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Relevant bibliographies by topics / Creutzfeldt-Jakob disease

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Academic literature on the topic 'Creutzfeldt-Jakob disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 17 June 2025

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Journal articles on the topic "Creutzfeldt-Jakob disease"

1

Kovacs, G. G., S. Horvath, T. Strobel, et al. "Genetic Creutzfeldt-Jakob disease mimicking variant Creutzfeldt-Jakob disease." Journal of Neurology, Neurosurgery & Psychiatry 80, no. 12 (2009): 1410–11. http://dx.doi.org/10.1136/jnnp.2008.163733.

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Martindale, Jennifer, Michael D. Geschwind, Stephen De Armond, et al. "Sporadic Creutzfeldt-Jakob Disease Mimicking Variant Creutzfeldt-Jakob Disease." Archives of Neurology 60, no. 5 (2003): 767. http://dx.doi.org/10.1001/archneur.60.5.767.

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Stricof, Rachel L., Patricia P. Lillquist, Nadia Thomas, Ermias D. Belay, Lawrence B. Schonberger, and Dale L. Morse. "An Investigation of Potential Neurosurgical Transmission of Creutzfeldt-Jakob Disease: Challenges and Lessons Learned." Infection Control & Hospital Epidemiology 27, no. 3 (2006): 302–4. http://dx.doi.org/10.1086/503017.

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In 2001, New York State health officials were notified about 2 patients with Creutzfeldt-Jakob disease who had undergone neurosurgical procedures at the same hospital within 43 days of each other. One patient had Creutzfeldt-Jakob disease at the time of surgery; the other patient developed Creutzfeldt-Jakob disease 6.5 years later. This investigation highlights the difficulties in assessing possible transmission of Creutzfeldt-Jakob disease.

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Yash Srivastav and Abdul Hameed. "Creutzfeldt-Jakob Disease (CJD): A Deadly Neurodegenerative Condition; Its Epidemiology, Monitoring, Current Status of Prevention and Circumvention." Asian Journal of Pharmaceutical Research and Development 12, no. 6 (2024): 125–30. https://doi.org/10.22270/ajprd.v12i6.1491.

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Creutzfeldt-Jakob Disease CJDis a rare brain ailment that causes dementia. It is often referred to as Creutzfeldt-Jakob. It is a member of a class of illnesses called prion disorders that affect both humans and animals. Alzheimer's disease and Creutzfeldt-Jakob disease symptoms can be comparable.A rare yet deadly neurodegenerative condition is Creutzfeldt-Jakob disease (CJD). According to reports, it affects one in one to one and a half million people worldwide each year, with less than 1,000 cases occurring in the US.A deadly neurodegenerative condition, Creutzfeldt-Jakob disease (CJD) is also referred to as subacute spongiform encephalopathy or neurocognitive dysfunction caused by prion disease. Memory issues, behavioural changes, poor coordination, and visual impairments are some of the early indications. Dementia, uncontrollable movements, blindness, paralysis, and coma are later signs. Within a year, almost 70% of people pass away.In 1922, Walther Spielmeyer coined the term "Creutzfeldt–Jakob disease" in honour of the German neurologists Hans Gerhard Creutzfeldt and Alfons Maria Jakob. A protein called a prion folds abnormally to cause CJD. Misfolded proteins known as infectious prions can cause other misfolded proteins to do the same.People with CJD experience a variety of symptoms, such as uncontrollable muscle spasms or mobility issues, memory loss, and cognitive challenges. Because CJD causes so much damage, it is ultimately fatal.The diseases CJD and variant CJD (vCJD) are not the same, despite their very similar names. They're both prion illnesses. But eating meat from cows with bovine spongiform encephalopathy, also known as Mad Cow Disease, is linked to variant CJD. CJD mostly happens seldom and is sometimes referred to as "classic CJD" to prevent confusion.Although there isn't a known cure for Creutzfeldt-Jakob disease (CJD), the National Prion Clinic is doing clinical research to look at potential therapies. Currently, the goal of treatment is to keep the patient as comfortable as possible while using medications to lessen symptoms.The present state of Creutzfeldt-Jakob disease (CJD), its underlying causes, and possible treatments are assessed in this article.

