The diagnosis of AD today is relying on memory tests and on some proteomics biomarkers, including β-amyloid (Aβ) and tau that can be further assessed by neuroimaging and cerebrospinal fluid (CSF) analysis. Aβ and tau are believed to cause disease when they form aggregates while their amount is increased in the central nervous system. Although the amount of these protein aggregates correlates with the stage of AD, no therapies against these proteins are available. Importantly, recent studies have highlighted the potential roles of metabolomics dysfunctions in the pathogenesis and progression of AD, suggesting that alterations in metabolomics and glyconomics profiles are not only the consequence of AD, but can cause the disease itself. Since the prevalence of AD is drastically elevated in the aging population, neither early biomarkers, nor therapies are available.
Goals
To identify which markers are associated with poor brain clearance function
To identify novel potential targets for pharmacologic interventions
To validate identified biomarkers in AD animal models
Project Facts
Project name: Metabolomics-Driven Biomarker Discovery of Alzheimer’s Disease
Project acronym: MetaboAD
Start date:
Duration: 36 months
Budget: € 812 881
Coordination: Iben Lundgaard, Department of Experimental Medical Science, Lund University, Sweden