Topic: APP

Flotillins are highly conserved integral membrane proteins which play a role in several key biological processes including vesicular trafficking, endocytosis, and cytoskeletal organization. Some studies have reported that flotillin-positive extracellular vesicles can be used as biomarker for AD diagnosis in blood samples. Due to its constitutive expression, flotillins can be expressed by many cell types. Our aim was to characterize the expression and localization of Flot1 in neurons and deduce the potential role of Flotillin-1 (Flot1) in AD. We use super-resolution microscopy methods such as A

Immunotherapy of Alzheimer’s disease (AD) is a promising approach to reduce the accumulation of amyloid-beta (Aβ) peptides, a critical event in the onset of the disease. Emerging evidence indicate that metabotropic glutamate receptors (mGluRs) are involved in the progression of AD, representing potential targets for new treatments. Studies have highlighted the potential role of group II mGluRs, mGluR2 and mGluR3, in the modulation of Aβ production, although their respective contribution remains unclear, due to the lack of specific tools to study them. Here, we showed in vitro that enhancing mG

NMDA receptors (NMDARs) are ionotropic receptors crucial for brain information processing. Yet, evidence also supports an ion flux-independent signaling mode mediating synaptic long-term depression (LTD) and spine shrinkage. How these different modes of NMDAR activity are controlled remains unknown. Here, we identify AETA (Aη), an amyloid-β precursor protein (APP) cleavage product, as an NMDAR modulator with the unique dual regulatory capacity to impact both signaling modes. AETA inhibits ionotropic NMDAR activity, principally of GluN2A containing heteromers, by competing with the co-agonist a

A growing body of evidence indicates a substantial role of the immune system and inflammation in the pathogenesis of Alzheimer’s disease (AD). In the current study, we investigated the effect of maternal immune activation (MIA) on AD-resembling pathological alterations in 12-month-old offspring. We also aimed to analyze whether inhibition of bromodomain and extraterminal domain (BET) proteins, the readers of the histone acetylation code, might impact these changes. In our study, we injected a viral mimetic polyinosinic-polycytidylic acid (PIC) at gestation day 17 to evoke MIA in wild-type mice