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Journal articles on the topic 'Raccoons as carriers of disease'

Author: Grafiati

Published: 4 June 2021

Last updated: 16 February 2022

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1

Nesterchuk, S. L., E. A. Makarova, and V. A. Ostapenko. "The importance of individual animal species in rabies virus transport in the Central federal district." Veterinariya, Zootekhniya i Biotekhnologiya 1, no. 4 (2020): 15–21. http://dx.doi.org/10.36871/vet.zoo.bio.202004002.

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The Rabies – a viral disease characterized by severe damage of the nervous system. The analysis of data from the Rospotrebnadzor for 4 years (from 2015 to 2018) on the varmint of animals with rabies in four regions of the Central Federal District with different population densities is carried out. The main carriers of rabies virus in the region are the red fox, raccoon dog, stray dogs and cats; the role of other species is not so significant and rarely exceeds 1% of the total number of animals with suspected rabies. It has been established that in areas with a low population (Tver region) the

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2

Mitchell, Sian, Jane Anscombe, and Julie Wessels. "Disease risks from raccoons and skunks." Veterinary Record 174, no. 20 (2014): 510–11. http://dx.doi.org/10.1136/vr.g3293.

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3

Hadi, Moch Irfan, Muhammad Yusuf Alamudi, Mei Lina Fitri Kumalasari, et al. "Dogs (Canis lupus familiaris) as Virus Carrier in Indonesia." Biotropic : The Journal of Tropical Biology 2, no. 2 (2018): 100–107. http://dx.doi.org/10.29080/biotropic.2018.2.2.100-107.

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A Virus is an individual that cannot be described as an animal or a plant. If animals and plants contain two nucleic acids (DNA and RNA), on the contrary, the virus only has one of them. These nucleic acids can stimulate a complete virus replication cycle. The virus can only replicate and live on a living host if the host is finally dead, then the virus will move on the cells that are still alive. The virus has genetic material which is a protective protein coat called a capsid. Viruses can infect various varieties of organisms, both eukaryotes (animals, plants, protists, and fungi) and prokar

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4

Moore, S. Jo, Jodi D. Smith, Jürgen A. Richt, and Justin J. Greenlee. "Raccoons accumulate PrPSc after intracranial inoculation of the agents of chronic wasting disease or transmissible mink encephalopathy but not atypical scrapie." Journal of Veterinary Diagnostic Investigation 31, no. 2 (2019): 200–209. http://dx.doi.org/10.1177/1040638718825290.

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Prion diseases are neurodegenerative diseases characterized by the accumulation of misfolded prion protein (PrPSc) in the brain and other tissues. Animal prion diseases include scrapie in sheep, chronic wasting disease (CWD) in cervids, and transmissible mink encephalopathy (TME) in ranch-raised mink. We investigated the susceptibility of raccoons to various prion disease agents and compared the clinicopathologic features of the resulting disease. Raccoon kits were inoculated intracranially with the agents of raccoon-passaged TME (TMERac), bovine-passaged TME (TMEBov), hamster-adapted drowsy (

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5

Hamir, A. N., N. Raju, C. Hable, and C. E. Rupprecht. "Retrospective Study of Testicular Degeneration in Raccoons with Canine Distemper Infection." Journal of Veterinary Diagnostic Investigation 4, no. 2 (1992): 159–63. http://dx.doi.org/10.1177/104063879200400207.

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A 6-year (1985–1990) retrospective survey of raccoons with canine distemper infection and an outbreak of the disease in 1988 on South Island, South Carolina, are described. During this epizootic, 3 male raccoons with the clinical disease had gross testicular lesions that, on histopathologic examination, revealed severe diffuse degeneration and mineralization of seminiferous tubules. The testicular pathology of canine distemper in raccoons has not been previously reported.

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6

Hamir, A. N., R. A. Kunkle, J. M. Miller, and J. A. Richt. "Second Passage of Sheep Scrapie and Transmissible Mink Encephalopathy (TME) Agents in Raccoons (Procyon lotor)." Veterinary Pathology 42, no. 6 (2005): 844–51. http://dx.doi.org/10.1354/vp.42-6-844.