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Le, Viet H. "Creutzfeldt-Jakob Disease." Journal of the American Osteopathic Association 119, no. 1 (2019): 63. http://dx.doi.org/10.7556/jaoa.2019.010.

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Coulthart, Michael B., and Beau M. Ances. "Creutzfeldt-Jakob disease." Neurology: Clinical Practice 5, no. 2 (2015): 99–101. http://dx.doi.org/10.1212/cpj.0000000000000103.

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Maldonado, Sonny, James B. Gross, and Eileen H. Bigio. "Creutzfeldt-Jakob Disease." Baylor University Medical Center Proceedings 11, no. 2 (1998): 89–98. http://dx.doi.org/10.1080/08998280.1998.11930089.

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MASTERS, COLIN L. "CREUTZFELDT-JAKOB DISEASE." Alzheimer Disease & Associated Disorders 3, no. 1 (1989): 46–51. http://dx.doi.org/10.1097/00002093-198903010-00006.

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9

Su, Ming-Shung, Shuu-Jiun Wang, Hung Chiang, et al. "Creutzfeldt- Jakob Disease." European Neurology 33, no. 3 (1993): 241–43. http://dx.doi.org/10.1159/000116945.

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Finkelstein, Lori E., Meryl H. Mendelson, Carmelita Tejero, and Jeanine Troccoli. "Creutzfeldt-Jakob Disease." American Journal of Nursing 98, no. 9 (1998): 66–67. http://dx.doi.org/10.1097/00000446-199809000-00054.

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Dissertations / Theses on the topic "Creutzfeldt-Jakob disease"

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Heslin, Donna E. "Lesion profiling in Creutzfeldt-Jakob disease." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ58829.pdf.

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Bunn, Tristan. "Prion protein biochemistry in Creutzfeldt-Jakob disease." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/23281.

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Macleod, Margaret-Ann. "The clinico-pathological phenotype of sporadic Creutzfeldt-Jakob disease." Thesis, University of Edinburgh, 2002. http://hdl.handle.net/1842/28507.

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Creutzfeldt-Jakob Disease (CJD) is a rare neurodegenerative disorder of the human central nervous system. It occurs in four main forms, defined essentially according to aetiology: sporadic, variant, iatrogenic and familial. All forms of the disease are characterised by the deposition of an abnormal cellular protein, the prion protein (PrP^sc), within the brain. Definitive diagnosis depends on identifying this along with other neuropathological changes such as spongiform degeneration and astrocytic gliosis. To date variant CJD has followed a relatively stereotyped clinical course with fairly consistent pathological findings. However, various clinico-pathological phenotypes of sporadic CJD have been described. It is believed the disease phenotype is influenced by a number of factors including agent strain (PrP^res isotype being used as a surrogate marker), and genotype (particularly a polymorphism at codon 129 of the prion protein gene). Data on 99 cases of sporadic CJD and 43 cases of variant CJD were analysed. The sporadic CJD cases were divided into 6 sub-groups, according to genotype at codon 129 (either methionine homozygous, valine homozygous or heterozygous) and PrP^res isotype (either type 1 or 2A). Some trends in clinico-pathological phenotype were found. Notably, the methionine homozygous cases with type 1 PrP^res isotype formed the majority of cases and followed a reasonably uniform disease course. The other groups tended to include atypical cases. These differences did not achieve statistical significance and there was considerable overlap amongst cases. 14-3-3 protein and the use of MR imaging were analysed. The results suggest that these investigations may improve the diagnostic classification of sporadic CJD. The variant CJD cases followed a relatively consistent clinico-pathological course, consistent with a distinct aetiology and probably a distinct strain. The data do not support the hypothesis that different strains of the sporadic CJD agent cause distinct clinico-pathological phenotypes.

