Basic Science and Pathogenesis.

Background: Alzheimer's disease (AD) is characterized by the accumulation of amyloid-beta (Aβ) in the extracellular space, which leads to various adverse effects such as oxidative stress, neuroinflammation, mitochondrial dysfunction, tau phosphorylation, synapse loss, and neurodegeneration. Therefore, therapeutic interventions that can reduce Aβ-toxicity and slow down the progression of cognitive dysfunction in AD have significance. One promising approach is to use extracellular vesicles (EVs) that are released by neural stem cells (NSCs) derived from human induced pluripotent stem cells (hiPSCs).

Residual microglia following short-term PLX5622 treatment in 5xFAD mice exhibit diminished NLRP3 inflammasome and mTOR signaling, and enhanced autophagy.

While moderately activated microglia in Alzheimer's disease (AD) are pivotal in clearing amyloid beta (Aβ), hyperactivated microglia perpetuate neuroinflammation. Prior investigations reported that the elimination of ~80% of microglia through inhibition of the colony-stimulating factor 1 receptor (CSF1R) during the advanced stage of neuroinflammation in 5xFamilial AD (5xFAD) mice mitigates synapse loss and neurodegeneration. Furthermore, prolonged CSF1R inhibition diminished the development of parenchymal plaques.

Residual Microglia Following Short-term PLX5622 Treatment in 5xFAD Mice Exhibit Diminished NLRP3 Inflammasome and mTOR Signaling, and Enhanced Autophagy.

Chronic neuroinflammation represents a prominent hallmark of Alzheimer's disease (AD). While moderately activated microglia are pivotal in clearing amyloid beta (Aβ), hyperactivated microglia perpetuate neuroinflammation. Prior investigations have indicated that the elimination of ∼80% of microglia through a month-long inhibition of the colony-stimulating factor 1 receptor (CSF1R) during the advanced stage of neuroinflammation in 5xFamilial AD (5xFAD) mice mitigates synapse loss and neurodegeneration without impacting Aβ levels.

Extracellular Vesicles from hiPSC-derived NSCs Protect Human Neurons against Aβ-42 Oligomers Induced Neurodegeneration, Mitochondrial Dysfunction and Tau Phosphorylation.

Background: One of the hallmarks of Alzheimer's disease (AD) is the buildup of amyloid beta-42 (Aβ-42) in the brain, which leads to various adverse effects. Therefore, therapeutic interventions proficient in reducing Aβ-42-induced toxicity in AD are of great interest. One promising approach is to use extracellular vesicles from human induced pluripotent stem cell-derived neural stem cells (hiPSC-NSC-EVs) because they carry multiple therapeutic miRNAs and proteins capable of protecting neurons against Aβ-42-induced pathological changes.

Can zinc aluminate-titania composite be an alternative for alumina as microelectronic substrate?

Alumina, thanks to its superior thermal and dielectric properties, has been the leading substrate over several decades, for power and microelectronics circuits. However, alumina lacks thermal stability since its temperature coefficient of resonant frequency (τ) is far from zero (-60 ppmK). The present paper explores the potentiality of a ceramic composite 0.