Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used for the palliative treatment of different degenerative diseases like diabetes, cirrhosis, and Parkinson’s, etc. The objective of this study was to assess the effectiveness of exogenous antioxidants, in particular, β carotene (1.02 and 2.05 mg/kg) against intracerebroventricular injected streptozotocin-induced memory impairment in mice. Streptozotocin (3 mg/kg, i.c.v) was administered in two separate doses (on 1st and 3rd days of treatment) for neurodegeneration. Fifty Albino mice (male) were selected in the protocol, and they were classified into five groups (Group I—control, Group II—disease, Group III—standard, Group IV–V—β-carotene-treated) to investigate the cognitive enhancement effect of selected antioxidants. The cognitive performance was observed following the elevated plus-maze, passive avoidance, and open field paradigms. Acetylcholine esterase, β-amyloid protein, and biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, and catalase were analyzed in brain homogenates. In silico activity against acetylcholinesterase (AChE) was determined by the molecular modeling of β-carotene. β-carotene at a dose of 2.05 mg/kg was found to attenuate the deleterious effects of streptozotocin-induced behavioral and biochemical impairments, including the inhibition of acetylcholinesterase activity. The in silico studies confirmed the binding capacity of β-carotene with the acetylcholinesterase enzyme. The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects, inhibition of acetylcholinesterase, and the reduction of amyloid β-protein fragments. These results suggest that β-carotene could be useful for the treatment of neurodegenerative diseases such as Alzheimer’s disease.

The purpose of this study was to characterize the variability and statistical distribution of electromagnetic induction measurements for salinity assessment on irrigated land. Such information is needed to optimize future sampling schemes. A detailed salinity survey was carried out with an electromagnetic device (Geonics EM38) in a representative experimental area of 37 ha near Faisalabad, Pakistan. The apparent electrical conductivity of the soil was measured at >3400 locations. In addition, a visual agronomic salinity survey was conducted. A linear relation between the standard deviation of the data and their means indicated that the salinity data were log‐normally distributed. Therefore, we recommend using log‐transformed data for statistical inferences. Geostatistical analysis of the log‐transformed data verified that the salinity of a field was principally determined by the irrigation management of the farmer. Significant salinity differences were found between abandoned, fallow, and cropped fields, but not between fields with different crops. We found that the electromagnetic induction meter (EM38) was in good agreement with the visual agronomic survey. The EM38 was superior because it had a better resolution, was more sensitive to salinity changes with depth and spatially, and could be conducted with or without a crop or at any stage of a crop. For random sampling schemes in our experimental area, the budgetary efficiency of the survey improved when entire fields rather than single points were selected for the survey. For salinity sampling with a stratified random sampling scheme, the strata can be based either on land use or on visually observed salinity status.

Alzheimer's disease (AD) is the neurodegenerative disorder characterized by impairment of higher intellectual dysfunctions associated with changes in the cognitive, behavioral, and social activities. Aim of the study: The current study was designed to evaluate the potential of aldosterone antagonist in the treatment of AD. Methodology: The study was conducted on albino mice of either sex (n = 60). Mice were subcategorized into six groups, each group having 10 mice. Group Inormal control (CMC 1 mL/kg), group IIdiseased [streptozotocin (STZ), 3 mg/kg, intracerebroventricular (i.c.v.)], group IIIstandard (piracetam, 200 mg/kg, i.p.), and groups IV−VI designated as the treatment group (eplerinone at dose levels of 4, 8, and 16 mg/kg, orally), respectively. The study was carried out for 14 consecutive days. STZ was administered through the i.c.v. route on first and third days of the study for memory impairment. The molecular docking was performed to investigate the chemical behavior of compounds to inhibit the AChE. Anti-Alzheimer's effect was assessed by using the behavioral paradigms such as passive avoidance, elevated plus maze, Morris water maze, open field, and balance beam. Various endogenous antioxidants such as SOD, GSH, nitrite, MDA, CAT, and AChE were identified in brain tissues of treated mice to assess the oxidative stress index. Biochemical markers for AD such as norepinephrine, dopamine, and serotonin, Aβ 1−40, Aβ 1−42, NF-κB, and tumor necrosis factor alpha were analyzed in brain tissues of mice. Expression of beta amyloid was observed by PCR. Results: The in silico study indicated the distinct mechanism of eplerinone to inhibit the AChE. The outcomes of the in vivo study manifested that eplerinone at the highest dose was found to be more effective in the treatment of AD. Conclusion: It may be concluded from the research work that eplerinone can be effective for cognitive improvement which proposes its therapeutic effect in many neurodegenerative disorders such as AD.