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Cordery, R. J. "The early diagnosis and management of Creutzfeldt-Jakob disease." Thesis, University College London (University of London), 2004. http://discovery.ucl.ac.uk/1446588/.

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This thesis describes work undertaken to improve the early diagnosis of variant Creutzfeldt-Jakob disease (vCJD), using existing clinical and research tools. Twenty-one cases referred to the National Hospital for Neurology and Neurosurgery and St. Mary's Hospital, London with suspected vCJD completed participation in the study. Fifteen cases were confirmed with definite or probable vCJD and six were given alternative diagnoses. These six cases with alternative diagnoses formed a control group. Further controls were recruited from patients referred with sporadic and familial forms of prion disease. A neuropsychiatry questionnaire comprising a battery of standardised tests was formulated. Of those with definite or probable vCJD, 86% exhibited anxiety, 93% irritability, 64% agitation and 79% displayed evidence of severe depressive symptoms. Fifty seven percent experienced simple delusions, most commonly of theft and suspicion and 36% described misidentifications (mean 8 months from illness onset). Behavioural change was common to all cases, 79% with aggression, 71% emotional lability and 79% sleep problems. Comprehensive neuropsychology assessments from those with vCJD were compared with sporadic and familial cases. Moderate to severe intellectual decline is characteristic of vCJD and impairment affects all cognitive domains. Only a minority of the vCJD cases presented with perceptual impairment compared with 50% of sporadic and familial cases. The proportion of cases with nominal impairment in the familial disease group was significantly lower than in the variant and sporadic groups. Serial volumetric MR imaging was only possible in a subgroup of cases with familial CJD. The annual mean rate of whole brain atrophy was 2.05% compared to 0.25% in normal controls. Single voxel proton magnetic spectroscopy performed in three cases with vCJD showed a 2.5 fold (150%) increase in the mean myo-inositol concentration and 50% reduction in N-acetylaspartate in the pulvinar region. Similar changes were seen in the caudate nucleus where no signal change was detected on T2 weighted images. The key to early diagnosis still relies on a high index of suspicion for vCJD and early referral to the appropriate specialist services. First hand experience of the problems faced by patients prompted a second, parallel project to be undertaken. A survey was conducted of all UK consultant neurologists and old age psychiatrists to assess current practices in the diagnosis and management of young people with dementia. It was concluded that young people may be under investigated if managed solely by an old age psychiatrist and may not receive adequate follow up services if managed solely by a neurologist.

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Mackay, Graham. "Clinico-pathological phenotypes of sporadic CJD in relation to PpPres type." Thesis, University of Aberdeen, 2012. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=202124.

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Zeidler, Martin. "A new variant of Creutzfeldt-Jakob disease in the United Kingdom." Thesis, University of Southampton, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274425.

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de, Vries Kay. "Caring for the person with variant Creutzfeldt-Jakob disease within the hospice service." Thesis, University of Surrey, 2006. http://epubs.surrey.ac.uk/842755/.

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This thesis explores the experience of caring for people with the new diseases of variant Creutzfeldt-Jakob disease (CJD) by hospice services. The experiences of the hospice staff and carers of five people, who had died, or were dying, as a result of variant CJD, at three different hospice sites in the South of England were explored. Data from four focus groups and 11 interviews, with hospice staff (included health care assistants, nurses, doctors and social workers) and family members, plus hospice patient records were analysed. Media material was also examined and used to inform the study. The thesis offers a theoretical explanation of these experiences developed through grounded theory methodology using an emergent fit design. It describes the event of the admission into the hospice service of a person with a new disease, that of variant CJD, and how the dying experience of these people was managed by both in-house and community hospice teams, 'Open systems' theory is used to assist in analysis and interpretation of the participant experiences, and as a means of 'contextualising' the hospice service. The hospice is presented as a metaphorical container within which dying is processed, and where the primary task of the organisation had a different emphasis and focus, depending on individual perspectives of participants. A theory of 'dealing with the unknown' was developed to explain the impact of this new disease on system equilibrium. The disease was a novelty and influenced admissions into the service and responses to the disease by others. It engendered the need for staff to use controlling practices to maintain the system balance. There were paradoxes between the practices of in-house and community teams, and between in- house and family member 'understanding' of how care was managed. The experience of caring for people with variant CJD was also profoundly humbling for participants. Humility was identified as a response to the realisation of limitations in relieving the suffering of people with variant CJD and their families. The study demonstrated change over time, where hospice staff moved from not knowing to becoming knowledgeable about managing the care of the person with variant CJD. The theory is complimented by and builds on existing theories of hospice practice.

