The most prominent morphological hallmarks of an AD brain are neurofibrillary tangles and neuritic or diffuse plaques. Tangles accumulate inside neurons and consist of hyperphosphorylated tau protein whereas extracellularly located plaques are mainly composed of amyloid-beta (Abeta). Abeta is considered to trigger hyperphosphorylation of tau and dementia in Alzheimer’s disease. With advancing pathology neurons are destroyed by the aggregating proteins. Since dead neurons are hardly regenerated, it is very important to diagnose AD as early as possible. Therefore, we started a project to identify blood biomarkers and to establish diagnostic assays that would allow assessing one’s individual risk to develop AD.
Even if an early diagnosis is possible, it is still necessary to find a treatment strategy that stops disease progression or even prevents its onset. We already showed that the action of specific proteins (ABC transporters) at the blood-brain barrier has a tremendous influence on the accumulation of Abeta in the brain. We also identified plant extracts and a synthetic drug that increase the activity of these transporters. We currently apply for funding for clinical testing of these new options for the patients.
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