of death worldwide and the third leading cause in the US. Among these maladies are many that can be classified as emerging diseases. Some of these disorders may be caused by truly novel pathogens. in others, the causative organisms have been present for many years (for some, probably millennia), but have escaped detection until recently. Still others represent the re-emergence of known pathogenic organisms after a long period of quiescence. The mention of emerging pathogens brings to mind sensational exotic and feared microorganisms such as Ebola virus, human immunodeficiency virus (HIV), hantavirus, West Nile virus, Yersinia pestis (plague), and prion diseases such as bovine spongiform encephalitis (BSE, “mad cow” disease) which have been associated with variant Creutzfeldt- Jakob disease (CJD) in humans. However, other organisms that have been known for some time can be classified as emerging pathogens as they continually mutate, recombine, and adapt, causing misery and death.
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Garcés, Moisés, Isabel M. Guijarro, Diane L. Ritchie, Juan J. Badiola, and Marta Monzón. "Novel Morphological Glial Alterations in the Spectrum of Prion Disease Types: A Focus on Common Findings." Pathogens 10, no. 5 (May 13, 2021): 596. http://dx.doi.org/10.3390/pathogens10050596.

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Human prion diseases are a group of rare fatal neurodegenerative diseases with sporadic, genetic, and acquired forms. They are neuropathologically characterized by pathological prion protein accumulation, neuronal death, and vacuolation. Classical immunological response has long been known not to play a major in prion diseases; however, gliosis is known to be a common feature although variable in extent and poorly described. In this investigation, astrogliosis and activated microglia in two brain regions were assessed and compared with non-neurologically affected patients in a representative sample across the spectrum of Creutzfeldt–Jakob disease (CJD) forms and subtypes in order to analyze the influence of prion strain on pathological processes. In this report, we choose to focus on features common to all CJD types rather than the diversity among them. Novel pathological changes in both glial cell types were found to be shared by all CJD types. Microglial activation correlated to astrogliosis. Spongiosis, but not pathological prion protein deposition, correlated to both astrogliosis and microgliosis. At the ultrastructural level, astrocytic glial filaments correlated with pathological changes associated with prion disease. These observations confirm that neuroglia play a prominent role in the neurodegenerative process of prion diseases, regardless of the causative prion type.
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Chapman, A. H., and Djalma Vieira e. Silva. "Creutzfeldt-Jakob disease a case report, with special attention to the electroencephalogram in this disorder and to its possible relationships to kuru, scrapie and «mad cow disease»." Arquivos de Neuro-Psiquiatria 51, no. 2 (June 1993): 258–66. http://dx.doi.org/10.1590/s0004-282x1993000200020.

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A case of Creutzfeldt-Jakob disease in a 58-year-old Brazillian cattle rancher and businessman is presented. The EEG was normal, which is consistent with the fact that it was made during the first half of his illness; in a later stage suppression of normal rhythms by slow moderate voltage waves would be expected. The resemblances of kuru, scrapie and "mad cow disease» to C-J disease are discussed. In each of these 4 illnesses the patient or affected animal (scrapie and «mad cow disease") (a) has a widespread spongiform encephalopathy and consequent dementia, myoclonic epilepsy and cerebellar and corticospinal symptoms, (b) Each illness is caused by a virus (or virus-like organism called a PrP or prion) which is unusually resistant to heat and entirely resistant to ultraviolet light and x-rays, (c) This causative agent can be transmitted to other mammals by intracerebral injection or, in the proved cases of 3 of them, by the oral route. Unresolved questions about C-J disease include the following: Are C-J disease, kuru, scrapie and "mad cow disease" essentially similar illnesses caused by the same virus or by subtle variants of it? What is the incubation period of C-J disease, and does its virus exist for long periods of time in some asymptomatic persons, some of whom may never become neurologically ill? How does this virus enter the bodies of most persons with C-J disease, and why does the clinical disease characteristically occur only in middle age?
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Gómez-López, Vıctor Manuel, Amparo Viramontes-Pintos, Miguel Ángel Ontiveros-Torres, Linda Garcés-Ramírez, Fidel de la Cruz, Ignacio Villanueva-Fierro, Marely Bravo-Muñoz, et al. "Tau Protein Phosphorylated at Threonine-231 is Expressed Abundantly in the Cerebellum in Prion Encephalopathies." Journal of Alzheimer's Disease 81, no. 2 (May 18, 2021): 769–85. http://dx.doi.org/10.3233/jad-201308.