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Choi, Young Pyo. "PrPSc complexity in different forms of Creutzfeldt-Jakob disease identified using biochemical approaches." Thesis, University of Edinburgh, 2010. http://hdl.handle.net/1842/4798.

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Transmissible spongiform encephalopathies (TSEs) or prion diseases are a group of fatal neurodegenerative diseases affecting humans and animal species. Prion diseases are characterized by the conversion of the host encoded prion protein (PrPC) into a disease-associated isoform (PrPSc), which (according to the prion hypothesis) is thought to be the main component of the infectious agent. PrPSc has been traditionally distinguished from PrPC by its biochemical properties, such as partial resistance to proteolysis and detergent-insolubility. In the absence of a foreign nucleic acid genome associated with prion diseases, efforts to provide a molecular basis for the biological diversity of prions have focused on biochemical characterization of PrPSc. In Creutzfeldt-Jakob disease (CJD) and other forms of human prion disease, the biochemical characterization of PrPSc has been largely restricted to the analysis of PK-resistant fragments of PrPSc (PrPres) by Western blot. However, given recent findings on the complexity of PrPSc identified in laboratory prion strains, PrPres analysis alone may not provide a complete description of PrPSc present in CJD brains. For a more complete characterization of PrPSc in human prion diseases, this study investigated biochemical properties of PrPSc in different forms of CJD by employing approaches that differ in principle from conventional Western blot analysis of PrPres. The novel biochemical approaches used in this study have identified further complexity of PrPSc accumulated in CJD brains, not only between different forms of CJD but also within single cases of individual disease entities. In this study, the two biochemical criteria most frequently used to define PrPSc (3F4 epitope accessibility versus resistance to limited proteolysis) did not always correlate, indicating probable non-uniform distribution of PK-sensitive isoform of PrPSc within the same CJD brains. In variant CJD (vCJD) brains, the thalamic region, which is characterized by distinct neuropathological features, could also be distinguished from frontal cortex and cerebellum by the sedimentation profiles of PrPC and PrPSc on sucrose step gradients. Moreover, the conformational stability of PrPSc was found not to be uniform among human prion diseases and did not correlate with PrPres type or prion protein genotype. Taken together, the results from this study provide a more complete description of PrPSc species occurring in CJD brains and contribute to a fuller understanding of the agents and the disease processes involved in humans.

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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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Ironside, James Wilson. "Neuropathology and molecular biology of iatrogenic Creutzfeldt-Jakob disease in UK human growth hormone recipients." Thesis, University of Edinburgh, 2017. http://hdl.handle.net/1842/28933.

