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Dataset results
454 results for “Preclinical”
A Donanemab (LY3002813) Study in Participants With Preclinical Alzheimer's Disease (TRAILBLAZER-ALZ 3)
ClinicalTrials.gov study NCT05026866. IPD Sharing: YES. Countries: 3. Publications: 1.
Prediction of Cognitive Decline by Neuroimaging Techniques and the Application in Diagnosis and Treatment of Preclinical AD
ClinicalTrials.gov study NCT03370744. IPD Sharing: UNDECIDED. Countries: 1. Publications: 12.
Next pErsonalized Cancer tX With mulTi-omics and Preclinical Model
ClinicalTrials.gov study NCT02141152. IPD Sharing: Not stated. Countries: 1. Publications: 1.
New Models for the Evaluation of Preclinical Treatment for Urothelial Carcinomas of the Upper Excretory Tract.
ClinicalTrials.gov study NCT04944550. IPD Sharing: Not stated. Countries: 1. Publications: 1.
E4D Compare Adapted to Preclinical Endodontics
ClinicalTrials.gov study NCT06567236. IPD Sharing: NO. Countries: 1. Publications: 1.
Education is associated with Aβ burden in preclinical familial and sporadic Alzheimer’s disease
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Data from: White matter hyperintensities and CSF AD biomarkers in preclinical Alzheimer's disease
Objective: Recent studies suggest that white matter hyperintensities (WMH) on MRI, which primarily reflect small vessel cerebrovascular disease, may play a role in the evolution of Alzheimer's disease (AD). In a longitudinal study, we investigated whether WMH promote the progression of AD pathology, or alter the association between AD pathology and risk of progression from normal cognition to mild cognitive impairment (MCI). Methods: Two sets of analyses were conducted. The relationship between whole brain WMH load, based on FLAIR MRI images, obtained in initially cognitively normal participants (n=274) and time to onset of symptoms of MCI (n=60) was examined using Cox regression models. In a subset of the participants with both MRI and CSF data (n=204), the interaction of WMH load and CSF AD biomarkers was also evaluated. Results: Baseline WMH load interacted with CSF t-tau with respect to symptom onset, but not with CSF abeta1-42 or p-tau181. WMH volume was associated with time to symptom onset of MCI among individuals with low t-tau [HR=1.35, CI=1.06-1.73, p=0.013], but not those with high t-tau [HR=0.86,CI=0.56-1.32, p=0.47]. The rate of change in the CSF biomarkers over time was not associated with the rate of change in WMH volumes. Conclusions and Relevance: These results suggest that WMH primarily affect the risk of progression when CSF measures of neurodegeneration or neuronal injury (as reflected by t-tau) are low. However, CSF biomarkers of amyloid and p-tau and WMH appear to have largely independent and non-synergistic effects on the risk of progression to MCI.
Data from: The relationship between risk of bias criteria, research outcomes, and study sponsorship in a cohort of preclinical thiazolidinedione animal studies: a meta-analysis
Introduction: There is little evidence regarding the influence of conflicts of interest on preclinical research. This study examines whether industry sponsorship is associated with increased risks of bias and/or effect sizes of outcomes in published preclinical thiazolidinedione (TZD) studies. Methods: We identified preclinical TZD studies published between January 1, 1965, and November 14, 2012. Coders independently extracted information on study design criteria aimed at reducing bias, results for all relevant outcomes, sponsorship source and investigator financial ties from the 112 studies meeting the inclusion criteria. The average standardized mean difference (SMD) across studies was calculated for plasma glucose (efficacy outcome) and weight gain (harm outcome). In subgroup analyses, TZD outcomes were assessed by sponsorship source and risk of bias criteria. Results: Seven studies were funded by industry alone, 17 studies funded by both industry and non-industry, 49 studies funded by non-industry alone and 39 studies had no disclosures. None of the studies used sample size calculations, intention-to-treat analyses, blinding of investigators or concealment of allocation. Most studies reported favourable results (88 of 112) and conclusions (95 of 112) supporting TZD use. Efficacy estimates were significantly larger in six studies sponsored by industry alone (−3.41; 95% CI −5.21, −1.53; I2 = 93%) versus 42 studies sponsored by non-industry sources (−0.97; 95% CI −1.37, −0.56; I2 = 81%; p-value = 0.01). Harms estimates were significantly larger in four studies sponsored by industry alone (5.00; 95% CI 1.22, 8.77; I2 = 93%) versus 38 studies sponsored by non-industry sources (0.30; 95% CI −0.08, 0.68; I2 = 79%; p-value = 0.02). TZD efficacy and harms did not differ by disclosure of financial COIs or risks of bias. Conclusions: Industry-sponsored TZD animal studies have exaggerated efficacy and harms outcomes compared with studies funded by non-industry sources. There was poor reporting of COIs.
