Alzheimer's disease (AD) is a neurodegenerative disease that affects the neurons in the hippocampus, resulting in cognitive and memory impairment. The most prominent clinical characteristics of AD are the production of amyloid-beta (Aβ) plaques, neurofibrillary tangles, and neuroinflammation in neurons. It has been proven that embelin (Emb) possesses antioxidant, anti-inflammatory, and neuroprotective properties. Therefore, we assessed the therapeutic potential of Emb in Benzo [α]pyrene (BaP)-induced cognitive impairment in experimental mice. BaP (5 mg/kg, i. p) was given to mice daily for 28 days, and Emb (2.5, 5, and 10 mg/kg, i. p) was given from 14 to 28 days of a protocol. In addition, locomotor activity was evaluated using open-field and spatial working, and non-spatial memory was evaluated using novel object recognition tasks (NORT), Morris water maze (MWM), and Y- maze. At the end of the study, the animal tissue homogenate was used to check biochemicals, neuroinflammation, and neurotransmitter changes. BaP-treated mice showed a significant decline in locomotor activity, learning and memory deficits and augmented oxidative stress (lipid peroxidation, nitrite, and GSH). Further, BaP promoted the release of inflammatory tissue markers, decreased acetylcholine, dopamine, GABA, serotonin, and norepinephrine, and increased glutamate concentration. However, treatment with Emb at dose-dependently prevented biochemical changes, improved antioxidant levels, reduced neuroinflammation, restored neurotransmitter concentration, and inhibited the NF-κB pathway. The current study's finding suggested that Emb improved cognitive functions through antioxidant, anti-inflammatory, and neuroprotective mechanisms and inhibition of acetylcholinesterase (AChE) enzyme activities and Aβ-42 accumulation.
Sudden phase changes are related to cortical phase transitions, which likely change in frequency and spatial distribution as epileptogenic activity evolves. A 100 s long section of micro-ECoG data obtained before and during a seizure was selected and analyzed. In addition, nine other short-duration epileptic events were also examined. The data was collected at 420 Hz, imported into MATLAB, downsampled to 200 Hz, and filtered in the 1–50 Hz band. The Hilbert transform was applied to compute the analytic phase, which was then unwrapped, and detrended to look for sudden phase changes. The phase slip rate (counts/s) and its acceleration (counts/s2) were computed with a stepping window of 1-s duration and with a step size of 5 ms. The analysis was performed for theta (3–7 Hz), alpha (7–12 Hz), and beta (12–30 Hz) bands. The phase slip rate on all electrodes in the theta band decreased while it increased for the alpha and beta bands during the seizure period. Similar patterns were observed for isolated epileptogenic events. Spatiotemporal contour plots of the phase slip rates were also constructed using a montage layout of 8 × 8 electrode positions. These plots exhibited dynamic and oscillatory formation of phase cone-like structures which were higher in the theta band and lower in the alpha and beta bands during the seizure period and epileptogenic events. These results indicate that the formation of phase cones might be an excellent biomarker to study the evolution of a seizure and also the cortical dynamics of isolated epileptogenic events.

