Potassium bromate (KBrO₃) is an oxidizing agent added to flour to improve bread quality. However, KBrO₃ is nephrotoxic, and a class B carcinogen banned in most countries, including Ghana. This study aimed to determine the residual KBrO₃ concentration in bread and to estimate the chemical and carcinogenic risk that is associated with the consumption of these breads in Ghana. A total of 285 samples of bread, consisting of 97 tea breads, 95 sugar breads, and 93 butter breads were randomly sampled from bakeries across ten regions of Ghana for this study. The bromate contents were qualitatively and quantitatively determined spectrophotometrically at 515 nm, based on the redox reaction between KBrO₃ and promethazine. The change in colour from colourless to pink indicated the presence of KBrO₃ in the sample. The data were analyzed with Microsoft Excel 365 Apps for Enterprise and GraphPad Prism and the map was plotted with QGIS. Out of the 285 bread samples analyzed, 12.28% (35/285) tested positive for KBrO₃ with concentrations ranging from 0.46 to 26.67 μg/g (mean 6.13 μg/g). This exceeded the permissible dose (0.02 μg/g) by 23–1334 times, respectively. Except Ashanti and Volta regions, all the other 8 regions had at least one bread type testing positive for KBrO₃. There was no statistically significant difference in the concentration of KBrO₃ between the bread types analyzed at p < 0.05. The hazard ratio ranged from 0.166 to 0.435 and the chronic hazard quotient ranged from 0.0037 to 0.00141. Breads from 8 regions of Ghana tested positive for KBrO_3, but their concentrations may not pose chemical or carcinogenic risks after regular consumption.

Background. In Ghana, Cymbopogon citratus leaves together with guava, pawpaw, and lime are processed into a decoction to treat fever. To encourage its usage, preclinical validation of the safety profile of the plant is required. The acute and subchronic toxicities of the conventional Soxhlet ethanolic Cymbopogon citratus leaves extract in Sprague–Dawley rats were investigated. Methods. Pulverized Cymbopogon citratus leaves were extracted with 98% ethanol using the conventional Soxhlet extraction (CSE) method and dried. In the acute toxicity study, a single dose of 5000 mg/kg body weight was administered to six female Sprague–Dawley rats and 1 ml/100 g body weight normal saline to control (6) once, and signs of toxicity were observed every hour for the first 12 hr, 24 hr, and 48 hr through to 14 days. In the subchronic study, the treatment groups were administered 200 mg/kg, 600 mg/kg, and 1200 mg/kg, respectively, of the CSE C. citratus leaves extract for six weeks. Analyses were conducted on the blood, urine, and serum samples of the rats. Histopathological examination of the liver, heart, kidney, spleen, and lungs was carried out at termination. Analysis of variance (ANOVA) was performed to determine statistically significant differences between the test and control rats at . Results. The results revealed that there were no statistically significant differences ( ) in the urinalysis and haematological analysis between control and test rats over the treatment period. Similarly, CSE C. citratus leaves extract did not induce any significant biochemical changes in the treatment group; however, there was a weight loss effect on the treated rats. There were no noticeable morphological changes in the heart, liver, spleen, lung, and kidney of the test rats compared to the control. Conclusion. CSE ethanolic C. citratus leaves extract has a weight loss effect, and long-term administration of the extract may not cause any organ-specific toxicity to the consumers.

Background: The global burden of dementia is escalating due to the aging population. While amyloid and tau biomarkers are central to Alzheimer's disease (AD) pathology, their causal roles across dementia subtypes are not fully understood. Objective: This study investigated the causal effects of cerebrospinal fluid (CSF) and plasma amyloid, tau, and hyperphosphorylated tau (p-tau) proteins on dementia [AD, frontotemporal dementia (FTD), and vascular dementia (VaD)] risk. Methods: In this study, we conducted a two-sample Mendelian randomization analysis using genome-wide association study (GWAS) summary statistics. The AD, CSF, and plasma amyloid, tau, and p-tau data were obtained from the GWAS catalog, while those for FTD and VaD were obtained from the FINNGEN database. The inverse variance weighting method, combined with sensitivity analysis, was used to obtain the estimates. Results: CSF p-tau in individuals with abnormal amyloid and APOE ε4 non-carriers was positively associated with AD risk [IVW: OR = 1.07, 95% CI = 1.01–1.13, p = 0.016; OR = 1.08, 95% CI = 1.02–1.14, p = 0.014, respectively]. CSF p-tau was also associated with VaD (IVW: OR = 1.11, 95% CI = 1.03–1.20, p = 0.008). Plasma Aβ ₁₋₄₂ reduced the odds of FTD (IVW: OR = 0.83, 95% CI = 0.70–0.98, p = 0.03), whereas CSF Aβ ₄₂ increased FTD risk (weighted median: OR = 1.58, 95% CI = 1.02–2.44, p = 0.041). Conclusions: The findings support the causal roles of tau and amyloid across dementia subtypes, reinforcing the value of biomarker-driven prevention and therapeutic strategies.