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To determine the transmissibility and pathogenicity of sheep scrapie and transmissible mink encephalopathy (TME) agents derived from raccoons (first passage), raccoon kits were inoculated intracerebrally with either TME (one source) or scrapie (two sources—each in separate groups of raccoons). Two uninoculated raccoon kits served as controls. All animals in the TME-inoculated group developed clinical signs of neurologic dysfunction and were euthanatized between postinoculation month (PIM) 6 and 8. Raccoons in the two scrapie-inoculated groups manifested similar clinical signs of disease, but s

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7

HAGIWARA, Katsuro, Youhei MATOBA, and Mitsuhiko ASAKAWA. "Borna Disease Virus in Raccoons (Procyon lotor) in Japan." Journal of Veterinary Medical Science 71, no. 8 (2009): 1009–15. http://dx.doi.org/10.1292/jvms.71.1009.

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8

Jarvis, Caitlin, and Mathieu Basille. "Facts about Wildlife Diseases: Raccoon-Borne Pathogens of Importance to Humans—The Raccoon Roundworm." EDIS 2020, no. 6 (2020): 7. http://dx.doi.org/10.32473/edis-uw480-2020.

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Diseases carried by northern raccoons present significant health hazards to both people and pets. This 7-page fact sheet written by Caitlin Jarvis and Mathieu Basille and published by the UF/IFAS Department of Wildlife Ecology and Conservation is part of a series addressing health hazards associated with raccoons. It describes the raccoon roundworm and the disease it causes, baylisascariasis, which normally causes little or no trouble to raccoons but in severe cases can make people and their pets very sick. Sick wild animals can act tame, but do not approach! Contact animal control or a wildli

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9

Peleg, L., A. Frisch, B. Goldman, et al. "Lower frequency of Gaucher disease carriers among Tay-Sachs disease carriers." European Journal of Human Genetics 6, no. 2 (1998): 185–86. http://dx.doi.org/10.1038/sj.ejhg.5200176.

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10

Mitchell, M. A., L. L. Hungerford, C. Nixon, et al. "SEROLOGIC SURVEY FOR SELECTED INFECTIOUS DISEASE AGENTS IN RACCOONS FROM ILLINOIS." Journal of Wildlife Diseases 35, no. 2 (1999): 347–55. http://dx.doi.org/10.7589/0090-3558-35.2.347.

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11

Ferson, Mark J. "Books as carriers of disease." Medical Journal of Australia 175, no. 11-12 (2001): 663–64. http://dx.doi.org/10.5694/j.1326-5377.2001.tb143769.x.

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12

Jones, Sir Keith. "Books as carriers of disease." Medical Journal of Australia 176, no. 4 (2002): 196. http://dx.doi.org/10.5694/j.1326-5377.2002.tb04368.x.

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13

Roche, John V. "Books as carriers of disease." Medical Journal of Australia 176, no. 9 (2002): 452. http://dx.doi.org/10.5694/j.1326-5377.2002.tb04497.x.

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14

Goker-Alpan, O. "Parkinsonism among Gaucher disease carriers." Journal of Medical Genetics 41, no. 12 (2004): 937–40. http://dx.doi.org/10.1136/jmg.2004.024455.

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15

Groot, Colin, Carole H. Sudre, Frederik Barkhof та ін. "Clinical phenotype, atrophy, and small vessel disease in APOEε2 carriers with Alzheimer disease". Neurology 91, № 20 (2018): e1851-e1859. http://dx.doi.org/10.1212/wnl.0000000000006503.

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ObjectiveTo examine the clinical phenotype, gray matter atrophy patterns, and small vessel disease in patients who developed prodromal or probable Alzheimer disease dementia, despite carrying the protective APOEε2 allele.MethodsWe included 36 β-amyloid-positive (by CSF or PET) APOEε2 carriers (all ε2/ε3) with mild cognitive impairment or dementia due to Alzheimer disease who were matched for age and diagnosis (ratio 1:2) to APOEε3 homozygotes and APOEε4 carriers (70% ε3/ε4 and 30% ε4/ε4). We assessed neuropsychological performance across 4 cognitive domains (memory, attention, executive, and l

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Brault, Aaron, Harry Savage, Nisha Duggal, Rebecca Eisen, and J. Staples. "Heartland Virus Epidemiology, Vector Association, and Disease Potential." Viruses 10, no. 9 (2018): 498. http://dx.doi.org/10.3390/v10090498.

