Alzheimer's disease (AD) is characterized by amyloid-beta (Aβ) plaques and tau tangles. However, recent research suggests that smaller, soluble Aβ oligomers (AβO) and tau oligomers (TauO) are more neurotoxic. These oligomers disrupt synaptic function and accelerate early AD progression by interfering with neuronal signaling. Calcineurin (CaN), a protein crucial for synaptic plasticity and memory, is implicated in AD due to its dysregulation in AβO-induced toxicity. However, its involvement in TauO-driven dysfunction is less understood.

Read this review where researchers used IVISense™ fluorescent labeling reagent and IVIS™ Spectrum imaging system to investigate whether inhibiting CaN with FK506 (Tacrolimus), an FDA-approved immunosuppressant, could impact TauO-induced pathology in AD using 2 mouse models:

• an acute model (recombinant TauO injected into healthy mouse brains) and
• a chronic model (3xTgAD mice with APP, tau, and presenilin-1 mutations).