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Journal articles on the topic '"AD-03."'

Author: Grafiati
Published: 4 June 2021
Last updated: 19 February 2022

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1

Jagust, William J. "F5-03-03: RESISTANCE TO AD OVER THE LIFECOURSE." Alzheimer's & Dementia 14, no. 7S_Part_31 (July 1, 2006): P1629. http://dx.doi.org/10.1016/j.jalz.2018.06.2978.

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Zetterberg, Henrik. "F1-03-02: How ad-Specific are ad CSF Biomarkers?" Alzheimer's & Dementia 12 (July 2016): P166. http://dx.doi.org/10.1016/j.jalz.2016.06.280.

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3

Frisoni, Giovanni B. "F1-03-04: How Ad-Specific are Ad-Like Mri Biomarkers?" Alzheimer's & Dementia 12 (July 2016): P167. http://dx.doi.org/10.1016/j.jalz.2016.06.282.

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4

Jagust, William J. "F1-03-03: How ad-Specific are ab and TAU Imaging Biomarkers?" Alzheimer's & Dementia 12 (July 2016): P166—P167. http://dx.doi.org/10.1016/j.jalz.2016.06.281.

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5

Sperling, Reisa A., and Paul S. Aisen. "F4-03-03: Anti-Amyloid Treatment of Asymptomatic Ad: A4 and Beyond." Alzheimer's & Dementia 12 (July 2016): P326—P327. http://dx.doi.org/10.1016/j.jalz.2016.06.598.

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6

Karlawish, Jason H. T., and Mark S. Cary. "O1-03-03: Home visits may improve recruitment in AD clinical trials." Alzheimer's & Dementia 3, no. 3S_Part_3 (July 2007): S171—S172. http://dx.doi.org/10.1016/j.jalz.2007.04.366.

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7

Federoff, Howard. "[S3-02-03]: AD Vaccination using HSV amplicons." Alzheimer's & Dementia 1 (July 2005): S107—S108. http://dx.doi.org/10.1016/j.jalz.2005.06.373.

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8

Zandi, Peter P., Chris A. Szekely, Robert C. Green, John C. Breitner, and Kathleen A. Welsh-Bohmer. "S1-03-03 Pooled analysis of the association between different NSAIDS and AD: preliminary findings." Neurobiology of Aging 25 (July 2004): S5—S6. http://dx.doi.org/10.1016/s0197-4580(04)80018-6.

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9

Rabinovici, Gil D., Daniel Schonhaut, Suzanne Baker, Andreas Lazaris, Nagehan Ayakta, Averill Cantwell, Sam Lockhart, et al. "F2-03-01: Tau and amyloid neuroimaging of ad phenotypes." Alzheimer's & Dementia 11, no. 7S_Part_3 (July 2015): P167. http://dx.doi.org/10.1016/j.jalz.2015.07.116.

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10

Hendrix, Suzanne B., and Noel Ellison. "F2-03-03: ADCOMS: A SENSITIVE MEASURE OF DISEASE PROGRESSION IN EARLY AD SUPPORTING BETTER DEVELOPMENT DECISIONS." Alzheimer's & Dementia 15 (July 2019): P520. http://dx.doi.org/10.1016/j.jalz.2019.06.4426.

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11

Skoog, Ingmar. "F5-03-03: DOES LATE-LIFE AD BEGIN ALREADY IN MIDLIFE? EVIDENCE FROM LONG TERM POPULATION STUDIES." Alzheimer's & Dementia 10 (July 2014): P284—P285. http://dx.doi.org/10.1016/j.jalz.2014.04.468.

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12

Duchesne, Simon, Kathy De Sousa, Christian Bocti, Howard Chertkow, and D. Louis Collins. "[O1-03-03]: Predicting MCI progression to AD via automated analysis of T1-weighted MR image intensity." Alzheimer's & Dementia 1 (July 2005): S83. http://dx.doi.org/10.1016/j.jalz.2005.06.294.

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13

Minoshima, Satoshi. "F1-03-01: How ad-Specific is Fdg as a Biomarker?" Alzheimer's & Dementia 12 (July 2016): P166. http://dx.doi.org/10.1016/j.jalz.2016.06.279.

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14

Scheltens, Philip. "S5-01-03: Added value of neuroimaging to diagnosis of AD." Alzheimer's & Dementia 2 (July 2006): S91. http://dx.doi.org/10.1016/j.jalz.2006.05.351.