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Creutzfeldt-Jakob disease (CJD) is the commonest form of human prion disease and occurs in sporadic, genetic and acquired forms. The causative agents (prions) appear to be composed entirely of a modified host protein, the prion protein, which undergoes misfolding to a disease-associated isoform closely associated with infectivity that is resistant to conventional methods of decontamination. Prions can be transmitted from one individual to another by medical and surgical procedures, resulting in iatrogenic CJD (iCJD). The commonest cause of iCJD is the inoculation of cadaveric pituitary-derived human growth hormone (hGH) to treat growth hormone deficiency in children; this form of treatment was abandoned in 1985 after the first UK case of iCJD in a hGH recipient was identified. Seventy-eight cases of iCJD have since occurred in the UK cohort of 1849 hGH recipients, including a case in 2016. This thesis describes a comprehensive tissue-based and molecular genetic analysis of the largest series (35 cases) of UK hGH-iCJD cases reported to date, including in vitro kinetic molecular modelling of genotypic factors influencing prion transmission. The results show that the polymorphism at codon 129 of the prion protein gene strongly influences the disease incubation period in hGH-iCJD (from 7.8-32.3 years in this series) and interacts with the infectious prion strain to govern the molecular and pathological characteristics of iCJD. The findings are consistent with the hypothesis that the UK hGH-iCJD epidemic resulted from transmission of the V2 human prion strain, which is found in the second most common form of sporadic CJD. The investigation also found accumulation of the amyloid beta (Aβ) protein associated with Alzheimer’s disease (AD) in the brains and cerebral blood vessels in 18/35 hGH-iCJD patients and 5/12 control patients who had been treated with hGH, but died from causes other than iCJD. In contrast, Aβ accumulation was markedly less prevalent in age-matched patients who died from sporadic CJD (1/15 cases) and variant CJD (2/33 cases). These results are consistent with the hypothesis that Aβ, which can accumulate in the pituitary gland, was present in the inoculated hGH preparations and seeded into the brains of around 50% of all hGH recipients, producing AD-like neuropathology and cerebral amyloid angiopathy (CAA). This provides further evidence of the prion-like properties of Aβ and gives insight into the potential for possible transmission of AD/CAA. It is uncertain whether any Aβ seeding within the brains of surviving patients in the UK hGH recipient cohort will ultimately result in clinical AD; however, the CAA in these patients may be complicated by intracerebral haemorrhage resulting from rupture of the blood vessels damaged by Aβ accumulation within their walls.

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Books on the topic "Creutzfeldt-Jakob disease"

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Society, Alzheimer's Disease, and Creutzfeldt-Jakob Disease Support Network, eds. Creutzfeldt-Jakob disease. 3rd ed. Alzheimer's Disease Society, 1996.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports., ed. Creutzfeldt-Jakob disease. The Institutes, 1998.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports, ed. Creutzfeldt-Jakob disease. The Institutes, 1998.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports, ed. Creutzfeldt-Jakob disease. The Institutes, 1998.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports, ed. Creutzfeldt-Jakob disease. The Institutes, 1998.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports., ed. Creutzfeldt-Jakob disease. The Institutes, 1998.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports., ed. Creutzfeldt-Jakob disease. The Institutes, 1998.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports, ed. Creutzfeldt-Jakob disease. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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National Institute of Neurological and Communicative Disorders and Stroke. Office of Scientific and Health Reports., ed. Creutzfeldt-Jakob disease. U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1986.

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Toshio, Mizutani, and Shiraki Hirotsugu 1917-, eds. Clinicopathological aspects of Creutzfeldt-Jakob disease. Elsevier, 1985.

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Book chapters on the topic "Creutzfeldt-Jakob disease"

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Valk, Jacob, and Marjo S. van der Knaap. "Creutzfeldt-Jakob Disease." In Magnetic Resonance of Myelin, Myelination, and Myelin Disorders. Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-02568-0_38.

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Sikorska, Beata, Richard Knight, James W. Ironside, and Paweł P. Liberski. "Creutzfeldt-Jakob Disease." In Advances in Experimental Medicine and Biology. Springer US, 2012. http://dx.doi.org/10.1007/978-1-4614-0653-2_6.

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Hawkins, Kari, Robert G. Will, and Narinder Kapur. "Creutzfeldt-Jakob Disease." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_547.

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Song, Wenyan, and Ruichi Zhang. "Creutzfeldt-Jakob Disease." In Radiology of Infectious Diseases: Volume 1. Springer Netherlands, 2015. http://dx.doi.org/10.1007/978-94-017-9882-2_11.

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Hawkins, Kari, Robert G. Will, and Narinder Kapur. "Creutzfeldt-Jakob Disease." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_547-3.

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Gibbs, Clarence J., and David M. Asher. "Creutzfeldt-Jakob Disease." In Abnormal States of Brain and Mind. Birkhäuser Boston, 1989. http://dx.doi.org/10.1007/978-1-4899-6768-8_15.

