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Article ; Online: Donanemab in Early Alzheimer's Disease. Reply.

Mintun, Mark A / Wessels, Alette M / Sims, John R

2021 Volume 385, Issue 7, Page(s) 667

MeSH term(s)	Alzheimer Disease ; Disease Progression ; Humans
Language	English
Publishing date	2021-08-11
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMc2109455
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Article ; Online: APOE ε4's impact on response to amyloid therapies in early symptomatic Alzheimer's disease: Analyses from multiple clinical trials.

Evans, Cynthia D / Sparks, JonDavid / Andersen, Scott W / Brooks, Dawn A / Hauck, Paula M / Mintun, Mark A / Sims, John R

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 19, Issue 12, Page(s) 5407–5417

Abstract: Introduction: Apolipoprotein E (APOE) ε4 may interact with response to amyloid-targeting therapies.: Methods: Aggregate data from trials enrolling participants with amyloid-positive, early symptomatic Alzheimer's disease (AD) were analyzed for ... ...

Abstract	Introduction: Apolipoprotein E (APOE) ε4 may interact with response to amyloid-targeting therapies. Methods: Aggregate data from trials enrolling participants with amyloid-positive, early symptomatic Alzheimer's disease (AD) were analyzed for disease progression. Results: Pooled analysis of potentially efficacious antibodies lecanemab, aducanumab, solanezumab, and donanemab shows slightly better efficacy in APOE ε4 carriers than in non-carriers. Carrier and non-carrier mean (95% confidence interval) differences from placebo using Clinical Dementia Rating Scale-Sum of Boxes (CDR-SB) were -0.30 (-0.478, -0.106) and -0.20 (-0.435, 0.042) and AD Assessment Scale-Cognitive subscale (ADAS-Cog) values were -1.01 (-1.577, -0.456) and -0.80 (-1.627, 0.018), respectively. Decline in the APOE ε4 non-carrier placebo group was equal to or greater than that in carriers across multiple scales. Probability of study success increases as the representation of the carrier population increases. Discussion: We hypothesize that APOE ε4 carriers have same or better response than non-carriers to amyloid-targeting therapies and similar or less disease progression with placebo in amyloid-positive trials. Highlights: Amyloid-targeting therapies had slightly greater efficacy in apolipoprotein E (APOE) ε4 carriers. Clinical decline is the same/slightly faster in amyloid-positive APOE ε4 non-carriers. Prevalence of non-carriers in trial populations could impact outcomes.
MeSH term(s)	Humans ; Alzheimer Disease/drug therapy ; Alzheimer Disease/genetics ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; Amyloid ; Amyloidogenic Proteins ; Disease Progression
Chemical Substances	donanemab ; Apolipoprotein E4 ; Apolipoproteins E ; Amyloid ; Amyloidogenic Proteins
Language	English
Publishing date	2023-05-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13128
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Article ; Online: Assessment of Efficacy and Safety of Zagotenemab: Results From PERISCOPE-ALZ, a Phase 2 Study in Early Symptomatic Alzheimer Disease.

Fleisher, Adam S / Munsie, Leanne M / Perahia, David G S / Andersen, Scott W / Higgins, Ixavier A / Hauck, Paula M / Lo, Albert C / Sims, John R / Brys, Miroslaw / Mintun, Mark

Neurology

2024 Volume 102, Issue 5, Page(s) e208061

Abstract: Background and objectives: Zagotenemab (LY3303560), a monoclonal antibody that preferentially targets misfolded, extracellular, aggregated tau, was assessed in the PERISCOPE-ALZ phase 2 study to determine its ability to slow cognitive and functional ... ...