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15

Strauss, G. M., A. Jemal, M. B. McKenna, J. A. Strauss, and K. M. Cummings. "Creation of an epidemic: The tobacco industry (TI) and smoking-related adenocarcinoma (AD) of the lung." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 7583. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.7583.

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7583 Background: When epidemiologic research first demonstrated an association between cigarette smoking (CS) and lung cancer (LC) in the 1950s, AD comprised about 5% of LCs and was only weakly related to CS. In the 1960s and 1970s, AD increased sharply, and became strongly related to CS. Methods: We conducted an epidemiological and ecological analysis correlating time trends in LC histology with changes in cigarette design and TI actions over the past 30 yrs. We utilized SEER data on 307,797 LCs diagnosed from 1975 to 2003 to analyze time trends of age-standardized incidence rates of each LC subtype: AD, squamous (SQ), small cell, and large cell. Comparisons were drawn based on sex, race, and age. Because SEER contains no data on CS, other sources were utilized to correlate changing histology to time trends in smoking prevalence, the changing cigarette, and TI actions. Results: Among all pts, AD surpassed SQ by 1980–84 to become the most common histology. AD increased 62% from 1975–79 to 1995–99, but fell 8% in 2000–03. SQ peaked in 1980–84 and dropped 35% by 2000–03. AD surpassed SQ in 1985–89 in men, while AD was already most common in women by 1975–79. AD rose 38% in men from 1975–79 to 1995–99, while it doubled in women during this interval. Among whites, AD surpassed SQ by 1980–84, although this did not occur among blacks for another decade. Nonetheless, AD incidence has consistently been higher in black men than in other subgroups. AD was already most common in pts <50 yrs by 1975–79, while AD rapidly increased and surpassed SQ in all other age groups by 1990–94. By 2000–03, AD comprised 47% of all LCs (42% in men; 52% in women; 59% in pts <50 yrs). Currently, AD is the most common histology in both sexes, races, and in all age groups. Trends in AD correlate with the wide-scale adoption by smokers of filtered and low tar cigarettes, and with increasing nitrosamine levels in cigarettes. Conclusions: The rise of AD, particularly in women and younger persons, is consistent with the hypothesis that changes in cigarette design and composition was responsible for this rise. These changes were introduced by the TI in response to mounting evidence that CS caused other forms of LC. While low tar cigarettes do not reduce LC risk, their adoption appears to be responsible for creating an epidemic of smoking-related lung AD. No significant financial relationships to disclose.
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16

Nyborg, Andrew C., Yona Levites, Thomas B. Ladd, Craig W. Zwizinski, Karen Jansen, and Todd E. Golde. "O3-03-03: Sortilin, SorLA, SorCS1: Just novel gamma-secretase substrates or more intimately involved in AD pathogenesis?" Alzheimer's & Dementia 2 (July 2006): S57. http://dx.doi.org/10.1016/j.jalz.2006.05.207.

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17

Hutchinson, Rachel S., and Alison F. Eardley. "The Accessible Museum: Towards an Understanding of International Audio Description Practices in Museums." Journal of Visual Impairment & Blindness 114, no. 6 (November 2020): 475–87. http://dx.doi.org/10.1177/0145482x20971958.

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Introduction: Audio description (AD) in museums is crucial for making them accessible for people with visual impairments. Nevertheless, there are limited museum-specific AD guidelines currently available. This research examines current varied international practitioner perspectives on museum AD, focusing on imagery, meaning, emotion and degrees of objectivity, and the regional differences (Europe and United States) in AD traditions, in order to better understand how AD can be used to enhance access to museums. Methods: Forty-two museum describers from 12 countries responded to a questionnaire requiring fixed-choice and free-text responses about the purpose and construction of museum AD. Results: Inference tests showed that European describers agreed more strongly than American describers that AD should “explore meaning” ( U = 91.00 , N1 = 24, N2 = 14, p = .03), and “create an emotional experience” ( U = 89.50, N1 = 24, N2 = 14, p = .03), rating the use of cognitive prompts as more important ( U = 85.50, N1 = 21, N2 = 14, p = .04). Qualitative data enriched this understanding by exploring participant responses on the themes of mental imagery, objectivity and interpretation and cognitive prompts. This highlighted broader agreement between regions on mental imagery, but more acceptance of interpretation in AD from the European respondents. Discussion: American and European describers’ opinions differ regarding the purpose of AD: whether it is about conveying visual information or whether broader interpretations should be incorporated into descriptions for audiences with visual impairments. Implications for practitioners: These findings indicate that further discussion is needed regarding the purpose of museum AD and, in particular, the way in which objectivity is contextualized. They raise questions about AD providing visual information and/or seeking to address a wider museum experience, including the stimulation of curiosity or emotion.
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18

