According to the modified amyloid hypothesis, in AD, extracellular amyloid-β (Aβ) plaques and intracellular neurofibrillary tau tangles are the pathognomonic hallmarks for the diagnosis and progression of AD.15 Lower levels of total tau-protein and elevated Aβ1-42-levels in CSF were recognised as important biomarkers and were identified as therapeutically relevant molecular targets.9 Pathological lesions are strongly associated with progressive loss of neurologic capacities, and it is hypothesised that prevention of these accumulations may improve symptoms of this disease.25 The gene discussed is MAPT; the disease is Alzheimer disease.