Data from: Evolution of ischemic damage and behavioural deficit over 6 months after MCAo in the rat: selecting the optimal outcomes and statistical power for multi-centre preclinical trials
Key disparities between the timing and methods of assessment in animal stroke studies and clinical trial may be part of the reason for the failure to translate promising findings. This study investigates the development of ischemic damage after thread occlusion MCAo in the rat, using histological and behavioural outcomes. Using the adhesive removal test we investigate the longevity of behavioural deficit after ischemic stroke in rats, and examine the practicality of using such measures as the primary outcome for future studies. Ischemic stroke was induced in 132 Spontaneously Hypertensive Rats which were assessed for behavioural and histological deficits at 1, 3, 7, 14, 21, 28 days, 12 and 24 weeks (n>11 per timepoint). The basic behavioural score confirmed induction of stroke, with deficits specific to stroke animals. Within 7 days, these deficits resolved in 50% of animals. The adhesive removal test revealed contralateral neglect for up to 6 months following stroke. Sample size calculations to facilitate the use of this test as the primary experimental outcome resulted in cohort sizes much larger than are the norm for experimental studies. Histological damage progressed from a necrotic infarct to a hypercellular area that cleared to leave a fluid filled cavity. Whilst absolute volume of damage changed over time, when corrected for changes in hemispheric volume, an equivalent area of damage was lost at all timepoints. Using behavioural measures at chronic timepoints presents significant challenges to the basic science community in terms of the large number of animals required and the practicalities associated with this. Multicentre preclinical randomised controlled trials as advocated by the MultiPART consortium may be the only practical way to deal with this issue.
Data from: Preclinical toxicity and pharmacokinetics of a new orally bioavailable flubendazole formulation and the impact for clinical trials and risk/benefit to patients.
Background: Flubendazole, originally developed to treat infections with intestinal nematodes, has been shown to be efficacious in animal models of filarial infections. For treatment of filarial nematodes, systemic exposure is needed. For this purpose, an orally bioavailable amorphous solid dispersion (ASD) formulation was developed. As this formulation results in improved systemic absorption, the pharmacokinetic and toxicological profile of flubendazole administered with this formulation have been assessed to ensure human safety before clinical trials could be initiated. Methods & Findings: Safety pharmacology, toxicity and genotoxicity studies have been conducted with the flubendazole ASD formulation. In animals, flubendazole has good oral bioavailability from an ASD formulation ranging from 15 % in dogs, 276 % in rats to more than 100% in jirds. In in vivo toxicity studies with the ASD formulation, high systemic exposure to flubendazole and its main metabolites was reached. Flubendazole, up to high peak plasma concentrations, does not induce Cmax related effects in the CNS or cardiovascular system. In repeated dose toxicity studies in rats and dogs, flubendazole-induced changes were observed in haematological, lymphoid and gastrointestinal systems and in testes. In dog, the liver was an additional target organ. Upon treatment cessation, at least partial recovery was observed for these changes in the dog. In rat, the low dose was the No Observed Adverse Effect Level (NOAEL) was , i.e. 5 mg (as base)/kg body weight/day (mg eq./kg/day)mg eq./kg/day in males and 2.5 mg eq./kg/day in females. In dog, the NOAEL was lower than the low dose, 20 mg eq./kg/day. Regarding genotoxicity, flubendazole was negative in the Ames test but positive in the in vivo micronucleus test. Conclusions: Based on these results, in combination with previously described genotoxicity and reproductive toxicity data and the outcome of the preclinical efficacy studies, it was concluded that no flubendazole treatment regimen can be selected that would provide efficacy in humans at safe exposure.