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Franceschi, Ana M., Michael J. Hoch, and Timothy M. Shepherd. "Creutzfeldt-Jakob Disease." In PET/MR Imaging. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-65106-4_127.

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Kovanlikaya, Ilhami, and Gloria C. Chiang. "Creutzfeldt-Jakob Disease." In Hybrid PET/MR Neuroimaging. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-82367-2_33.

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Hawkins, Kari, R. G. Will, and Narinder Kapur. "Creutzfeldt-Jakob Disease." In Encyclopedia of Clinical Neuropsychology. Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_547.

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Peters, Nils, Martin Dichgans, Sankar Surendran, et al. "Creutzfeldt-Jakob Disease." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8505.

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Conference papers on the topic "Creutzfeldt-Jakob disease"

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Chatterjee, Rishit, and Kazutaka Takahashi. "A nested cross validation approach to machine learning model performance evaluation on a small dataset for Creutzfeldt-Jakob disease diagnosis." In 2024 46th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2024. https://doi.org/10.1109/embc53108.2024.10782803.

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Guelli, Mariana Sandoval Terra Campos, Daniela Bastos de Almeida Zampier, Lorena Araújo Silva Dias, and Marina de Oliveira Nunes Ibrahim. "Creutzfeldt-Jakob Disease - a literature review." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.126.

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Background: Creutzfeldt-Jakob disease (CJD) is a progressive, rare, fatal and rapid human neurodegenerative disease that occurs in the etiologies: sporadic (CJD), familial, iatrogenic (CJD) and CJD variant (CJV) in which cell prion protein (PrP) can be transmitted through animals. Objectives: Literature review about Creutzfeldt-Jakob diseaseDesign and setting: Literature review development in the Centro Universitário de Volta Redonda, Rio de Janeiro, Brazil. Methods: The Creutzfeldt-Jakob disease, infectious diseases and neuroinfection indexes were used in the PUBMED and Scielo databases. Results:CJD has different etiologies with different clinical and pathological phenotypes. CJDV shows psychiatric behaviors and symptoms followed by abnormalities, ataxia and dementia. The sporadic form is the most common, with a progressive clinical course with generalized brain deposition of abnormal prion protein aggregates (PrPTSE) that leads to spongiform change, gliosis and neuronal loss. CJD progresses to dementia and two or more symptoms: cerebellar or visual impairments; pyramidal or extrapyramidal signs; myoclonus; and akinetic mutism. Complex periods of acute wave in the electroencephalogram (EEG) are strongly suggestive of prionic diseases. Rapidly evolving field neuroimmune disorders have shown an increasing in autoantibody testing; attempt to diagnose a range of immune-mediated conditions. Evidence indicates that diffusion-weighted magnetic resonance imaging (DWI) is more sensitive for detecting signal abnormalities. Conclusion: The disease progresses to dementia, accompanied by myoclonus, pyramidal signs and characteristic EEG. It is a complex pathology, which has only symptomatic treatment and requires strict control of reservoirs and risk of contamination.

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WILL, R. G. "CREUTZFELDT-JAKOB DISEASE AND BLOOD TRANSFUSION." In The 32nd Session of International Seminars and International Collaboration. WORLD SCIENTIFIC, 2005. http://dx.doi.org/10.1142/9789812701787_0013.

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Brooks, Joseph Bruno Bidin, Fábio César Prosdócimi, Fernanda Stoffel Covolan, et al. "Sporadic Creutzfeldt-Jakob disease. Case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.184.

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Context: Creutzfeldt-Jakob disease (CJD) is a rare disease that belongs to the category of transmissible spongiform encephalopathies. The condition is invariably fatal and progresses with severe dementia with psychiatric signs and, with cortical, subcortical and cerebellar signs. This case report was approved by the Ethics Committee of Universidade Metropolitana de Santos. Case Report: We present the case of a 59-year-old male patient who presented with a subacute onset of behavioral changes associated with myoclonus and changes in coordination. Associated with the described symptoms, he presented aphasia of expression, cerebellar incoordination and spasticity was also present in the four limbs. Conclusions: The usual forms of transmission could not be confirmed for this patient, who died four months after the onset of symptoms.

