Backgound: Extracellular deposits of amyloid-β (Aβ) in neuronal synapse have been considered as a major hallmark of Alzheimer’s disease. Purpose: Here in we have investigated the neuroprotective potential of embelin Aβ-42 induced neurotoxicity in rats. Material and Methods: Amyloid β1-42 oligomer was infused (3nmol/3µl) intracerebroventrically twice on day-1to induced Alzheimer’s type dementia in rats. Spatial and non- spatial memory was assessed at different time intervals and terminally biochemical, neurochemical and neuroinflammatory parameters were determined in rat hippocampal brain tissue. One week following Aβ1-42 infused rats were treated with different doses of embelin (2.5, 5 and 10mg/kg/p.o.) till 21st day. Results: Amyloid β1-42 infusion produced significant deterioration in learning and memory while hippocampal tissue showed elevation in AChE activity, oxidative stress, and pro-inflammatory cytokine levels (TNF-α, IL-β etc.) and disturbed pattern of GABA/glutamate levels in Aβ1-42 infused rats. On the other side, embelin significantly attenuated Aβ1-42 induced cognitive deficit & other biochemical changes in rats. Embelin treated rats showed improved learning and memory was able to reduce the burden of hippocampal oxidative stress and pro-inflammatory cytokines and also restored the GABA/glutamate balance in rats. Conclusion and Implication: The pro-cognitive effect of embelin may be due to its antioxidant and anti-inflammatory actions. The observed results indicate the therapeutic potential of embelin in cognitive disorders. Key words: Alzheimer’s disease; Embelin; Amyloid-β; Neuroprotection; Dementia; Cognitive deficit.

The novel corona virus, previously dubbed 2019-nCoV and now officially named SARS-CoV-2 and COVID-19 has caused major outbreaks of deadly pneumonia in the 21st century has began in Wuhan, China in late 2019 and now become a destructive to global health and therefore the utmost need of the hour is to develop therapeutic candidates or vaccines against it (Zhu et al., 2020). Numerous corona viruses, first discovered in domestic poultry in the 1930s, 2002 and 2012 cause respiratory, gastrointestinal, liver, and neurologic diseases in animals. Only 7 corona viruses are known to cause disease in humans. There is an urgent need to identify specific targets to design promising therapeutic agents against severe acute respiratory syndrome coronavirus aetiological agent of coronavirus disease 2019 (COVID-19) characterised by pulmonary infection in humans. The need exists for additional treatment options addressing antiviral replication, and against SARS-CoV-2. Virus entry and replication strategies are potential targets for antiviral drug treatments. Since NF-κB pathway is often targeted by viral pathogens to enhance viral replication, host cell survival and host immune evasion. Viruses may activate or suppress NF-kB. (Marta et al., 2014). There have many studies on SARS-COV since 2002-2003 SARS epidemics. SARS-COV2 (COVID-19) belongs to the same family of corona viruses and shares many similarities (3), including SARS-CoV-1. Here we discuss the possible mechanisms of NFκB inhibitor interference with the SARS-CoV-2 replication cycle.