What is it and what does it include?
The study included 124 people between the ages of 50 and 80 and with mild to moderate Alzheimer's disease, and compared 250 mg of Rilapladib taken once daily to placebo. This study primarily evaluated rilapladib's effect on CSF Aβ and tau biomarkers, as well as on a composite score of working memory and executive function. CSF samples were taken via lumbar puncture at baseline and Week 24 for biomarker analyses related to Alzheimer's disease. Blood samples were collected throughout the study for pharmacokinetics and a range of biomarker analyses. A range of safety and tolerability assessments were also performed (including vital signs, laboratory tests, eye examinations and ECGs).
How can I use this dataset to advance my research?
This dataset is ideal if:
- you’re investigating the effects of Rilapladib on biomarkers related to the Alzheimer's disease, and cognitive function.
- your research encompasses cerebrovascular oxidative stress and inflammation.
- you’re studying the effect on inhibition of Lp-PLA2 and its potential to reduce peripheral measures of inflammation.
- you’re investigating the extent to which the mechanisms observed in preclinical models of peripheral reduction of the production of proinflammatory and toxic mediators and restoration of the brain-blood barrier integrity are present in subjects with AD and CVD and whether any downstream impact on neurodegenerative biomarkers or cognition could be detected over a 24-week treatment period.
- you’re interested in studying the ability of Rilapladib to reduce brain-blood barrier permeability in human models.
Has this dataset helped researchers understand Alzheimer’s and other dementias better?
Of course!
- AD & cognition and CSF biomarkers of AD:
In 2015, researchers found Rilapladib to be well tolerated with no significant safety concerns. A significant difference from placebo was observed for rilapladib on change from baseline in their executive function/working memory score. They also found no significant difference between groups on the change from baseline in CSF Aβ1–42. Preliminary evidence of effects was detected on other mechanistic (albumin quotient) and disease-related biomarkers (tau/P-tau and neurofilament light chain). Overall, these data provide initial evidence supporting Lp-PLA2 inhibition as a novel treatment for dementia. June 2015 – DOI: https://doi.org/10.1016/j.trci.2015.06.003