Albert, Marilyn S., Anja Soldan, Ola Selnes, Michael Miller, Tilak Ratnanather, Susumu Mori, Abhay Moghekar, et al. "F1-03-02: Using combinations of variables to identify individuals with preclinical ad." Alzheimer's & Dementia 11, no. 7S_Part_2 (July 2015): P118. http://dx.doi.org/10.1016/j.jalz.2015.07.015.

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19

Dagher, Alain, Yashar Zeighami, and D. Louis Collins. "F4-04-03: Brain Networks as Targets of Neurodegeneration in Pd and Ad." Alzheimer's & Dementia 12 (July 2016): P328—P329. http://dx.doi.org/10.1016/j.jalz.2016.06.602.

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20

Malek-Ahmadi, Michael, Kewei Chen, Sylvia E. Perez, and Elliott J. Mufson. "O2-03-04: CEREBRAL AMYLOID ANGIOPATHY CORRELATES WITH COGNITIVE DECLINE IN PRECLINICAL AD." Alzheimer's & Dementia 14, no. 7S_Part_11 (July 1, 2006): P617. http://dx.doi.org/10.1016/j.jalz.2018.06.2654.

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21

Ropacki, Michael T., Kristin Hannesdottir, Suzanne Hendrix, Mark F. Gordon, Diane Stephenson, Stephen J. Coons, and Robert A. Stern. "O1-05-03: CONSORTIA DRIVEN APPROACH TO ADDRESSING CLINICAL MEANINGFULNESS IN EARLY AD." Alzheimer's & Dementia 10 (July 2014): P137. http://dx.doi.org/10.1016/j.jalz.2014.04.082.

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22

Chetelat, Gaël, Béatrice Desgranges, Florence Mézenge, Brigitte Landeau, Vincent de la Sayette, Jean-Claude Baron, and Francis Eustache. "O2-02-03: Relationships between white matter density loss and hypometabolism in AD." Alzheimer's & Dementia 3, no. 3S_Part_3 (July 2007): S185. http://dx.doi.org/10.1016/j.jalz.2007.04.037.

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23

Poirier, Judes, Anne Labonté, Dorothy Dea, Jennifer Tremblay-Mercier, Melissa Savard, Pedro Rosa-Neto, Pierre E. Etienne, Pierre Bellec, and John C. S. Breitner. "F1-03-03: Mapping the progression of CSF and imaging biomarkers in “at-risk” healthy subjects: The prevent-ad program." Alzheimer's & Dementia 11, no. 7S_Part_2 (July 2015): P118. http://dx.doi.org/10.1016/j.jalz.2015.07.016.

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24

Lim, Wee Shiong, Mei Sian Chong, Laura Tay, Noorhazlina Ali, Audrey Yeo, and Mark Chan. "O3-03-03: Differential impact of disease pre-progression on baseline and one-year caregiver burden in Alzheimer's dementia (AD)." Alzheimer's & Dementia 11, no. 7S_Part_5 (July 2015): P222—P223. http://dx.doi.org/10.1016/j.jalz.2015.07.250.

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25

Loprinzi, Paul D. "Need for Increased Promotion of Physical Activity Among Adults at Risk for Alzheimer’s Disease: A Brief Report." Journal of Physical Activity and Health 12, no. 12 (December 2015): 1601–4. http://dx.doi.org/10.1123/jpah.2014-0554.

