Betanin combined with virgin coconut oil inhibits neuroinflammation in aluminum chloride-induced toxicity in rats by regulating NLRP3 inflammasome.

Background And Aim: Activating NLRP3 (NOD-, LRR-, and pyrin domain-containing protein 3) is crucial in the pathogenesis of Alzheimer's disease (AD). A multimodal treatment intervention is the most feasible way to alter the course of AD progression. Hence, the current study was conducted to study the combination of betanin (BET) and virgin coconut oil (VCO) on NLRP3 regulation in aluminum chloride-induced AD in Wistar rats.

A current review on P2X7 receptor antagonist patents in the treatment of neuroinflammatory disorders: a patent review on antagonists.

Chronic inflammation is defined by an activated microglial state linked to all neurological disorders, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (a motor neuron disease that affects the brain and spinal cord). P2X7 receptors (P2X7R) are ATP-activated ion-gated channels present on microglial surfaces. Prolonged ATP release under pathological settings results in sustained P2X7R activation, which leads to inflammasome development and cytokine release.

Betanin mitigates scopolamine-induced cognitive impairment by restoring cholinergic function, boosting brain antioxidative status, and increasing BDNF level in the zebrafish model.

Betalains obtained from Beta vulgaris (family Caryophyllales) are regularly consumed as part of the regular diet with medicinal benefits due to antioxidant and anti-inflammatory properties. The objective of this article was to evaluate betanin's neuroprotective properties in a scopolamine-induced zebrafish paradigm. Betanin (BET) (50, 100, and 200 mg/L), and donepezil (10 mg/L) were delivered to zebrafish in a treatment tank once a day for 8 days, while memory impairment was produced by scopolamine (100 µM), which was given 60 min before behavioral assessments.

Zebrafish as a Promising Tool for Modeling Neurotoxin-Induced Alzheimer's Disease.

Drug discovery and development for Alzheimer's disease (AD) are complex and challenging due to the higher failure rate in the drug development process. The overproduction and deposition of Aβ senile plaque and intracellular neurofibrillary tangle (NFT) formation are well-recognized diagnostic hallmarks of AD. Numerous transgenic models of Alzheimer's disease have restrictions on cost-effectiveness and time in the preclinical setup.

Inhibitors of NF-κB and P2X7/NLRP3/Caspase 1 pathway in microglia: Novel therapeutic opportunities in neuroinflammation induced early-stage Alzheimer's disease.

Microglial activation is a distinguished attribute in many neurodegenerative diseases of aging. Compelling evidence suggests that neuroinflammation stimulated by microglia, the resident macrophage-like immune cells in the brain, play a contributing role in the pathogenesis of Alzheimer's disease (AD). Postmortem brain tissue of individuals with AD has credibly demonstrated that neuroinflammation is likely to be a key driver of the disease.