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WILL, R. G., R. S. G. KNIGHT, and M. D. SPENCER. "NEUROPSYCHIATRIC ASPECTS OF VARIANT CREUTZFELDT-JAKOB DISEASE." In Proceedings of the International Seminar on Nuclear War and Planetary Emergencies — 27th Session. WORLD SCIENTIFIC, 2003. http://dx.doi.org/10.1142/9789812705150_0074.

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Gouvêa, Sabrina Vechini, Victor Guimarães Correa, Giovana Barros e. Silva Ribeiro, et al. "A Creutzfeldt-Jakob disease mimics: case report." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.562.

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Introduction: Creutzfeld-Jakob Disease (CJD) is an important differential diagnoses in patients with rapidly progressive dementia (RPD). Several inflammatory, immune-mediated, vascular, granulomatous and neurodegenerative conditions can mimic this disease. Objectives: Report a curious case of CJD mimics that was a limbic encephalitis. Methods: A 71-year-old man, with diabetes mellitus. His initial symptoms included visual hallucinations and temporo-spatial disorientation. Over the course of a month, he lost his critical judgment, and began with aggressive behavior and disinhibition. He progressed with gait apraxia and diffuse myoclonic jerks, as well as loss of both bladder and bowel sphincter incontinence and dysphagia. Blood tests results were normal. Cerebrospinal fluid presented increase in proteins (82) without any further alterations. Brain magnetic resonance imaging showed a bilateral increase in T2/FLAIR (T2- weighted-Fluid-Attenuated Inversion Recovery) signal intensity from the hippocampus to the amygdala. Also presented alterations in white matter suggesting microangiopathy (Fazekas 2). Brain PET-CT (Positron Emission Tomography-Computed Tomography) scan showed hypermetabolism in bilateral basal ganglia and mesial temporal regions. EEG evidenced moderate to severe disorganization of background activity and myoclonic jerks with no electroencephalographic correlation. Detection of 14-3-3 protein in cerebrospinal fluid was negative. Results: Patient received 1 g of methylprednisolone for five days and presented significant improvement of clinic symptoms, stopping myoclonic jerks and dysphagia with better tenacity, self-orientation and improved gait. However, he presented persistently short term memory alteration with signs of disinhibition (hyperphagia) that didn`t get better with a second immunotherapy treatment with cyclophosphamide. Conclusion: immune-mediated conditions as encephalitis must be kept in mind when assessing differential diagnoses of RPD and treated as soon as possible

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Bhakta, Arnav, and Carolyn Byrne. "Creutzfeldt-Jakob Disease Prediction Using Machine Learning Techniques." In 2021 IEEE 9th International Conference on Healthcare Informatics (ICHI). IEEE, 2021. http://dx.doi.org/10.1109/ichi52183.2021.00101.

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BROWN, PAUL. "IATROGENIC CREUTZFELDT-JAKOB DISEASE IN THE YEAR 2000." In International Seminar on Nuclear War and Planetary Emergencies 25th Session. World Scientific Publishing Co. Pte. Ltd., 2001. http://dx.doi.org/10.1142/9789812797001_0025.

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WILL, R. G. "VARIANT CREUTZFELDT-JAKOB DISEASE AND BOVINE SPONGIFORM ENCEPHALOPATHY: CURRENT STATUS." In Proceedings of the International Seminar on Nuclear War and Planetary Emergencies — 27th Session. WORLD SCIENTIFIC, 2003. http://dx.doi.org/10.1142/9789812705150_0073.

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Vahabzadeh, A., L. M. De Rose, A. Y. A. Mohamed, I. Singh, and J. W. Lee. "A Case of Creutzfeldt- Jakob Disease Masked by Concomitant Mumps." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a6082.

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