Abstract	Background and objectives: Zagotenemab (LY3303560), a monoclonal antibody that preferentially targets misfolded, extracellular, aggregated tau, was assessed in the PERISCOPE-ALZ phase 2 study to determine its ability to slow cognitive and functional decline relative to placebo in early symptomatic Alzheimer disease (AD). Methods: Participants were enrolled across 56 sites in North America and Japan. Key eligibility criteria included age of 60-85 years, Mini-Mental State Examination score of 20-28, and intermediate levels of brain tau on PET imaging. In this double-blind study, participants were equally randomized to 1,400 mg or 5,600 mg of zagotenemab, or placebo (IV infusion every 4 weeks for 100 weeks). The primary outcome was change on the Integrated AD Rating Scale (iADRS) assessed by a Bayesian Disease Progression model. Secondary measures include mixed model repeated measures analysis of additional cognitive and functional endpoints as well as biomarkers of AD pathology. Results: A total of 360 participants (mean age = 75.4 years; female = 52.8%) were randomized, and 218 completed the treatment period. Demographics and baseline characteristics were reasonably balanced among arms. The mean disease progression ratio (proportional decline in the treated vs placebo group) with 95% credible intervals for the iADRS was 1.10 (0.959-1.265) for the zagotenemab low-dose group and 1.05 (0.907-1.209) for the high-dose, where a ratio less than 1 favors the treatment group. Secondary clinical endpoint measures failed to show a drug-placebo difference in favor of zagotenemab. No treatment effect was demonstrated by flortaucipir PET, volumetric MRI, or neurofilament light chain (NfL) analyses. A dose-related increase in plasma phosphorylated tau181 and total tau was demonstrated. Zagotenemab treatment groups reported a higher incidence of adverse events (AEs) (85.1%) compared with the placebo group (74.6%). This difference was not attributable to any specific AE or category of AEs. Discussion: In participants with early symptomatic AD, zagotenemab failed to achieve significant slowing of clinical disease progression compared with placebo. Imaging biomarker and plasma NfL findings did not show evidence of pharmacodynamic activity or disease modification. Trial registration information: ClinicalTrials.gov: NCT03518073. Classification of evidence: This study provides Class II evidence that for patients with early symptomatic AD, zagotenemab does not slow clinical disease progression.
MeSH term(s)	Aged ; Aged, 80 and over ; Female ; Humans ; Middle Aged ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/drug therapy ; Alzheimer Disease/psychology ; Antibodies, Monoclonal/therapeutic use ; Bayes Theorem ; Disease Progression ; Double-Blind Method ; Treatment Outcome ; Male
Chemical Substances	Antibodies, Monoclonal
Language	English
Publishing date	2024-02-22
Publishing country	United States
Document type	Randomized Controlled Trial ; Clinical Trial, Phase II ; Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000208061
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Article ; Online: Early tau detection in flortaucipir images: validation in autopsy-confirmed data and implications for disease progression.

Kotari, Vikas / Southekal, Sudeepti / Navitsky, Michael / Kennedy, Ian A / Lu, Ming / Morris, Amanda / Zimmer, Jennifer Ann / Fleisher, Adam S / Mintun, Mark A / Devous, Michael D / Pontecorvo, Michael J

Alzheimer's research & therapy

2023 Volume 15, Issue 1, Page(s) 41

Abstract: Background: There is an increasing interest in utilizing tau PET to identify patients early in Alzheimer's disease (AD). In this work, a temporal lobe composite (Eτ) volume of interest (VOI) was evaluated in a longitudinal flortaucipir cohort and ... ...

Abstract	Background: There is an increasing interest in utilizing tau PET to identify patients early in Alzheimer's disease (AD). In this work, a temporal lobe composite (Eτ) volume of interest (VOI) was evaluated in a longitudinal flortaucipir cohort and compared to a previously described global neocortical VOI. In a separate autopsy-confirmed study, the sensitivity of the Eτ VOI for identifying intermediate (B2) neurofibrillary tangle (NFT) pathology was evaluated. Methods: A total of 427 subjects received flortaucipir, florbetapir, MRI, and cognitive evaluation at baseline and 18 months. In a separate autopsy study, 67 subjects received ante-mortem flortaucipir scans, and neuropathological findings were recorded according to NIA-AA recommendations by two experts. Two VOIs: Eτ comprising FreeSurfer volumes (bilateral entorhinal cortex, fusiform, parahippocampal, and inferior temporal gyri) transformed to MNI space and a previously published global AD signature-weighted neocortical VOI (AD Results: Sixty-four out of 390 analyzable subjects were identified as Eτ+/AD Conclusion: The Eτ VOI identified subjects with elevated temporal but not global tau (Eτ+/AD
MeSH term(s)	Humans ; Autopsy ; Alzheimer Disease/diagnostic imaging ; Apolipoprotein E4 ; Disease Progression
Chemical Substances	7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole (J09QS3Z3WB) ; Apolipoprotein E4
Language	English
Publishing date	2023-02-28
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-023-01160-6
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Article ; Online: Tau as a diagnostic instrument in clinical trials to predict amyloid in Alzheimer's disease.