Figure 6 from: Shannag S, Nuseir K, Tahaineh L, Hananeh W (2024) Curcumin is comparable to metformin for the treatment of PCOS in rats: a preclinical study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e119708
Figure 6 Ovarian section from G6 group showing disrupted follicular development, lack of corpora lutea and presence of follicular cysts.
Figure 3 from: Shannag S, Nuseir K, Tahaineh L, Hananeh W (2024) Curcumin is comparable to metformin for the treatment of PCOS in rats: a preclinical study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e119708
Figure 3 Hormonal and metabolic serum levels over time. Changes in serum levels of testosterone, estradiol, progesterone, and glucose before and after treatment with metformin, curcumin, metformin + curcumin, and olive oil compared to control rats' side by side. Data expressed as mean ± SEM (n = 16–17).
Figure 5 from: Shannag S, Nuseir K, Tahaineh L, Hananeh W (2024) Curcumin is comparable to metformin for the treatment of PCOS in rats: a preclinical study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e119708
Figure 5 Ovarian section from G3 group showing multiple variably sized follicular cysts with disrupted normal follicular development.
Figure 2 from: Shannag S, Nuseir K, Tahaineh L, Hananeh W (2024) Curcumin is comparable to metformin for the treatment of PCOS in rats: a preclinical study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e119708
Figure 2 Hormonal and metabolic serum levels. Changes in serum levels of testosterone, estradiol, progesterone, and glucose before and after treatment with metformin, curcumin, metformin + curcumin, and olive oil compared to control rats. Data expressed as mean ± SEM (n = 16–17). *Significantly different form control. A. Testosterone levels in ng/ml following letrozole injections and before treatment at age 9 weeks; B. Estradiol levels in pg/ml following letrozole injections and before treatment at age 9 weeks; C. Progesterone levels in ng/ml following letrozole injections and before treatment at age 9 weeks; D. Glucose serum levels mg/dl following letrozole injections and before treatment at age 9 weeks; E. Testosterone levels in ng/ml following treatment at age 12 weeks; F. Estradiol levels in pg/ml following treatment at age 12 weeks; G. Progesterone levels in ng/ml following treatment at age 12 weeks; H. Glucose serum levels mg/dl following treatment at age 12 weeks.
Figure 4 from: Shannag S, Nuseir K, Tahaineh L, Hananeh W (2024) Curcumin is comparable to metformin for the treatment of PCOS in rats: a preclinical study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e119708
Figure 4 Ovarian section from control group showing different stages of follicular development and normal ovarian morphology.
Figure 1 from: Shannag S, Nuseir K, Tahaineh L, Hananeh W (2024) Curcumin is comparable to metformin for the treatment of PCOS in rats: a preclinical study. Pharmacia 71: 1-10. https://doi.org/10.3897/pharmacia.71.e119708
Figure 1 Changes in body weight before (DI, week 6) PCOS induction, after PCOS induction (T, week 9), and following treatments (sac, week 12) with metformin, curcumin, combination of met +cur and olive oil. Data expressed as mean ± SEM (n = 16–17). ** significant difference from control group.
