Ophidism is a public health problem in tropical countries, occurring predominantly in rural areas. In Colombia, among the species responsible for snakebite envenomation, inflicting high mortality, is the Chocoan bushmaster, Lachesis acrochorda, better known locally by the names “verrugosa (warty)” and “pudridora (rot-causing)”. In this research, the cardiotoxic effect of the venom of L. acrochorda in male Wistar rats weighing 230 ± 20 g was evaluated. A statistical design of randomized blocks was implemented with three treated groups, injected with lyophilized venom (doses of 3.22 μg/g, 6.43 μg/g, 12.86 μg/g), and a control group injected with 0.9% saline solution. Electrocardiographic (ECG) recordings were taken from the anesthetized animals, revealing an increase in the amplitude of the P and T waves and an increase in the duration of the QT intervals in the electrocardiographic recordings. These increases were not observed in the control biomodels. In the analysis of the CK and CK-MB enzyme levels, increases were also observed in the levels of cardiac isoenzymes in the injected animals, but none in the control animals. The histopathological analyses carried out reveal that the injected animals showed effects such as interfibrillar and perivascular edema, cellular shortening of the cardiomyocytes, foci with tissue destructuring, and necrosis with contraction bands. In conclusion, the venom of the Lachesis acrochorda snake increases the P and T waves and the QT interval and increases the CK and CK-MB enzymes in the blood. Additionally, it causes interfibrillar and perivascular edema in the cardiac tissue, cardiocytolysis, and contraction bands.

Background: Inflammation plays a key role in Alzheimer's disease (AD) progression. Interleukin 8 (CXCL8) has emerged as an important cytokine involved in neuroinflammation. It is known as an inflammatory factor that induces a chemotactic response to sites of injury, involving the infiltration of neutrophils. In AD, interactions between CXCL8, Aβ42, and Tau suggest that CXCL8 amplifies inflammatory reactivity induced by Aβ42 and increases Tau phosphorylation and subsequent NFT formation. Our main objective was to determine the CXCL8 profile and its relationship with AD biomarkers in clinical and biological groups in a cohort of Brazilian older adults.Method: seventy‐four older adults were recruited and grouped based on different cognitive profile: Alzheimer’s dementia (n=33), Mild Cognitive Impairment (MCI) (n= 22) and normal cognition (NC) (n=19). CSF samples were collected by lumbar puncture and levels of Aβ42, p‐Tau, t‐Tau and, CXCL8 were assessed by the Luminex xMAP technique. Subsequently, based on biological criteria, the participants were classified in accordance with the AT(N) system into two groups AD continuum and non‐AD. Spearman correlation test and comparison between groups using the Mann‐Whitney U‐test and Kruskal‐Wallis's test were performed. Significant associations between CSF levels of Aβ42, p‐Tau, and p‐Tau/Aβ42 and CXCL8 were further explored in multiple linear regression analyses adjusted for age, sex, education, and APOE allele ε4 carrier status.Result: A significant correlation was found between CSF IL‐8 levels and the pTau/Aβ42 ratio (r=‐.456; p=.009) only in individuals with AD. We observed decreased CSF CXCL8 levels in the AD continuum compared to the non‐AD group [U=450.0; p=.022]. Considering clinical groups, we also observed decreased CXCL8 levels in AD group compared to the MCI group [X2 (2): 8.2; p=.016]. A significant positive association adjusted by sex, age, formal education and allele Ɛ4 was found between CXCL8 and Aβ42 (ß=.316; p=.016) and a negative association with pTau/Aß42 ratio (ß=. ‐257; p=.036).Conclusion: a decrease in CXCL8 levels was observed in the AD‐related groups and there was an increase in the MCI group, suggesting that IL‐8 may be more active in the prodromal stage of the disease and then its activity decreases as the disease progresses.

Background: The neuroinflammatory process in Alzheimer’s disease (AD) is characterized by increased reactivity of astrocytes and microglia, along with elevated production and release of immune mediators. Studies have shown that the reactive microglial phenotype in AD contributes to heightened levels of these mediators, which in turn exacerbate amyloid and tau pathology, ultimately leading to a sustained and robust inflammatory response. Brazil’s genetically diverse population offers a unique opportunity to investigate these immune mechanisms, potentially revealing population‐specific inflammatory profiles. This study aims to profile Alzheimer's disease biomarkers and immune mediators across clinical stages of the disease in a cohort of Brazilian older adults. Method: One hundred and eight older adults were recruited and categorized based on clinical profiles in three different groups: Alzheimer’s Disease Dementia (ADD) ( n =54), Mild Cognitive Impairment (MCI) ( n =33), and Healthy Controls (HC) ( n =21). Cerebrospinal fluid (CSF) Aβ42, p ‐Tau, t‐Tau, p ‐Tau/ Aβ42 and Aβ42/ Aβ40 and 27 immune mediators were assessed using the Luminex xMAP technique. Fold change analyses were conducted to identify differential expression patterns of biomarkers and immune mediators across clinical stages. To evaluate their discriminatory potential, receiver operating characteristic (ROC) and two‐graph ROC (TG‐ROC) analyses were performed on the inflammatory mediators and biomarkers that exhibited the highest area under the curve (AUC) values. Result: The fold change results demonstrated significant increases in CCL11, CCL5, IFN‐γ, and PDGF in the MCI/HC profile, along with a decrease in CCL4. The DDA/HC profile showed increases in Aβ40, p ‐Tau, t‐Tau, the p ‐Tau/Aβ42 ratio, CCL11, and PDGF, while decreases were observed in Aβ42, the Aβ42/Aβ40 ratio, CXCL8, and IL‐1Ra. In the ADD/MCI profile, p ‐Tau, the p ‐Tau/Aβ42 ratio, CCL3, and G‐CSF exhibited increased fold changes, whereas Aβ42, the Aβ42/Aβ40 ratio, CCL2, and the IFN‐γ ratio were decreased. CCL11 was able to discriminate between MCI and HC groups, while p ‐Tau effectively distinguished ADD from both MCI and HC. Conclusion: Our findings provide new insights into the role of neuroinflammation in AD, contributing to a deeper understanding of the dynamics of biomarkers and immune mediators in the pathophysiology of the disease.