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First identified in two Missouri farmers exhibiting low white-blood-cell and platelet counts in 2009, Heartland virus (HRTV) is genetically closely related to severe fever with thrombocytopenia syndrome virus (SFTSV), a tick-borne phlebovirus producing similar symptoms in China, Korea, and Japan. Field isolations of HRTV from several life stages of unfed, host-seeking Amblyomma americanum, the lone star tick, implicated it as a putative vector capable of transstadial transmission. Laboratory vector competence assessments confirmed transstadial transmission of HRTV, demonstrated vertical infect

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17

Rees, Erin E., Bruce A. Pond, Catherine I. Cullingham, et al. "Landscape modelling spatial bottlenecks: implications for raccoon rabies disease spread." Biology Letters 5, no. 3 (2009): 387–90. http://dx.doi.org/10.1098/rsbl.2009.0094.

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A landscape genetic simulation modelling approach is used to understand factors affecting raccoon rabies disease spread in southern Ontario, Canada. Using the Ontario Rabies Model, we test the hypothesis that landscape configuration (shape of available habitat) affects dispersal, as indicated by genetic structuring. We simulated range expansions of raccoons from New York into vacant landscapes in Ontario, in two areas that differed by the presence or absence of a landscape constriction. Our results provide theoretical evidence that landscape constriction acts as a vicariant bottleneck. We disc

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18

Gonzalez-Astudillo, Viviana, Matthew F. Sheley, Francisco A. Uzal, and Mauricio A. Navarro. "Pathology of cryptosporidiosis in raccoons: case series and retrospective analysis, 1990–2019." Journal of Veterinary Diagnostic Investigation 33, no. 4 (2021): 721–27. http://dx.doi.org/10.1177/10406387211011949.

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Cryptosporidiosis is an intestinal protozoal disease of public health importance caused by Cryptosporidium spp. Despite the high synanthropism of raccoons, studies describing the pathology of Cryptosporidium spp. infections in this species are lacking. Therefore, we characterized the pathology of cryptosporidiosis in 2 juvenile raccoons. In addition, we conducted a retrospective search of the database of the California Animal Health and Food Safety laboratory for 1990–2019 and found 6 additional cases of cryptosporidiosis in raccoons. Sequencing of cryptosporidia was performed in one autopsied

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19

Hamir, A. N., J. M. Miller, R. C. Cutlip, et al. "Experimental inoculation of scrapie and chronic wasting disease agents in raccoons (Procyon lotor)." Veterinary Record 153, no. 4 (2003): 121–23. http://dx.doi.org/10.1136/vr.153.4.121.

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20

Beltrán-Beck, Beatriz, Francisco José García, and Christian Gortázar. "Raccoons in Europe: disease hazards due to the establishment of an invasive species." European Journal of Wildlife Research 58, no. 1 (2011): 5–15. http://dx.doi.org/10.1007/s10344-011-0600-4.

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21

Sugden, A. M. "ECOLOGY/EVOLUTION: Conquest by Disease Carriers." Science 299, no. 5615 (2003): 1947c—1947. http://dx.doi.org/10.1126/science.299.5615.1947c.

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22

Floeter, Mary K., Bryan J. Traynor, Jennifer Farren, et al. "Disease progression in C9orf72 mutation carriers." Neurology 89, no. 3 (2017): 234–41. http://dx.doi.org/10.1212/wnl.0000000000004115.

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Objective:To assess changes in 3 clinical measures, the Revised ALS Functional Rating Scale (ALSFRS-R), letter fluency, and Frontal Behavioral Inventory (FBI), over time in C9orf72 mutation carriers (C9+) with varied clinical phenotypes.Methods:Thirty-four unrelated participants with mutations in C9orf72 were enrolled in a prospective natural history study. Participants were classified as asymptomatic, amyotrophic lateral sclerosis (ALS), ALS–familial frontotemporal dementia (FTD), or behavioral-variant FTD by clinical diagnostic criteria. Diagnostic cognitive and motor tests were repeated at

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23

Kawai, H., K. Yokoi, M. Akaike, et al. "Graves' disease in HTLV-I carriers." Journal of Molecular Medicine 73, no. 2 (1995): 85–88. http://dx.doi.org/10.1007/bf00270582.