Shcherbinin, Sergey / Morris, Amanda / Higgins, Ixavier A / Tunali, Ilke / Lu, Ming / Deveau, Carmen / Southekal, Sudeepti / Kotari, Vikas / Evans, Cynthia D / Arora, Anupa K / Collins, Emily C / Pontecorvo, Michael / Mintun, Mark A / Sims, John R

Alzheimer's & dementia (New York, N. Y.)

2023 Volume 9, Issue 3, Page(s) e12415

Abstract: ... positivity was ≥93% for all three trials using various A+ and T+ definitions, including visual, quantitative ... and combination methods. Population characteristics did not have an impact on A+ predictability ... consistent among visual and quantitative A+ definitions (: Discussion: These findings suggest ...

Abstract	Introduction: Alzheimer's disease (AD) is characterized by the presence of both amyloid and tau pathology. In vivo diagnosis can be made with amyloid and tau positron emission tomography (PET) imaging. Emergent evidence supports that amyloid and tau accumulation are associated and that amyloid accumulation may precede that of tau. This report further investigates the relationship between amyloid and tau to assess whether elevated cortical tau can predict elevated amyloid in participants with early symptomatic AD. Methods: Florbetapir F18 and flortaucipir F18 uptake were evaluated from baseline PET scans collected in three multi-center studies with cognitively impaired participants, including A05 ( Results: PPV for amyloid positivity was ≥93% for all three trials using various A+ and T+ definitions, including visual, quantitative, and combination methods. Population characteristics did not have an impact on A+ predictability. Regional analyses (early tau (Eτ) volume of interest (VOI), temporal, parietal, frontal) revealed significant area under the ROC curve in Eτ VOI compared to frontal region, regardless of reference region and consistent among visual and quantitative A+ definitions ( Discussion: These findings suggest that a positive tau PET scan is associated (≥93%) with amyloid positivity in individuals with early symptomatic AD, with the potential benefits of reducing clinical trial and health care expenses, radiation exposure, and participant time. Highlights: Positron emission tomography (PET) evaluates candidates for Alzheimer's disease (AD) research. A positive tau PET scan is associated (≥93%) with amyloid positivity.A positive amyloid PET is not necessarily associated with tau positivity.Tau PET could be the sole diagnostic tool to confirm candidates for AD trials.
Language	English
Publishing date	2023-08-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	2832891-7
ISSN	2352-8737 ; 2352-8737
ISSN (online)	2352-8737
ISSN	2352-8737
DOI	10.1002/trc2.12415
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Article: FDG and amyloid positron emission tomography.

Mintun, Mark A

CNS spectrums

2008 Volume 13, Issue 10 Suppl 16, Page(s) 21–24

MeSH term(s)	Aged ; Alzheimer Disease/diagnosis ; Alzheimer Disease/pathology ; Brain/metabolism ; Fluorodeoxyglucose F18/pharmacokinetics ; Humans ; Plaque, Amyloid/metabolism ; Plaque, Amyloid/pathology ; Positron-Emission Tomography ; Radiopharmaceuticals/pharmacokinetics
Chemical Substances	Radiopharmaceuticals ; Fluorodeoxyglucose F18 (0Z5B2CJX4D)
Language	English
Publishing date	2008-10-24
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2008418-3
ISSN	2165-6509 ; 1092-8529
ISSN (online)	2165-6509
ISSN	1092-8529
DOI	10.1017/s1092852900027000
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Article ; Online: Association of Amyloid Reduction After Donanemab Treatment With Tau Pathology and Clinical Outcomes: The TRAILBLAZER-ALZ Randomized Clinical Trial.