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Background:We have a limited understanding of the physical activity (PA) and sedentary levels among individuals at risk and not at risk for developing Alzheimer’s disease (AD), which was the purpose of this study.Methods:Data from the 2003–2004 NHANES were used, from which 3015 participants were evaluated with 416 indicating a family history of AD. Physical activity and sedentary behavior were assessed via accelerometry with individuals at risk for AD self-reporting a family history of AD.Results:For the entire sample, those at risk for AD engaged in more sedentary behavior than those not at risk (494.9 vs. 477.9 min/day, P = .03, respectively). Similarly, those at risk for AD engaged in less total MVPA than those not at risk (22.4 vs. 24.3 min/day, P = .05, respectively). Results were also significant for various subgroups at risk for AD.Conclusion:Despite the beneficial effects of PA in preventing AD and prolonging the survival of AD, adults at risk for AD tend to engage in more sedentary behavior and less PA than those not at risk for AD. This finding even persisted among minorities (Hispanics and non-Hispanic blacks) who are already at an increased risk of developing AD.
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26

Town, Terrence, Kavon Rezai-Zadeh, Daniel Ye, Altan Rentsendorj, Stephen Johnson, Inna Spivak, Yasmin Bholat, et al. "S4-03-05: Elucidation of the Amyloid Cascade Hypothesis in the TgF344-AD Rat." Alzheimer's & Dementia 6 (July 2010): e14-e14. http://dx.doi.org/10.1016/j.jalz.2010.08.044.

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27

Hao, Ke. "F1-02-03: MULTISCALE COMPUTATIONAL APPROACH ILLUMINATING NOVEL COMMON PATHWAYS BETWEEN DIABETES AND AD." Alzheimer's & Dementia 10 (July 2014): P126. http://dx.doi.org/10.1016/j.jalz.2014.04.049.

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28

Murray, Melissa Erin, Neill R. Graff-Radford, Amanda M. Liesinger, Ashley D. Cannon, Bhupendra Rawal, Ronald Carl Petersen, Clifford R. Jack, et al. "O1-12-03: THAL AMYLOID PHASE: CLINICOPATHOLOGIC AND PIB-PET IMPLICATIONS OF AD PATHOPHYSIOLOGY." Alzheimer's & Dementia 10 (July 2014): P153—P155. http://dx.doi.org/10.1016/j.jalz.2014.04.124.

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29

Chen, Peijun, Peter D. Guarino, Maurice W. Dysken, Muralidhar Pallaki, Sanjay Asthana, Maria D. Llorente, Susan Love, Julia E. Vertrees, Gerard D. Schellenberg, and Mary Sano. "Neuropsychiatric Symptoms and Caregiver Burden in Individuals With Alzheimer’s Disease: The TEAM-AD VA Cooperative Study." Journal of Geriatric Psychiatry and Neurology 31, no. 4 (July 2018): 177–85. http://dx.doi.org/10.1177/0891988718783897.

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Objectives: To assess the prevalence of neuropsychiatric symptoms (NPS) in mild-to-moderate Alzheimer disease (AD) and their association with caregiver burden. Methods: Secondary analyses of baseline data from the Trial of Vitamin E and Memantine in Alzheimer's Disease (TEAM-AD) (N=613). Neuropsychiatric Inventory were used to measure severity of NPS and caregiver activity survey to measure caregiver burden. Results: A total of 87% of patients displayed at least 1 NPS; 70% displayed clinically meaningful NPS. The most common symptoms were apathy (47%), irritability (44%), agitation (42%), and depression (40%). Those with moderate AD had more severe NPS than those with mild AD ( P = .03). Neuropsychiatric symptoms were significantly associated with caregiver time after adjusting for age, education, cognitive function, and comorbidity ( P-value < .0001) with every point increase in NPS associated with a 10-minute increase in caregiver time. Conclusion: Neuropsychiatric symptoms were prevalent in both mild and moderate AD, even in patients receiving treatment with an acetylcholinesterase inhibitors, and were more severe in moderate AD and associated with greater caregiver time.
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30

Polito, Letizia, Francesca Prato, Serena Rodilossi, Eleonora Ateri, Daniela Galimberti, Elio Scarpini, Francesca Clerici, Claudio Mariani, Gianluigi Forloni, and Diego Albani. "A Novel Study and Meta-Analysis of the Genetic Variation of the Serotonin Transporter Promoter in the Italian Population Do Not Support a Large Effect on Alzheimer's Disease Risk." International Journal of Alzheimer's Disease 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/312341.

