Servizio Comunitario di Informazione in materia di Ricerca e Sviluppo - CORDIS


BIOFINDER Sintesi della relazione

Project ID: 311292
Finanziato nell'ambito di: FP7-IDEAS-ERC
Paese: Sweden

Mid-Term Report Summary - BIOFINDER (New biomarkers for Alzheimer’s & Parkinson’s diseases - key tools for early diagnosis and drug development)

The pathologies of Alzheimer's (AD) and Parkinson's (PD) start 10-20 years before overt clinical symptoms, opening a window for early diagnosis and treatment. To exploit this opportunity we intend to develop methods for early and accurate diagnosis so that treatment can be initiated before irreversible neurodegeneration has occurred. Efforts to advance diagnosis as well as developing new therapies will require research on humans, and we will therefore use our solid and successful clinical research experience to create a new human experimental system for AD and PD. We include well-characterized and clinically relevant populations of
patients and healthy elderly that are followed prospectively for at least 4 years. Participants repeatedly undergo cognitive and psychiatric evaluation, provide blood and cerebrospinal fluid, and have brain imaging using advanced MRI protocols and amyloid PET. Tissue samples for isolating cells that can be reprogrammed into brain cells are also obtained and experimental cell biology data will be individually linked to clinical data. Blood, CSF and cell samples will be analyzed with e.g. quantitative mass spectrometry and high sensitivity immunoassays. New knowledge about the molecular pathologies of AD and PD will be vital for improving the clinical diagnostic work-up and drug discovery. Such advances would ease the human and societal burden of these diseases with an anticipated dramatic increase in prevalence as the elderly population grows.

Recently, we have e.g. shown that cerebrospinal fluid (CSF) Aβ42/40 ratio as well as amyloid positron emission tomography (PET) can be used with high accuracy to detect AD during the prodromal stages, i.e. before the patients have become demented. Further, we have shown that CSF AD biomarker can be used reliably in clinical routine practice. Together these results strongly imply that CSF AD biomarkers and amyloid PET imaging should be in the diagnostic work-up of AD in the clinic as well as when selecting patients with prodromal AD for clinical trials evaluating novel disease-modifying therapies. Further, we have found evidence that neuroinflammation might occur very early in AD, even before amyloid pathology is evident, a finding that might have implications for the development of novel therapies for AD. In Parkinson's disease we have found that we can distinguish this disorder from atypical parkinsonian disorders using a novel blood-based assay to quantify plasma levels of neurofilament light, which might be used in the clinic in the future. We have also found that CSF biomarkers reflecting α-synuclein pathology predict future worsening in motor function and cognitive speed, and CSF Aβ42 predict future memory impairment in patients with PD. These markers could consequently be used to predict different future outcomes in PD patients. Finally, we are studying tau pathology using PET and we have found that Tau PET imaging can be used to reliably detect this pathology in Alzheimer's disease but not in other tauopathies like progressive supranuclear palsy.

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