Alzheimer's disease (AD) is a complex neurodegenerative disease. There is epidemiological evidence that heart failure (HF) patients are at higher risk of developing AD, and the impact of sacubitril/valsartan, the first angiotensin receptor-neprilysin inhibitor (ARNI) approved for HF, on cognitive functions is still controversial. To investigate the effect of sacubitril/valsartan on cognitive functions in colchicine-induced AD rat model. Forty adult male Wistar rats were equally allocated into four groups (each of 10 rats): Group I: normal control, Group II: intracerebroventricular injection of colchicine (15 μg/5 μl/bilaterally), Group III: colchicine (15 μg/5 μl/bilaterally, icv) + oral sacubitril/valsartan (100 mg/kg/day) for 25 days, and Group IV: colchicine (15 μg/5 μl/bilaterally, icv) + oral valsartan (50 mg/kg/day) for 25 days. Behavioral assessment was done using Morris water maze and passive avoidance tasks. Biochemically, β-amyloid (1-40 and 1-42) peptides, oxidative stress (malondialdehyde and superoxide dismutase) and inflammatory (tumor necrosis factor-alpha) parameters were measured in hippocampus and prefrontal cortex. Sacubitril/valsartan exaggerated colchicine-induced cognitive impairment in both Morris water maze and passive avoidance tasks and was associated with significant increase in β-amyloid accumulation, oxidative stress, and inflammation versus valsartan. Sacubitril/ valsartan caused deleterious effect on cognitive impairment and biochemical alterations in colchicine-induced AD rat model. Hence, special caution should be taken following long-term intake of ARNI on cognitive functions.
Purpose: Molar Incisor Hypomineralization (MIH) is a congenital defect of unknown etiology that has been recently identified and is currently considered an increasing concern to dental clinicians. The defect involves enamel mineralization of one to four permanent first molars usually associated with similarly affected permanent incisors. The purpose of this retrospective study was to investigate the prevalence, severity, and location of MIH in the permanent molars and incisors of patients with unilateral and bilateral cleft lip and palate (CLP) as compared with controls.
Methods:The sample consisted of intra-oral photographs of 71 CLP patients which were divided into two groups (unilateral versus bilateral cleft) and a modified Weerheijm ranking of enamel defects was compared to a control sample of 60 children without CLP who were age matched. Pearson chi-square tests were used to compare the groups for differences in the presence of hypomineralization, and Mantel-Haenszel chi-square tests were used to compare the groups for differences in MIH scores. Cochran-Mantel-Haenszel chi-square tests for stratified categorical data were used to compare the cleft and non-cleft sides for differences in the prevalence of hypomineralization and MIH scores within the CLP unilateral subjects. Significance was defined as p<0.05.Results: MIH scores were significantly lower for controls than for CLP bilateral and CLP unilateral groups (p<.0001). CLP bilateral had significantly higher MIH scores than CLP unilateral (p ≤ 0.01). The MIH scores were not significantly different between the cleft and non-cleft sides in the CLP unilateral subjects. However, two of the individual teeth -the maxillary-lateral (p=0.03) and maxillary central incisors (p ≤ 0.01) -did show significantly higher scores for the cleft side as compared with the non-cleft side.Conclusions: Cleft patients are at higher risk of MIH than controls and children with bilateral clefts present with the most severe hypomineralization.
Yucca aloifolia L. fruit (Yucca or Spanish bayonet, family Asparagaceae) is recognized for its purplish red color reflecting its anthocyanin content, which has a powerful antioxidant activity. This study aimed to investigate yucca (YA) fruit extract’s protective effect on Parkinson’s disease (PD). In vitro study, the anti-inflammatory activity of yucca fruit extracts was explored by measuring tumor necrosis factor receptor 2 (TNF-R2) and nuclear factor kappa B (NF-KB) to choose the most effective extract. Afterward, a detailed in vivo investigation of the protective effect of the most active extract on rotenone-induced PD was performed on male albino Wister rats. First, the safety of the extract in two different doses (50 and 100 mg/kg in 0.9% saline orally) was confirmed by a toxicological study. The rats were divided into four groups: 1) normal control (NC); 2) rotenone group; and third and fourth groups received 50 and 100 mg/kg yucca extract, respectively. The neurobehavioral and locomotor activities of the rats were tested by rotarod, open field, and forced swim tests. Striatal dopamine, renal and liver functions, and oxidative stress markers were assessed. Western blot analysis of brain tissue samples was performed for p-AMPK, Wnt3a, and β-catenin. Histopathological examination of striatal tissue samples was performed by light and electron microscopy (EM). The metabolites of the active extract were characterized using high-resolution LC-MS/MS, and the results showed the prevalence of anthocyanins, saponins, phenolics, and choline. Biochemical and histopathological tests revealed a dose-dependent improvement with oral Yucca extract. The current study suggests a possible neuroprotective effect of the acidified 50% ethanol extract (YA-C) of the edible Yucca fruit, making it a promising therapeutic target for PD.
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