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Alzheimer’s disease (AD) is a neurodegenerative disorder whose clinical onset is mainly characterized by memory loss. During AD progression, behavioral and psychological symptoms of dementia (BPSD) frequently occur. In this paper we evaluated the association between AD and the short/long (S/L) functional polymorphism of the promoter region of the 5-hydroxytryptamine (5-HT) transporter gene (SLC6A4). The S-allele shows a 2-fold reduced transcriptional rate, causing an imbalance in 5-HT intracellular availability that might in turn trigger behavioral and cognitive alterations. We also genotyped theSLC6A4promoter functional variantrs25531(A→G). By comparing the genotypic and allelic frequencies in an Italian population of 235 AD and 207 controls, we found an association between5-HTTLPRand AD (odds ratio for the L-allele versus the S-allele: 0.74, associatedPvalue = .03), while no difference was found for thers25531. A meta-analysis of studies in Italy assessing5-HTTLPRand AD risk gave an estimation of odds ratio for the L-allele versus the S-allele of 0.85 (associatedPvalue = .08). Overall, our findings are not supportive of a large genetic effect of the explored polymorphisms on AD risk.
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31

Nordberg, Agneta, Henry Engler, Gunnar Blomqvist, Ove Almkvist, Birgitta Ausén, Anders Wall, and Bengt Lngström. "O3-03-08 Imaging of amyloid in brain in vivo in MCI and AD patients." Neurobiology of Aging 25 (July 2004): S59. http://dx.doi.org/10.1016/s0197-4580(04)80198-2.

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32

Goldman, Stewart, Mark Kieran, Sabine Mueller, Jill Buck, Richard MacKenna, John Barrett, Laurence Cooper, and Francois Lebel. "PDCT-03. PHASE 1 STUDY OF Ad-RTS-hIL-12 + VELEDIMEX IN PEDIATRIC BRAIN TUMORS." Neuro-Oncology 19, suppl_6 (November 2017): vi184. http://dx.doi.org/10.1093/neuonc/nox168.747.

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33

Lucey, Brendan P., Cristina D. Toedebusch, Jennifer S. McLeland, Eric C. Landsness, Lena McCue, Chengjie Xiong, Austin McCullough, Tammie L. S. Benzinger, John C. Morris, and Dave M. Holtzman. "F4-05-03: ASSOCIATION OF AD PATHOLOGY AND NON-RAPID EYE MOVEMENT SLOW WAVE ACTIVITY." Alzheimer's & Dementia 14, no. 7S_Part_26 (July 1, 2006): P1390. http://dx.doi.org/10.1016/j.jalz.2018.06.2882.

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34

Felsenstein, Kevin M., Hyo-Jin Park, Yong Ran, Joo-In Jung, Oliver Holmes, Lisa Smithson, Carolina Ceballos-Diaz, et al. "O2-06-03: CAN WE TARGET CORTICOTROPIN RELEASING FACTOR (CRF) FOR THERAPEUTIC BENEFIT IN AD?" Alzheimer's & Dementia 10 (July 2014): P175. http://dx.doi.org/10.1016/j.jalz.2014.04.188.

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35

Scarmeas, Nikos. "F5-03-04: DOES LATE ONSET AD BEGIN IN MIDDLE-LIFE? CLINICAL AND BIOMARKER DATA." Alzheimer's & Dementia 10 (July 2014): P285. http://dx.doi.org/10.1016/j.jalz.2014.04.469.

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36

Betterle, Corrado, Riccardo Scarpa, Silvia Garelli, Luca Morlin, Francesca Lazzarotto, Fabio Presotto, Graziella Coco, et al. "Addison's disease: a survey on 633 patients in Padova." European Journal of Endocrinology 169, no. 6 (December 2013): 773–84. http://dx.doi.org/10.1530/eje-13-0528.