The study investigated the toxicological profile of lemongrass leaf extract obtained by ultrasound- assisted ethanolic (UAE) technique in Sprague Dawley (SD) rats. Extracts of dried lemongrass leaves were obtained by the UAE technique. A single oral dose of 5000mg/kg body weight of the extract was administered by gavage to ten (10) female SD rats, and 1 mL/100g bw.t of normal saline was used as a vehicle for the control rats for acute toxicity studies. An hourly observation was made on the rats for the first 12 hours, and a 24-hour observation was made after 24, 48 hours, up to 14 days for any indications of acute toxicity. Another set of rats was also administered, respectively, with 200, 600, and 1200mg/kg bw.t doses of the extract for six weeks to determine its maximum permissible dosage and long-term toxicological effect. The SD rats› body weights were recorded. Urine and blood samples were collected for urinalysis, clinical chemistry, and haematological analysis, respectively. The heart, kidney, liver, spleen, and lungs were harvested after sacrificing the rats for histopathological examination after the termination of the experiment. At the end of the study, no mortality or morbidity was recorded for both the acute and subchronic studies nor were any signs of clinical abnormality presented by the rats. Moreover, the biochemical, haematological, and urine analysis data were in the same trend as the vehicle-treated rats, and histopathological alterations in the selected organs were not observed. The study revealed that the lemongrass leaves extract obtained by the UAE technique is safe with LD50 > 5000mg/kg bw.t.

Background: While All-cause dementia (ACD) may often be characterized by the abnormal deposition of extracellular β-amyloid (Aβ) in the brain cortex and hyperphosphorylated tau (p-tau) as neurofibrillary tangles intracellularly, there is a need to identify early metabolic changes that may accompany these pathological changes. Objective: This study evaluated the predictive value of fatty acids in cerebrospinal fluid (CSF) fractions in differentiating cognitively unimpaired (CU), mild cognitive impairment (MCI), and ACD participants. Methods: CSF fatty acid profiles were analyzed from CU (n=68), MCI (n=38), and ACD (n=37) individuals aged 77.3 ± 7.7 years, sourced from the Huntington Medical Research Institutes (HMRI). Multivariable binary logistic regression identified the most effective CSF fatty acid biomarkers for distinguishing CU, MCI, and ACD groups. The top-performing CSF fatty acid biomarkers were combined with Aβ ₄₂ , tau, and the Aβ ₄₂ /tau ratio to evaluate their collective diagnostic performance. The model was adjusted for covariates, including age, sex, smoking status, hypertension, diabetes, and APOE genotype. Receiver operating characteristic (ROC) curves were generated for the top 10 CSF fatty acids ranked by area under the curve (AUC), sensitivity, and specificity, and their significance was assessed using the DeLong test. Results: The top 10 fatty acids in CSF fractions demonstrated superior discrimination between CU individuals and those with MCI compared to traditional markers such as Aβ ₄₂ , tau, and the Aβ ₄₂ /tau ratio. Furthermore, incorporating a panel of these fatty acid biomarkers alongside Aβ ₄₂ /tau significantly improved diagnostic accuracy. Age, sex, smoking, hypertension, APOE genotype, and diabetes did not significantly influence the model’s performance. Conclusion: This study suggests that changes in fatty acid metabolism occur in early ACD pathology. Thus, strategies that regulate fatty acid metabolism may prevent cognitive decline in an older population. Highlights: This study revealed that CSF fractions’ fatty acids have a better discriminatory power for CU from MCI than CSF Aβ ₄₂ , tau, and Aβ ₄₂ /tau ratio. A panel of CSF fraction fatty acids combined with Aβ ₄₂ /tau remarkably improved its diagnostic performance for differential diagnosis of CU, MCI, and ACD. Clinical evaluation of these fatty acids will strengthen the detection of early cognitive impairment. A prospective large cohort multicenter study of the diagnostic utility of CSF fractions’ fatty acids will provide robust evidence before extensive clinical usage of these fatty acids.

Background: Although fatty acids are integral structural components of neuronal membranes, knowledge of their metabolism and contribution to cognition is sparse and limited. This study aimed to evaluate the diagnostic performance of fatty acids in cerebrospinal fluid (CSF) fractions in the differential diagnosis of mild cognitive impairment (MCI) from cognitively unimpaired (CU) older adults. Method: Saturated fatty acids (SAFA), monounsaturated fatty acids (MUFA), and polyunsaturated fatty acids (PUFA) from three CSF fractions (unesterified, supernatant fluid and nanoparticles) were obtained from the Huntington Medical Research Institutes (HMRI) Aging Study. The data consisted of 68 CU and 38 MCI. The socio‐demographic data were summarized where continuous variables were reported as mean ± SD and categorical variables as counts and percentages. Multivariable binary logistic regression analysis was performed to differentiat CU from MCI. The best fitting CSF fatty acids biomarker was integrated with CSF Aβ ₄₂ , tau, and Aβ ₄₂ /tau ratio to assess their impact on the diagnostic performance. The model was adjusted for covariates; age, sex, smoking status, hypertension, diabetes, and APOE genotype. ROC curves were generated for the top 10 CSF fatty acids based on the area under the curve (AUC), sensitivity, and specificity and statistical significance differences between the groups using the DeLong test. Result: The palmitoleic acid/palmitic acid ratio, alpha‐linolenic acid, and palmitoleic acid in CSF unesterified, supernatant fluid, and nanoparticles fraction respectively effectively differentiated MCI from CU than Aβ, tau, and Aβ/tau with AUC of 0.70, 0.66 and 0.71 respectively which were significantly different from the AUC of Aβ ₄₂ , tau and Aβ ₄₂ /tau ratio (0.53, 0.54, 0.55) respectively. Moreover, integrating a panel of these fatty acids with Aβ ₄₂ /tau significantly improved its diagnostic accuracy. Age, sex, smoking, hypertension, APOE genotype and diabetes did not influence the model performance. Conclusion: Our study suggests that changes in fatty acid metabolism precede abnormalities in amyloid and tau in MCI. Thus, strategies that regulate fatty acid metabolism may stem off early cognitive decline in an older population.