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Background: Transmissible spongiform encephalopathies (TSEs) are rare neurodegenerative disorders that affect animals and humans. Bovine spongiform encephalopathy (BSE) in cattle, and Creutzfeld-Jakob Disease (CJD) in humans belong to this group. The causative agent of TSEs is called “prion”, which corresponds to a pathological form (PrPSc) of a normal cellular protein (PrPC) expressed in nerve cells. PrPSc is resistant to degradation and can induce abnormal folding of PrPC, and TSEs are characterized by extensive spongiosis and gliosis and the presence of PrPSc amyloid plaques. CJD presents initially with clinical symptoms similar to Alzheimer’s disease (AD). In AD, tau aggregates and amyloid-β protein plaques are associated with memory loss and cognitive impairment in patients. Objective: In this work, we study the role of tau and its relationship with PrPSc plaques in CJD. Methods: Multiple immunostainings with specific antibodies were carried out and analyzed by confocal microscopy. Results: We found increased expression of the glial fibrillary acidic protein (GFAP) and matrix metalloproteinase (MMP-9), and an exacerbated apoptosis in the granular layer in cases with prion disease. In these cases, tau protein phosphorylated at Thr-231 was overexpressed in the axons and dendrites of Purkinje cells and the extensions of parallel fibers in the cerebellum. Conclusion: We conclude that phosphorylation of tau may be a response to a toxic and inflammatory environment generated by the pathological form of prion.
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Dissertations / Theses on the topic "Creutzfeldt-Jakob disease; Alzheimers; Causative"

1

Betmouni, Samar. "Inflammatory response in a mouse model of scrapie." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.361753.

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Book chapters on the topic "Creutzfeldt-Jakob disease; Alzheimers; Causative"

1

Sanz, Marta Gonzalez, and Caoimhe Nic Fhogartaigh. "Zoonotic Infections." In Tutorial Topics in Infection for the Combined Infection Training Programme. Oxford University Press, 2019. http://dx.doi.org/10.1093/oso/9780198801740.003.0046.

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The term zoonosis comes from the Greek: ζῷον (zoon) ‘animal’ and νόσος (nosos) ‘sickness’, and means an infection transmissible from animals to humans. Infected animals can be symptomatic or asymptomatic, and humans usually become accidental hosts through close contact with the reservoir animal. Six out of ten infections in humans globally are spread from animals, and 75% of emerging infections are zoonotic. Some occur worldwide e.g. E. coli O157:H7, whereas some are more restricted geographically, e.g. Ebola virus. The highest burden is in developing countries. There are various classifications of zoonoses. ● Causative pathogen: bacterial (anthrax, non-typhoidal Salmonelloses); viral (rabies, Yellow Fever, hantaviruses); parasitic (hookworm, Giardia, toxoplasmosis); fungal (dermatophytes, histoplasmosis); or prion (new-variant Creutzfeldt-Jakob disease). ● Mode of transmission (see Section 35.3 and Table 35.1 below) ● Distribution: endemic zoonoses are continually present in a population (e.g. leptospirosis, brucellosis); epidemic zoonoses occur intermittently (e.g. anthrax, Rift Valley Fever); emerging zoonoses are new infections, or existing infections that are increasing in incidence or geographical range (e.g. Nipah virus, Middle East Respiratory Syndrome coronavirus). ● Direct contact: infectious particles are present on an infected animal, in its body fluids, and in its excreta. Q fever, caused by Coxiella burnetii, and brucellosis may be acquired by direct contact with infected animals, particularly during parturition; cat-scratch disease caused by Bartonella henselae, and Pasteurella spp. may be acquired by bites or scratches from cats, and rabies from canine bites. Many zoonoses are also transmitted via indirect animal contact through exposure to soil or water contaminated by infectious material, e.g. leptospirosis may be acquired when water contaminated with infected rats’ urine comes into contact with broken skin or mucous membranes. ● Ingestion: infection occurs by ingesting contaminated food or water, e.g. unpasteurized milk, poorly processed or undercooked meat, or by eating/ drinking after handling animals without handwashing. Listeria, bovine tuberculosis, and brucellosis may be transmitted by unpasteurized milk and dairy produce; Hepatitis E through processed pork, and Ebola and Marburg through bushmeat. ● Vector-borne: infection is transmitted through a biting arthropod vector. Examples include West Nile Virus and Japanese encephalitis from mosquitoes, Lyme disease, tick-borne encephalitis, and Rocky Mountain Spotted Fever from ticks, and Rickettsia typhi from rat fleas.
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