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ObjectiveAddison's disease (AD) is a rare endocrine condition.DesignWe aimed to evaluate clinical, immunologic, adrenal imaging, and genetic features in 633 Italian patients with AD followed up since 1967.MethodsAdrenal cortex autoantibodies, presence of other autoimmune and nonautoimmune diseases, nonadrenal autoantibodies, adrenal imaging, and genetic profile for HLA-DRB1 and AIRE were analyzed.ResultsA total of 492 (77.7%) patients were found to be affected by autoimmune AD (A-AD), 57 (9%) tuberculous AD, 29 (4.6%) genetic-associated AD, 10 (1.6%) adrenal cancer, six (0.94%) post-surgical AD, four (0.6%) vascular disorder-related AD, three (0.5%) post-infectious AD, and 32 (5.1%) were defined as idiopathic. Adrenal cortex antibodies were detected in the vast majority (88–100%) of patients with recent onset A-AD, but in none of those with nonautoimmune AD. Adrenal imaging revealed normal/atrophic glands in all A-AD patients: 88% of patients with A-AD had other clinical or subclinical autoimmune diseases or were positive for nonadrenal autoantibodies.Based on the coexistence of other autoimmune disorders, 65.6% of patients with A-AD were found to have type 2 autoimmune polyendocrine syndrome (APS2), 14.4% have APS1, and 8.5% have APS4. Class II HLA alleles DRB1*03 and DRB1*04 were increased, and DRB1*01, DRB1*07, DRB1*013 were reduced in APS2 patients when compared with controls. Of the patients with APS1, 96% were revealed to have AIRE gene mutations.ConclusionsA-AD is the most prevalent form of adrenal insufficiency in Italy, and ∼90% of the patients are adrenal autoantibody-positive at the onset. Assessment of patients with A-AD for the presence of other autoimmune diseases should be helpful in monitoring and diagnosing APS types 1, 2, or 4 and improving patients' care.
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Fujimura, Masato, Yoshinobu Nakatsuji, Subaru Fujiwara, Christophe Rème, and Hugues Gatto. "Spot-On Skin Lipid Complex as an Adjunct Therapy in Dogs with Atopic Dermatitis: An Open Pilot Study." Veterinary Medicine International 2011 (2011): 1–5. http://dx.doi.org/10.4061/2011/281846.

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The purpose of this paper was to evaluate the efficacy of topical skin lipid complex (SLC) in canine atopic dermatitis (AD). Eight dogs with chronic AD and no improvement of main therapy in symptoms, erythema, lichenification, excoriation, and alopecia in the previous month were treated with SLC topically as adjunct therapy at lesion sites twice weekly for 12 weeks. A statistically significant reduction (26.0%, ) in the third version of the Canine Atopic Dermatitis Extent and Severity Index (CADESI-03) modification from baseline was recorded 6 weeks after treatment, with marked reduction in the erythema subscore (36.2%, ). A significant reduction in excoriation and alopecia subscores was observed 6 weeks after treatment (39.9%, and 19.9%, , resp.). However, the lichenification subscore was not reduced significantly at 6 or 12 weeks. These findings suggest that topical SLC may have therapeutic and clinical benefits in dogs with AD.
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38

van den Berg, E., J. M. Poos, L. C. Jiskoot, L. M. Heijnen, S. Franzen, R. M. E. Steketee, R. Meijboom, et al. "Differences in Discriminability and Response Bias on Rey Auditory Verbal Learning Test Delayed Recognition in Behavioral Variant Frontotemporal Dementia and Alzheimer’s Disease." Journal of the International Neuropsychological Society 26, no. 9 (April 27, 2020): 918–26. http://dx.doi.org/10.1017/s1355617720000375.

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AbstractObjective:Episodic memory is impaired in Alzheimer’s disease (AD) dementia but thought to be relatively spared in behavioral variant frontotemporal dementia (bvFTD). This view is challenged by evidence of memory impairment in bvFTD. This study investigated differences in recognition memory performance between bvFTD and AD.Method:We performed a retrospective analysis on the recognition trial of the Rey Auditory Verbal Learning Test in patients with bvFTD (n = 85), AD (n = 55), and control participants (n = 59). Age- and education-adjusted between-group analysis was performed on the total score and indices of discriminative ability and response bias. Correlations between recognition and measures of memory, language, executive functioning, and construction were examined.Results:Patients with AD had a significantly lower total recognition score than patients with bvFTD (control 28.8 ± 1.5; bvFTD 24.8 ± 4.5; AD 23.4 ± 3.6, p < .01). Both bvFTD and AD had worse discriminative ability than controls (A’ control 0.96 ± 0.03; bvFTD 0.87 ± 0.03; AD 0.84 ± 0.10, p < .01), but there was no difference in response bias (B” control 0.9 ± 0.2; bvFTD 1.6 ± 1.47; AD 1.4± 1.4, p < .01). AD had worse discriminability than bvFTD (p < .05). Discriminability was associated with memory for both patient groups (median correlation coefficient r = .34) and additionally associated with language (r = .31), but not executive functioning (r = −.03) in bvFTD. Response bias was unrelated to other cognitive functions (r = −.02).Conclusions:Discriminability, but not response bias, differentiated patients with bvFTD from AD. The presence of an impaired discrimination index suggests a “pure” (recognition) memory deficit in bvFTD.
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39

Bartolomei, Francesca. "Il segreto come identit�. Omaggio ad Antonio Tabucchi (24/09/1943, Pisa - 25/03/2012, Lisbona)." Sigila N�30, no. 2 (2012): 17. http://dx.doi.org/10.3917/sigila.030.0017.

