Topic: Pick bodies

Therapeutic interventions’ lackluster performance in Alzheimer dementia (AD) may in part be due to the irreversibly advanced stage of the pathological process underlying cognitive decline once the latter is diagnosed. Currently, clinical diagnosis of AD is supported by in vivo molecular imaging of disease-related Aβ and Tau aggregates in the brain, and analysis of cerebrospinal fluid. Positron Emission Tomography, Single Photon Emission Computed Tomography, and Magnetic Resonance imaging are the most common methods used. They are costly, which limits their use in routine screening. We used flu

Tau accumulation is clearly linked to pathogenesis in Alzheimer’s disease and other Tauopathies. However, processes leading to Tau fibrillization and reasons for its pathogenicity remain largely elusive. Mical emerged as a novel interacting protein of human Tau expressed in Drosophila brains. Mical is characterized by the presence of a flavoprotein monooxygenase domain that generates redox potential with which it can oxidize target proteins. In the well-established Drosophila Tauopathy model, we use genetic interactions to show that Mical alters Tau interactions with microtubules and the Actin