Shcherbinin, Sergey / Evans, Cynthia D / Lu, Ming / Andersen, Scott W / Pontecorvo, Michael J / Willis, Brian A / Gueorguieva, Ivelina / Hauck, Paula M / Brooks, Dawn A / Mintun, Mark A / Sims, John R

JAMA neurology

2022 Volume 79, Issue 10, Page(s) 1015–1024

Abstract: Importance: β-amyloid plaques and neurofibrillary tau deposits biologically define Alzheimer disease.: Objective: To perform post hoc analyses of amyloid reduction after donanemab treatment and assess its association with tau pathology and clinical ... ...

Abstract	Importance: β-amyloid plaques and neurofibrillary tau deposits biologically define Alzheimer disease. Objective: To perform post hoc analyses of amyloid reduction after donanemab treatment and assess its association with tau pathology and clinical measures. Design, setting, and participants: The Study of LY3002813 in Participants With Early Symptomatic Alzheimer's Disease (TRAILBLAZER-ALZ) was a phase 2, placebo-controlled, randomized clinical trial conducted from December 18, 2017, to December 4, 2020, with a double-blind period of up to 76 weeks and a 48-week follow-up period. The study was conducted at 56 centers in the US and Canada. Enrolled were participants from 60 to 85 years of age with gradual and progressive change in memory function for 6 months or more, early symptomatic Alzheimer disease, elevated amyloid, and intermediate tau levels. Interventions: Donanemab (an antibody specific for the N-terminal pyroglutamate β-amyloid epitope) dosing was every 4 weeks: 700 mg for the first 3 doses, then 1400 mg for up to 72 weeks. Blinded dose-reduction evaluations occurred at 24 and 52 weeks based on amyloid clearance. Main outcomes and measures: Change in amyloid, tau, and clinical decline after donanemab treatment. Results: The primary study randomized 272 participants (mean [SD] age, 75.2 [5.5] years; 145 female participants [53.3%]). The trial excluded 1683 of 1955 individuals screened. The rate of donanemab-induced amyloid reduction at 24 weeks was moderately correlated with the amount of baseline amyloid (Spearman correlation coefficient r, -0.54; 95% CI, -0.66 to -0.39; P < .001). Modeling provides a hypothesis that amyloid would not reaccumulate to the 24.1-centiloid threshold for 3.9 years (95% prediction interval, 1.9-8.3 years) after discontinuing donanemab treatment. Donanemab slowed tau accumulation in a region-dependent manner as measured using neocortical and regional standardized uptake value ratios with cerebellar gray reference region. A disease-progression model found a significant association between percentage amyloid reduction and change on the integrated Alzheimer Disease Rating Scale only in apolipoprotein E (APOE) ε4 carriers (95% CI, 24%-59%; P < .001). Conclusions and relevance: Results of post hoc analyses for donanemab-treated participants suggest that baseline amyloid levels were directly associated with the magnitude of amyloid reduction and inversely associated with the probability of achieving complete amyloid clearance. The donanemab-induced slowing of tau was more pronounced in those with complete amyloid clearance and in brain regions identified later in the pathologic sequence. Data from other trials will be important to confirm aforementioned observations, particularly treatment response by APOE ε4 status. Trial registration: ClinicalTrials.gov Identifier: NCT03367403.
MeSH term(s)	Aged ; Alzheimer Disease/drug therapy ; Alzheimer Disease/pathology ; Amyloid ; Amyloid beta-Peptides ; Amyloidosis ; Apolipoprotein E4 ; Epitopes/therapeutic use ; Female ; Humans ; Infant ; Plaque, Amyloid/drug therapy ; Plaque, Amyloid/pathology ; Positron-Emission Tomography ; Pyrrolidonecarboxylic Acid/therapeutic use ; tau Proteins
Chemical Substances	Amyloid ; Amyloid beta-Peptides ; Apolipoprotein E4 ; Epitopes ; tau Proteins ; Pyrrolidonecarboxylic Acid (SZB83O1W42)
Language	English
Publishing date	2022-09-12
Publishing country	United States
Document type	Clinical Trial, Phase II ; Journal Article ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2022.2793
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Article ; Online: Association of Donanemab Treatment With Exploratory Plasma Biomarkers in Early Symptomatic Alzheimer Disease: A Secondary Analysis of the TRAILBLAZER-ALZ Randomized Clinical Trial.