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40

De Santi, Susan, Maciek Bobinski, Juan Li, Isabel Monteiro, Istvan Boksay, Steven Ferris, Barry Reisberg, and Mony J. de Leon. "O1-02-03 A 4-year, 3 timepoint MRI hippocampal study of MCI transition to AD." Neurobiology of Aging 25 (July 2004): S12. http://dx.doi.org/10.1016/s0197-4580(04)80038-1.

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ten Kate, Mara, Alberto Redolfi, Enrico Peira, Isabelle Bos, Stephanie J. B. Vos, Philip Scheltens, Sebastiaan Engelborghs, et al. "F1-02-03: MRI PREDICTORS OF AMYLOID PATHOLOGY: RESULTS FROM THE EMIF-AD BIOMARKER DISCOVERY STUDY." Alzheimer's & Dementia 14, no. 7S_Part_3 (July 1, 2006): P202—P204. http://dx.doi.org/10.1016/j.jalz.2018.06.2309.

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Darst, Burcu F., Qiongshi Lu, Rebecca L. Koscik, Erin Jonaitis, Lindsay R. Clark, Kirk J. Hogan, Sterling C. Johnson, and Corinne D. Engelman. "O3-03-05: INTEGRATIVE NETWORK ANALYSIS IDENTIFIES RELATIONSHIPS BETWEEN METABOLOMICS, GENOMICS, AND RISK FACTORS FOR AD." Alzheimer's & Dementia 14, no. 7S_Part_19 (July 1, 2006): P1016—P1017. http://dx.doi.org/10.1016/j.jalz.2018.06.2786.

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Yang, Ting, Yifan Dang, Beth Ostaszewski, David Mengel, Verena Steffen, Christina Rabe, Tobias Bittner, Dominic M. Walsh, and Dennis J. Selkoe. "DT-02-03: TARGET ENGAGEMENT IN AN AD TRIAL: CRENEZUMAB LOWERS Aβ OLIGOMER LEVELS IN CSF." Alzheimer's & Dementia 14, no. 7S_Part_31 (July 1, 2006): P1669—P1670. http://dx.doi.org/10.1016/j.jalz.2018.07.012.

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Hosford, David A., Jill F. B. Altman, Ann M. Saunders, Marc E. Risner, Marina E. Zvartau-Hind, George C. Ormandy, and Allen D. Roses. "O4-03-07: Efficacy of rosiglitazone (RSG) in patients with mild to moderate Alzheimer's disease (AD)." Alzheimer's & Dementia 2 (July 2006): S81. http://dx.doi.org/10.1016/j.jalz.2006.05.315.

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Wong, Roger. "LIFESTYLE BEHAVIORS AND RACIAL DIFFERENCES IN ALZHEIMER’S DISEASE RISK." Innovation in Aging 3, Supplement_1 (November 2019): S468—S469. http://dx.doi.org/10.1093/geroni/igz038.1748.

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Abstract There is substantial evidence indicating that among all racial groups, Blacks have the highest Alzheimer’s disease (AD) risk. Despite the wide support for this disparity, the reasons for these racial differences in AD risk remain unclear. The purpose of this study was to examine how lifestyle behaviors (physical activity, smoking, and social contacts) mediate and moderate the relationship between race and AD risk among Black and White older adults. This study used seven annual waves (2011-2017) of prospective data from the National Health and Aging Trends Study (NHATS), a large nationally representative U.S. sample of older adults. At each wave, physical activity was measured as whether they engaged in vigorous physical activities; smoking was measured as whether they were cigarette smokers; and social contacts was measured as whether they visited friends/family outside of their home. The dependent variable was age of AD diagnosis. Multivariate analyses were conducted using the Cox proportional hazards model. Blacks had a 1.3 times significantly higher risk for AD compared to Whites (Hazard Ratio [HR]=1.31, p=.03). After controlling for lifestyle behaviors as a mediator, racial differences in AD risk were attenuated and no longer significantly different between Blacks and Whites (HR=1.05, p=.74). For the moderation model, interactions between race and each lifestyle behavior generated no statistically significant results. Our findings indicate lifestyle behaviors contribute to racial differences in AD risk between Blacks and Whites. Future research is needed among Black populations to identify specific lifestyle behaviors that are especially protective against AD as targets of intervention.
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Ginsberg, Stephen D. "PL-03-03: Expression profiling of vulnerable neuronal populations during the progression of AD: Lessons from postmortem human brains and relevant animal models of neurodegeration." Alzheimer's & Dementia 6 (July 2010): S115. http://dx.doi.org/10.1016/j.jalz.2010.05.357.

