VX-765 attenuates secondary damage and β-amyloid accumulation in ipsilateral thalamus after experimental stroke in rats.

Focal cortical infarction can result both in the accumulation of Aβ in as well as further secondary damage and inflammation within the ipsilateral thalamus. VX-765 is a potent and selective small-molecule capable of inhibiting caspase-1, which has been shown to exhibit active neuroprotection properties in multiple disease. However, the neuroprotection efficacy of VX-765 as a means of attenuating secondary damage after MCAO remains uncertain.

Can ischemic stroke patients with mTICI of 2b achieve similar outcomes compared to those with complete recanalization following endovascular therapy?

Background And Purpose: Endovascular therapy (EVT) has been used as a standard treatment method for patients with large vessel ischemic stroke within 24 h of the onset. The extent of recanalization after EVT can be assessed using the modified thrombolysis in cerebral infarction (mTICI) scale as an accepted angiographic grading system. In this study, we aimed to investigate whether patients with a mTICI grade of 2b achieve similar outcomes compared to those with complete recanalization (mTICI of 3) following EVT for acute ischemic stroke.

Targeted brain delivery of RVG29-modified rifampicin-loaded nanoparticles for Alzheimer's disease treatment and diagnosis.

Alzheimer's disease (AD) is an aging-related neurodegenerative disease. The main pathological features of AD are β-amyloid protein (Aβ) deposition and tau protein hyperphosphorylation. Currently, there are no effective drugs for the etiological treatment of AD.

Dl-butylphthalide inhibits rotenone-induced oxidative stress in microglia via regulation of the Keap1/Nrf2/HO-1 signaling pathway.

Activated microglia are a source of superoxide which often increases oxidative stress in the brain microenvironment, increase production of reactive oxygen species (ROS) and directly or indirectly lead to dopaminergic neuronal death in the substantia nigra. Thus superoxide contributes to the pathogenesis of Parkinson's disease (PD). Evidence suggests that mitochondria are the main source of ROS, which cause oxidative stress in cells.

Rifampicin ameliorates lipopolysaccharide-induced cognitive and motor impairments via inhibition of the TLR4/MyD88/NF-κB signaling pathway in mice.

Objectives: Aberrant microglial responses promote neuroinflammation in neurodegenerative diseases. However, rifampicin's effect on cognitive and motor sequelae of inflammation remains unknown. Therefore, we investigated whether rifampicin exerts neuroprotection against lipopolysaccharide (LPS)-induced cognitive and motor impairments.

Inhibition of Caspase-1 Ameliorates Ischemia-Associated Blood-Brain Barrier Dysfunction and Integrity by Suppressing Pyroptosis Activation.

Ischemic cerebral infarction represents a significant cause of disability and death worldwide. Caspase-1 is activated by the NLRP3/ASC pathway and inflammasomes, thus triggering pyroptosis, a programmed cell death. In particular, this death is mediated by gasdermin D (GSDMD), which induces secretion of interleukin (IL)-1β and IL-18.

Rifampicin Suppresses Amyloid-β Accumulation Through Enhancing Autophagy in the Hippocampus of a Lipopolysaccharide-Induced Mouse Model of Cognitive Decline.

Background: Alzheimer's disease (AD) is characterized by amyloid-β (Aβ) deposition. The metabolism of Aβ is critically affected by autophagy. Although rifampicin is known to mediate neuroinflammation, the underlying mechanism by which rifampicin regulates the cognitive sequelae remains unknown.

Neuroprotective mechanisms of 3-n-butylphthalide in neurodegenerative diseases.

Since 3-n-butylphthalide (NBP) was approved by the China Food and Drug Administration for the treatment of acute ischemia stroke in 2002, a number of studies have investigated NBP worldwide. In recent years, NBP has also demonstrated potential as treatment of several neurodegenerative diseases, which has increased the interest in its mechanisms of protection and action. Clinical studies and studies that used cell or animal models, have directly demonstrated neuroprotective effects of NBP via the following mechanisms: i) Inhibiting the inflammatory reaction; ii) reducing mitochondrial oxidative stress; iii) regulating apoptosis and autophagy; iv) inducing resistance to endoplasmic reticulum stress; and v) decreasing abnormal protein deposition.