Theophylline‐7‐acetic acid (acefylline) (3) and its derivatives are pharmacologically active compounds and generally recognized as bronchodilators for the treatment of respiratory diseases like acute asthma for over 70 years. In this article, synthesis of 2‐((5‐((1,3‐dimethyl‐2,6‐dioxo‐2,3‐dihydro‐1H‐purin‐7(6H)‐yl)methyl)‐1,3,4‐oxadiazol‐2‐yl)thio)‐N‐arylacetamides (10a‐j) has been reported. All the synthesized derivatives (10a‐j) were structurally verified by FT‐IR, 1H NMR, 13C NMR and evaluated for their anti‐cancer (using MTT assay), hemolytic and thrombolytic potential. N‐(4‐Chlorophenyl)‐2‐(5‐((1,3‐dimethyl‐2,6‐dioxo‐2,3‐dihydro‐1H‐purin‐7(6H)‐yl)methyl)‐1,3,4‐oxadiazol‐2‐ylthio)acetamide (10g) was found to be the most active against human liver cancer cell lines (Huh7) having cell viability 53.58 ± 1.28 using 100 μg/mL concentration of compound which was further in‐silico modelled to describe the possible mechanistic insights for its anti‐proliferative activity. The results of hemolytic and thrombolytic activities indicated that these derivatives were less toxic and hold considerable potential as a drug candidate. 2‐(5‐((1,3‐Dimethyl‐2,6‐dioxo‐2,3‐dihydro‐1H‐purin‐7(6H)‐yl)methyl)‐1,3,4‐oxadiazol‐2‐ylthio)‐N‐(2‐fluorophenyl)acetamide (10c) of the series was found to be least toxic with 0.1% hemolysis relative to ABTS (95.5%) as positive control. 2‐(5‐((1,3‐Dimethyl‐2,6‐dioxo‐2,3‐dihydro‐1H‐purin‐7(6H)‐yl)methyl)‐1,3,4‐oxadiazol‐2‐ylthio)‐N‐(tetrahydro‐2H‐pyran‐4‐yl)acetamide (10j) exhibited potent clot lysis activity (90%) as compared to negative control DMSO (0.57%).

Tribulus terrestris (T.T.) is a rich source of flavonoids and saponins, which have been reported to have neuroprotective and antioxidant potential. The current study was planned to investigate the anti-Parkinson’s activity of T. terrestris methanol extract (TTME). It was hypothesized that TTME possessed antioxidant potential and can ameliorate Parkinson’s disease (PD) via modulation of α-synuclein, acetylcholinesterase (AChE), TNF-α, and IL-1β. To test this hypothesis, in silico and in vivo studies were performed. The PD model in rats was prepared by giving haloperidol, 1 mg/kg, i.p. Rats were divided into six groups: control, disease control, standard, and treatment groups receiving TTME orally at 100, 300, and 1000 mg/kg dose levels for 21 days. Behavioral observations and biochemical analyses were done. The TTME modulatory effect on mRNA expression of α-synuclein, AChE, TNF-α, and interleukins in the brain homogenate was estimated by RT-PCR. Compounds detected in HPLC analysis disrupted the catalytic triad of AChE in in silico studies. Behavioral observations showed significant ( p < 0.05) improvement in a reversal of catatonia, muscular strength, locomotor functions, stride length, and exploration in a dose-dependent manner (1000 >300 >100 mg/kg) of PD rats. Endogenous antioxidant enzyme levels CAT, SOD, GSH, and GPx were significantly restored at a high dose ( p < 0.05) with a notable ( p < 0.05) decrease in the MDA level in TTME-treated groups. TTME at a high dose significantly ( p < 0.05) decreased the level of acetylcholinesterase. RT-PCR results are showing down-regulation in the mRNA expression levels of IL-1β, α -synuclein, TNF-α, and AChE in TTME-treated groups compared to the disease control group, indicating neuroprotection. It is concluded that TTME has potential to ameliorate the symptoms of Parkinson’s disease.