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Godio, M., M. Preve, N. E. Suardi, E. Bolla, R. A. Colombo, and R. Traber. "Quetiapine XR reduce impulsivity and dissociation in a sample of alcoholic patients." European Psychiatry 33, S1 (March 2016): S312—S313. http://dx.doi.org/10.1016/j.eurpsy.2016.01.1068.

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IntroductionAlcohol dependence (AD) is a major public health problem. Currently, three drugs for the treatment of AD have been approved: acamprosate, disulfiram and oral naltrexone. Quetiapine XR is an atypical antipsychotic has been shown to be a promising medication for the treatment of alcoholism [1,2]. The aim of our study is evaluate quetiapine efficacy on impulsivity in a sample of alcoholic patients.MethodA sample of alcoholic patients (n = 40) was assessed at the entrance and 2 months with: SCID-P, Brief-Temps, BIS-11, GSR, BPRS, SCI-DER, and CGI. The medium dosage of quetiapine is 300 mg.ResultsUsing the last observation carried forward, the mean total BIS score decreased from 60.8 at baseline to 40.2 at the final visit (P = .03). More pronounced improvement was observed in motor impulsiveness (P < .03) and attentional impulsiveness (P < .05) compared with non-planning impulsiveness (P = .09). We observed an improvement in SCI-DER total score (P = .02), in particular in derealization (P = .03) and autopsychic depersonalization (P = .04). A mean weight gain of 4.8 kg was observed. There is not significant different related to the different affective temperament.Discussion and conclusionAnalyses revealed a significant effect of Quetiapine XR in improving impulsivity and dissociation, in particular motor and attentional impulsiveness, derealization and autopsychic depersonalization. Moreover, an improvement of dissociative symptoms is probably connected with the blockade of postsynaptic 5-HT1A receptors [3]. Methodological limitations, clinical implications and suggestions for future research directions are considered.Disclosure of interestThe authors have not supplied their declaration of competing interest.
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Lukiw, Walter, Surjyadipta Bhattacharjee, Yuan Y. Li, Peter N. Alexandrov, Aileen I. Pogue, and Yuhai Zhao. "S3-02-03: Upregulation of micro RNA (miRNA) signaling in Alzheimer's disease (AD) and related neurological disorders." Alzheimer's & Dementia 8, no. 4S_Part_11 (July 2012): P421. http://dx.doi.org/10.1016/j.jalz.2012.05.1123.

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Gordon, Brian A., Tyler M. Blazey, Jon Christensen, Shaney Flores, Aylin Dincer, Sarah Keefe, Eric McDade, et al. "O3-13-03: THE RELATIONSHIP BETWEEN TAU PET AND OTHER AD BIOMARKERS IN AUTOSOMAL DOMINANT ALZHEIMER DISEASE." Alzheimer's & Dementia 14, no. 7S_Part_19 (July 1, 2006): P1056—P1057. http://dx.doi.org/10.1016/j.jalz.2018.06.2845.

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Devanand, Davangere P., Jesse G. Strickler, Elizabeth Crocco, Brent Forester, Mustafa Husain, Ipsit Vahia, Edward Huey, and Gregory H. Pelton. "F4-02-03: LITHIUM TREATMENT OF AGITATION IN ALZHEIMER'S DISEASE (LIT-AD): CLINICAL RATIONALE AND STUDY DESIGN." Alzheimer's & Dementia 14, no. 7S_Part_26 (July 1, 2006): P1384—P1385. http://dx.doi.org/10.1016/j.jalz.2018.06.2870.

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