Pontecorvo, Michael J / Lu, Ming / Burnham, Samantha C / Schade, Andrew E / Dage, Jeffrey L / Shcherbinin, Sergey / Collins, Emily C / Sims, John R / Mintun, Mark A

JAMA neurology

2022 Volume 79, Issue 12, Page(s) 1250–1259

Abstract: Importance: Plasma biomarkers of Alzheimer disease may be useful as minimally invasive pharmacodynamic measures of treatment outcomes.: Objective: To analyze the association of donanemab treatment with plasma biomarkers associated with Alzheimer ... ...

Abstract	Importance: Plasma biomarkers of Alzheimer disease may be useful as minimally invasive pharmacodynamic measures of treatment outcomes. Objective: To analyze the association of donanemab treatment with plasma biomarkers associated with Alzheimer disease. Design, setting, and participants: TRAILBLAZER-ALZ was a randomized, double-blind, placebo-controlled clinical trial conducted from December 18, 2017, to December 4, 2020, across 56 sites in the US and Canada. Exploratory biomarkers were prespecified with the post hoc addition of plasma glial fibrillary acidic protein and amyloid-β. Men and women aged 60 to 85 years with gradual and progressive change in memory function for at least 6 months were included. A total of 1955 participants were assessed for eligibility. Key eligibility criteria include Mini-Mental State Examination scores of 20 to 28 and elevated amyloid and intermediate tau levels. Interventions: Randomized participants received donanemab or placebo every 4 weeks for up to 72 weeks. The first 3 doses of donanemab were given at 700 mg and then increased to 1400 mg with blinded dose reductions as specified based on amyloid reduction. Main outcomes and measures: Change in plasma biomarker levels after donanemab treatment. Results: In TRAILBLAZER-ALZ, 272 participants (mean [SD] age, 75.2 [5.5] years; 145 [53.3%] female) were randomized. Plasma levels of phosphorylated tau217 (pTau217) and glial fibrillary acidic protein were significantly lower with donanemab treatment compared with placebo as early as 12 weeks after the start of treatment (least square mean change difference vs placebo, -0.04 [95% CI, -0.07 to -0.02]; P = .002 and -0.04 [95% CI, -0.07 to -0.01]; P = .01, respectively). No significant differences in plasma levels of amyloid-β 42/40 and neurofilament light chain were observed between treatment arms at the end of treatment. Changes in plasma pTau217 and glial fibrillary acidic protein were significantly correlated with the Centiloid percent change in amyloid (Spearman rank correlation coefficient [R] = 0.484 [95% CI, 0.359-0.592]; P < .001 and R = 0.453 [95% CI, 0.306-0.579]; P < .001, respectively) following treatment. Additionally, plasma levels of pTau217 and glial fibrillary acidic protein were significantly correlated at baseline and following treatment (R = 0.399 [95% CI, 0.278-0.508], P < .001 and R = 0.393 [95% CI, 0.254-0.517]; P < .001, respectively). Conclusions and relevance: Significant reductions in plasma biomarkers pTau217 and glial fibrillary acidic protein compared with placebo were observed following donanemab treatment in patients with early symptomatic Alzheimer disease. These easily accessible plasma biomarkers might provide additional evidence of Alzheimer disease pathology change through anti-amyloid therapy. Usefulness in assessing treatment response will require further evaluation. Trial registration: ClinicalTrials.gov Identifier: NCT03367403.
Language	English
Publishing date	2022-10-25
Publishing country	United States
Document type	Journal Article
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2022.3392
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Article: Utilizing advanced imaging and surrogate markers across the spectrum of Alzheimer's disease.