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24

Löwy, Ilana. "Hidden Perils: Diagnosing Asymptomatic Disease Carriers." Medicine Anthropology Theory 8, no. 2 (2021): 1–29. http://dx.doi.org/10.17157/mat.8.2.5106.

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COVID-19, a disease induced by SARS-CoV-2, became a worldwide pandemic while SARS, a disease induced by a closely related virus, SARS-CoV, was successfully contained. This is because COVID-19, unlike SARS, can be spread by people who do not display any symptoms of disease, either because they are in the early stages of the infection or because their infection remains clinically silent. This research article traces the complex history of the diagnosis of symptom-free (or asymptomatic) carriers of pathogens, a term inseparably linked to the rise of the laboratory diagnosis of pathogens. Only suc

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25

Lin, Ai-Ling, David Allan Butterfield, and Arlan Richardson. "mTOR: Alzheimer's disease prevention for APOE4 carriers." Oncotarget 7, no. 29 (2016): 44873–74. http://dx.doi.org/10.18632/oncotarget.10349.

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26

Belkin, N. L. "Testing for carriers of Creutzfeldt-Jakob disease." Journal of Hospital Infection 55, no. 2 (2003): 153–54. http://dx.doi.org/10.1016/s0195-6701(03)00259-7.

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27

Belkin, Nathan L. "Creutzfeldt-Jakob Disease Identifying Prions and Carriers." AORN Journal 78, no. 2 (2003): 204–10. http://dx.doi.org/10.1016/s0001-2092(06)60771-0.

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28

ISHIKAWA, Koh-ichi, Yutaka TAKEBE, Rika KISHIMOTO, Takeshi KURATA, and Takashi KAWANA. "Sexually Transmitted Disease Infection in HIV Carriers." Journal of the Japanese Association for Infectious Diseases 68, no. 4 (1994): 474–78. http://dx.doi.org/10.11150/kansenshogakuzasshi1970.68.474.

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29

van Duijn, E., E. M. Kingma, and R. C. van der Mast. "Psychopathology in Verified Huntington’s Disease Gene Carriers." Journal of Neuropsychiatry and Clinical Neurosciences 19, no. 4 (2007): 441–48. http://dx.doi.org/10.1176/jnp.2007.19.4.441.

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30

Kotka, Maria, Agne Lieden, Sven Pettersson, Vito Trinchieri, Alessandra Masci, and Mauro DʼAmato. "Solute Carriers (SLC) in Inflammatory Bowel Disease." Journal of Clinical Gastroenterology 42 (September 2008): S133—S135. http://dx.doi.org/10.1097/mcg.0b013e31815f5ab6.

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31

Sekhon, L., Z. Luscher, T. G. Nazem, J. Lee, L. Grunfeld, and A. B. Copperman. "Gaucher’s disease carriers demonstrate improved art outcome." Fertility and Sterility 110, no. 4 (2018): e142. http://dx.doi.org/10.1016/j.fertnstert.2018.07.420.

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32

Becker, Joanna G., Gregory M. Pastores, Alessandro Di Rocco, Marissa Ferraris, Jerome J. Graber, and Swati Sathe. "Parkinson’s disease in patients and obligate carriers of Gaucher disease." Parkinsonism & Related Disorders 19, no. 1 (2013): 129–31. http://dx.doi.org/10.1016/j.parkreldis.2012.06.023.

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33

Duke, John E., Jesse D. Blanton, Melissa Ivey, and Charles Rupprecht. "Modeling enzootic raccoon rabies from land use patterns - Georgia (USA) 2006-2010." F1000Research 2 (December 27, 2013): 285. http://dx.doi.org/10.12688/f1000research.2-285.v1.