CSF synaptic biomarkers in the preclinical stage of Alzheimer's disease and their association with MRI and PET markers of neurodegeneration: a cross-sectional study
<p>Objective: To determine whether CSF synaptic biomarkers are altered in the early preclinical stage of the Alzheimer's <i>continuum</i> and associated with Alzheimer's disease (AD) risk factors, primary pathology, and neurodegeneration markers.</p> <p>Methods: Cross-sectional study in the ALFA+ cohort, comprising middle-aged cognitively unimpaired participants. CSF neurogranin and GAP-43 were measured using immunoassays and SNAP-25 and synaptotagmin-1 using immunoprecipitation mass spectrometry. AD CSF biomarkers Aβ42/40, p-tau and t-tau, and the neurodegeneration biomarker NfL were also measured. Participants underwent structural MRI, and <span>fluorodeoxyglucose and</span> Aβ<span> PET imaging. General linear modeling was used to test the associations between CSF synaptic biomarkers and risk factors, </span>Aβ<span> pathology, tau pathology, and neurodegeneration markers.</span></p> <p>Results: All CSF synaptic biomarkers increased with age. CSF neurogranin was higher in females, while CSF SNAP-25 was higher in <i>APOE-</i>ε4 carriers. All CSF synaptic biomarkers increased with higher Aβ load (as measured by CSF Aβ42/40 and Aβ PET Centiloid values) and, importantly, the synaptic biomarkers were increased even in individuals in the earliest stages of Aβ deposition. Higher CSF synaptic biomarkers were also associated with higher CSF p-tau and NfL. Higher CSF neurogranin and GAP-43 were significantly associated with higher brain metabolism, but lower cortical thickness in AD-related brain regions.</p> <p>Conclusion: CSF synaptic biomarkers increase in early preclinical stages of the Alzheimer's <i>continuum </i>even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, <i>APOE-</i>ε4<i>,</i> and markers of neurodegeneration.</p>
Association of CSF biomarkers with hippocampal-dependent memory in preclinical Alzheimer disease
<p><b>Objective: </b>To determine if memory tasks with demonstrated sensitivity to hippocampal function can detect variance related to preclinical Alzheimer's disease (AD) biomarkers, we examined associations between performance in three memory tasks and CSF Ab<sub>42</sub>/Ab<sub>40 </sub>and p-tau<sub>181</sub> in cognitively unimpaired older adults (CU).</p> <p><b>Methods: </b>CU enrolled in the Stanford Aging and Memory Study (N=153; age 68.78 ± 5.81 yrs; 94 female) completed a lumbar puncture and memory assessments. CSF Ab<sub>42</sub>,<sub> </sub>Ab<sub>40</sub>, and phosopho-tau<sub>181</sub> (p-tau<sub>181</sub>) were measured with the automated Lumipulse G system in a single-batch analysis. Episodic memory was assayed using a delayed recall composite, paired associate (word-picture) cued recall, and a mnemonic discrimination task that involves discrimination between studied 'target' objects, novel 'foil' objects, and perceptually similar 'lure' objects. Analyses examined cross-sectional relationships between memory performance, age, and CSF measures, controlling for sex and education.</p> <p><span><b>Results: </b>Age and lower Ab<sub>42</sub>/Ab<sub>40 </sub>were independently associated with elevated p-tau<sub>181</sub>. Age, Ab<sub>42</sub>/Ab<sub>40,</sub> and p-tau<sub>181</sub> were each associated with a) poorer associative memory and b) diminished improvement in mnemonic discrimination performance across levels of decreased task difficulty (i.e., target-lure similarity). P-tau mediated the effect of Ab<sub>42</sub>/Ab<sub>40 </sub>on memory. Relationships between CSF proteins and delayed recall were similar but non-significant. CSF Ab<sub>42 </sub>was not significantly associated with p-tau<sub>181 </sub>or memory. </span></p> <p><b>Conclusions: </b>Tests designed to tax hippocampal function are sensitive to subtle individual differences in memory among CU, and correlate with early AD-associated biomarker changes in CSF. These tests may offer utility for identifying cognitively unimpaired older adults with preclinical AD pathology.<b> </b></p>
Peripheral mononuclear blood cell apheresis in a preclinical ovine model
<p>Dataset relating to sheep blood values</p>
Ecotoxicants within the maximum permissible concentration affect clinical and laboratory parameters of patients with rheumatoid arthritis and individuals at risk at preclinical stages
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.