Mintun, Mark A

CNS spectrums

2005 Volume 10, Issue 11 Suppl 18, Page(s) 13–16

Abstract: Alzheimer's disease is a degenerative neurological condition characterized by the presence of beta-amyloid plaques and neurofibrillary tangles in the limbic and neocortical regions of the brain. Pittsburgh Compound-B (PIB), a benzothiazole analog, has ... ...

Abstract	Alzheimer's disease is a degenerative neurological condition characterized by the presence of beta-amyloid plaques and neurofibrillary tangles in the limbic and neocortical regions of the brain. Pittsburgh Compound-B (PIB), a benzothiazole analog, has recently been found to specifically label amyloid deposits in positron emission tomography (PET) studies of the brain, opening the door for a wide range of applications related to Alzheimer's disease. In this article, data demonstrating the specificity of PIB as a PET tracer for beta-amyloid lesions are reviewed, and the potential clinical applications of PIB PET imaging is discussed. Because amyloid plaques are common even in elderly individuals who are not suffering from dementia, the primary diagnostic function of PIB PET imaging presumably would be to rule out, rather than definitively confirm, Alzheimer's diagnoses in elderly patients. Other possible uses include monitoring plaque loads in patients receiving anti-amyloid therapy for Alzheimer's disease, as well as assessing plaque formation in unaffected individuals as a means of evaluating future Alzheimer's disease.
MeSH term(s)	Aged ; Alzheimer Disease/diagnosis ; Alzheimer Disease/immunology ; Alzheimer Disease/metabolism ; Amyloid beta-Protein Precursor/immunology ; Amyloid beta-Protein Precursor/metabolism ; Antibody Formation ; Biomarkers ; Brain/metabolism ; Brain/pathology ; Cerebral Cortex/immunology ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Humans ; Limbic System/immunology ; Limbic System/metabolism ; Limbic System/pathology ; Magnetic Resonance Imaging ; Neurofibrillary Tangles/metabolism ; Positron-Emission Tomography
Chemical Substances	Amyloid beta-Protein Precursor ; Biomarkers
Language	English
Publishing date	2005-07-26
Publishing country	United States
Document type	Journal Article
ZDB-ID	2008418-3
ISSN	2165-6509 ; 1092-8529
ISSN (online)	2165-6509
ISSN	1092-8529
DOI	10.1017/s1092852900014188
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Article ; Online: PET amyloid imaging as a tool for early diagnosis and identifying patients at risk for progression to Alzheimer's disease.

Pontecorvo, Michael J / Mintun, Mark A

Alzheimer's research & therapy

2011 Volume 3, Issue 2, Page(s) 11

Abstract: Current theory suggests that β-amyloid accumulation may be an early step in the cascade that leads to cognitive impairment in Alzheimer's disease. β-Amyloid targeted positron emission tomography (PET) imaging potentially provides a direct, relatively ... ...

Abstract	Current theory suggests that β-amyloid accumulation may be an early step in the cascade that leads to cognitive impairment in Alzheimer's disease. β-Amyloid targeted positron emission tomography (PET) imaging potentially provides a direct, relatively noninvasive estimate of brain β-amyloid burden. This has recently been supported by demonstration that amyloid plaque binding on PET was strongly correlated with brain β-amyloid burden at autopsy. Additionally, there is growing consensus that PET imaging can identify subjects with elevated β-amyloid burden, even at early stages of disease. Finally, preliminary evidence suggests that abnormal β-amyloid accumulation, as evidenced by PET imaging, has implications for both present nd future cognitive performance. Although large longitudinal studies like the ongoing ADNI trial will be required for definitive evaluation, present data suggest that PET amyloid imaging has the potential to promote earlier and more specific diagnosis of dementia.
Language	English
Publishing date	2011-03-29
Publishing country	England
Document type	Journal Article
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/alzrt70
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