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We analyzed how land-use patterns and changes in urbanization influence reported rabid raccoons in Georgia from 2006 - 2010. Using Geographical Information Systems and rabies surveillance data, multivariate analysis was conducted on 15 land-use variables that included natural topography, agricultural development, and urbanization to model positive raccoon rabies cases while controlling for potential raccoon submission bias associated with higher human population densities. Low intensity residential development was positively associated with reported rabid raccoons while a negative association

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Duke, John E., Jesse D. Blanton, Melissa Ivey, and Charles Rupprecht. "Modeling enzootic raccoon rabies from land use patterns - Georgia (USA) 2006-2010." F1000Research 2 (March 18, 2014): 285. http://dx.doi.org/10.12688/f1000research.2-285.v2.

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We analyzed how land-use patterns and changes in urbanization influence reported rabid raccoons in Georgia from 2006 - 2010. Using Geographical Information Systems and rabies surveillance data, multivariate analysis was conducted on 15 land-use variables that included natural topography, agricultural development, and urbanization to model positive raccoon rabies cases while controlling for potential raccoon submission bias associated with higher human population densities. Low intensity residential development was positively associated with reported rabid raccoons while a negative association

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35

Burrell, Caitlin E., Chris Anchor, Nadia Ahmed, Jennifer Landolfi, Keith W. Jarosinski, and Karen A. Terio. "Characterization and Comparison of SLAM/CD150 in Free-Ranging Coyotes, Raccoons, and Skunks in Illinois for Elucidation of Canine Distemper Virus Disease." Pathogens 9, no. 6 (2020): 510. http://dx.doi.org/10.3390/pathogens9060510.

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Canine distemper virus (CDV) is a cause of significant disease in canids and increasingly recognized as a multi-host pathogen, particularly of non-canid families within Carnivora. CDV outbreaks in sympatric mesocarnivores are routinely diagnosed in the Forest Preserve District of Cook County, Illinois. CDV is diagnosed more commonly and the disease more severe in raccoons and striped skunks than in coyotes. Research in other species suggests host cell receptors may play a role in variable disease outcome, particularly, the signaling lymphocyte activation molecule (SLAM) located on lymphoid cel

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36

Deng, Xiao, Bin Xiao, John Carson Allen, et al. "Parkinson’s disease GWAS-linked Park16 carriers show greater motor progression." Journal of Medical Genetics 56, no. 11 (2019): 765–68. http://dx.doi.org/10.1136/jmedgenet-2018-105661.

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BackgroundData on the long-term motor outcomes of genome-wide association study (GWAS)-linked Parkinson disease (PD) carriers are useful for clinical management.ObjectivesTo characterise the association between GWAS-linked PARK16 gene variant and disease progression in PD over a 9-year time frame.MethodsOver a 9-year period, carriers of PARK16 rs11240572 variant and non-carriers were followed up and evaluated using the modified Hoehn and Yahr (H&Y) staging scale and Unified Parkinson’s Disease Rating Scale (UPDRS) part III. A longitudinal, linear mixed model was performed to compare the ch

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37

Weigel, Ronald M., Edwin C. Hahn, and Gail Scherba. "Survival and immunization of raccoons after exposure to pseudorabies (Aujeszky’s disease) virus gene-deleted vaccines." Veterinary Microbiology 92, no. 1-2 (2003): 19–24. http://dx.doi.org/10.1016/s0378-1135(02)00350-4.

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38

Rosatte, Rick, Mark Ryckman, Karen Ing, et al. "Density, movements, and survival of raccoons in Ontario, Canada: implications for disease spread and management." Journal of Mammalogy 91, no. 1 (2010): 122–35. http://dx.doi.org/10.1644/08-mamm-a-201r2.1.

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39

Dharmarajan, Guha, James C. Beasley, Jennifer A. Fike, et al. "Effects of kin-structure on disease dynamics in raccoons (Procyon lotor) inhabiting a fragmented landscape." Basic and Applied Ecology 13, no. 6 (2012): 560–67. http://dx.doi.org/10.1016/j.baae.2012.08.010.

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40

Dubey, J. P., W. J. A. Saville, J. F. Stanek, et al. "Sarcocystis neurona infections in raccoons (Procyon lotor): evidence for natural infection with sarcocysts, transmission of infection to opossums (Didelphis virginiana), and experimental induction of neurologic disease in raccoons." Veterinary Parasitology 100, no. 3-4 (2001): 117–29. http://dx.doi.org/10.1016/s0304-4017(01)00500-3.

