Basic Science and Pathogenesis.

Background: Stroke and AD patients with gut complications often present worsened neurological outcomes. The goal of this study was to examine the role of extracellular vesicle (EV)-mediated pyroptosis in the bi-directional gut-brain axis after photothrombotic stroke (PTS) in aged 3xTg mice and wildtype (WT) controls.

Method: Twelve-month 3xTg and WT male and female mice underwent PTS using a YAG laser.

Basic Science and Pathogenesis.

Background: Neurogranin (Ng) is considered a biomarker for synaptic dysfunction in Alzheimer's disease (AD). In contrast, the inflammasome complex has been shown to exacerbate AD pathology.

Method: We investigated the protein expression, morphological differences of Ng and correlated Ng to hyperphosphorylated tau in the postmortem brains of 17 AD cases and 17 age and sex-matched controls.

Basic Science and Pathogenesis.

Background: The global ageing population is rising with each year, and with that, the percentage of individuals with Alzheimer's disease (AD) is expected to rise in parallel. Along with age, traumatic brain injury (TBI) is another risk factor for AD. TBI and AD patients demonstrate abnormal inflammatory responses, including that of the inflammasome.

Cracking down on vapochromic salts: unveiling vapomechanical stress in gas-sorbing platinum complexes.

This study explores the vapochromic and vapoluminescent behaviors of [Pt(tpy)Cl]PF host molecules (tpy = 2,2':6',2''-terpyridine) under acetonitrile (CHCN) vapor guest, challenging the conventional view that these phenomena arise solely from direct host-guest interactions. Our findings reveal a cooperative mechanism where mechanochromic surface perturbations prime the Pt(II) host for guest incorporation, leading to initial color and luminescence changes prior to significant structural alterations. While the color transition between the yellow [Pt(tpy)Cl]PF form and the red/orange [Pt(tpy)Cl]PF·CHCN form is reversible, repeated vapor cycling induces a loss of crystallinity, as indicated by diffraction peak broadening and emission shifts.

Catecholamine-Induced Inflammasome Activation in the Heart Following Photothrombotic Stroke.

Cerebrovascular stroke patients exhibit an increased incidence of cardiac arrhythmias. The pathomechanisms underlying post-traumatic cardiac dysfunction include a surge of catecholamines and an increased systemic inflammatory response, but whether inflammasome activation contributes to cardiac dysfunction remains unexplored. Here, we used a mouse model of photothrombotic stroke (PTS) to investigate the role of inflammasome activation in post-stroke cardiac dysfunction by catecholamines and to evaluate the effectiveness of the inflammasome inhibitor IC100 on inflammasome activation.