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41

Srithayakumar, Vythegi, Hariharan Sribalachandran, Rick Rosatte, Susan A. Nadin-Davis, and Christopher J. Kyle. "Innate immune responses in raccoons after raccoon rabies virus infection." Journal of General Virology 95, no. 1 (2014): 16–25. http://dx.doi.org/10.1099/vir.0.053942-0.

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Zoonotic wildlife diseases pose significant health risks not only to their primary vectors but also to humans and domestic animals. Rabies is a lethal encephalitis caused by rabies virus (RV). This RNA virus can infect a range of terrestrial mammals but each viral variant persists in a particular reservoir host. Active management of these host vectors is needed to minimize the negative impacts of this disease, and an understanding of the immune response to RV infection aids strategies for host vaccination. Current knowledge of immune responses to RV infection comes primarily from rodent models

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Jayasinghe, R. D., S. R. Gunawardane, M. A. M. Sitheeque, and S. Wickramasinghe. "A Case Report on Oral Subcutaneous Dirofilariasis." Case Reports in Infectious Diseases 2015 (2015): 1–4. http://dx.doi.org/10.1155/2015/648278.

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Dirofilariasis is an uncommon zoonotic parasitic infection affecting human. The natural hosts for this nematode are animals such as dogs, cats, foxes, jackals, and raccoons. This disease is endemic in South Eastern United States, Australia, Europe, and Central and Southern Asia.Dirofilaria immitisandD. repensare the common mosquito borne filarial nematodes that cause infection. Several species of mosquitos includingMansonia uniformis,M. annulifera, andAedes aegyptiare the potential vectors for this disease in Sri Lanka. Two rare cases of dirofilariasis presenting as facial and intraoral lumps

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Drozdzik, Marek, Maria Drozdzik, and Stefan Oswald. "Membrane Carriers and Transporters in Kidney Physiology and Disease." Biomedicines 9, no. 4 (2021): 426. http://dx.doi.org/10.3390/biomedicines9040426.

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The growing information suggests that chronic kidney disease may affect expression and function of membrane carriers and transporters in the kidney. The dysfunction of carriers and transporters entails deficient elimination of uremic solutes as well as xenobiotics (drugs and toxins) with subsequent clinical consequences. The renal carriers and transporters are also targets of drugs used in clinical practice, and intentional drug–drug interactions in the kidney are produced to increase therapeutic efficacy. The understanding of membrane carriers and transporters function in chronic kidney disea

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Verhoeven, AJ, ML van Schaik, D. Roos, and RS Weening. "Detection of carriers of the autosomal form of chronic granulomatous disease." Blood 71, no. 2 (1988): 505–7. http://dx.doi.org/10.1182/blood.v71.2.505.505.

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Abstract The NADPH:O2 oxidoreductase catalyzing the respiratory burst in activated phagocytes from healthy individuals is not operative in phagocytes from patients with chronic granulomatous disease (CGD). In a microscopic slide test using the dye nitroblue tetrazolium (NBT), carriers of X-linked CGD can be recognized by a mosaic pattern of NBT- positive and NBT-negative cells, governed by the expression of an unaffected or an affected X chromosome, respectively. Until now, it has not been possible to detect carriers of the autosomal form of CGD (other than by family studies) because all cells

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Verhoeven, AJ, ML van Schaik, D. Roos, and RS Weening. "Detection of carriers of the autosomal form of chronic granulomatous disease." Blood 71, no. 2 (1988): 505–7. http://dx.doi.org/10.1182/blood.v71.2.505.bloodjournal712505.

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The NADPH:O2 oxidoreductase catalyzing the respiratory burst in activated phagocytes from healthy individuals is not operative in phagocytes from patients with chronic granulomatous disease (CGD). In a microscopic slide test using the dye nitroblue tetrazolium (NBT), carriers of X-linked CGD can be recognized by a mosaic pattern of NBT- positive and NBT-negative cells, governed by the expression of an unaffected or an affected X chromosome, respectively. Until now, it has not been possible to detect carriers of the autosomal form of CGD (other than by family studies) because all cells of these

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46

Robins Wahlin, Tarja-Brita, Mary A. Luszcz, Åke Wahlin, and Gerard J. Byrne. "Non-Verbal and Verbal Fluency in Prodromal Huntington's Disease." Dementia and Geriatric Cognitive Disorders Extra 5, no. 3 (2015): 517–29. http://dx.doi.org/10.1159/000441942.

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Background: This study examines non-verbal (design) and verbal (phonemic and semantic) fluency in prodromal Huntington's disease (HD). An accumulating body of research indicates subtle deficits in cognitive functioning among prodromal mutation carriers for HD. Methods: Performance was compared between 32 mutation carriers and 38 non-carriers in order to examine the magnitude of impairment across fluency tasks. The predicted years to onset (PYTO) in mutation carriers was calculated by a regression equation and used to divide the group according to whether onset was predicted as less than 12.75

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Cacabelos, Ramón, Juan Carril, Natalia Cacabelos, et al. "Sirtuins in Alzheimer’s Disease: SIRT2-Related GenoPhenotypes and Implications for PharmacoEpiGenetics." International Journal of Molecular Sciences 20, no. 5 (2019): 1249. http://dx.doi.org/10.3390/ijms20051249.

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Sirtuins (SIRT1-7) are NAD+-dependent protein deacetylases/ADP ribosyltransferases with important roles in chromatin silencing, cell cycle regulation, cellular differentiation, cellular stress response, metabolism and aging. Sirtuins are components of the epigenetic machinery, which is disturbed in Alzheimer’s disease (AD), contributing to AD pathogenesis. There is an association between the SIRT2-C/T genotype (rs10410544) (50.92%) and AD susceptibility in the APOEε4-negative population (SIRT2-C/C, 34.72%; SIRT2-T/T 14.36%). The integration of SIRT2 and APOE variants in bigenic clusters yields

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Baena, Ana, Yamile Bocanegra, Valeria Torres, et al. "Neuroticism Is Associated with Tau Pathology in Cognitively Unimpaired Individuals with Autosomal Dominant Alzheimer’s Disease." Journal of Alzheimer's Disease 82, no. 4 (2021): 1809–22. http://dx.doi.org/10.3233/jad-210185.

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Abstract:

Background: Greater neuroticism has been associated with higher risk for Alzheimer’s disease (AD) dementia. However, the directionality of this association is unclear. We examined whether personality traits differ between cognitively-unimpaired carriers of autosomal-dominant AD (ADAD) and non-carriers, and are associated with in vivo AD pathology. Objective: To determine whether personality traits differ between cognitively unimpaired ADAD mutation carriers and non-carriers, and whether the traits are related to age and AD biomarkers. Methods: A total of 33 cognitively-unimpaired Presenilin-1

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Vilaplana, Eduard, Elena Rodriguez-Vieitez, Daniel Ferreira, et al. "Cortical microstructural correlates of astrocytosis in autosomal-dominant Alzheimer disease." Neurology 94, no. 19 (2020): e2026-e2036. http://dx.doi.org/10.1212/wnl.0000000000009405.

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ObjectiveTo study the macrostructural and microstructural MRI correlates of brain astrocytosis, measured with 11C-deuterium-L-deprenyl (11C-DED)–PET, in familial autosomal-dominant Alzheimer disease (ADAD).MethodsThe total sample (n = 31) comprised ADAD mutation carriers (n = 10 presymptomatic, 39.2 ± 10.6 years old; n = 3 symptomatic, 55.5 ± 2.0 years old) and noncarriers (n = 18, 44.0 ± 13.7 years old) belonging to families with mutations in either the presenilin-1 or amyloid precursor protein genes. All participants underwent structural and diffusion MRI and neuropsychological assessment, a

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Mencacci, Niccolò E., Ioannis U. Isaias, Martin M. Reich, et al. "Parkinson’s disease in GTP cyclohydrolase 1 mutation carriers." Brain 137, no. 9 (2014): 2480–92. http://dx.doi.org/10.1093/brain/awu179.

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