Parkinson’s disease (PD) is characterized by a range of motor signs, but cognitive dysfunction is also observed. Supplementation with folic acid and vitamin B12 is expected to prevent cognitive impairment. To test this in PD, we promoted a lesion within the substantia nigra pars compacta of rats using the neurotoxin rotenone. In the sequence, the animals were supplemented with folic acid and vitamin B12 for 14 consecutive days and subjected to the object recognition test. We observed an impairment in object recognition memory after rotenone administration, which was prevented by supplementation (p < 0.01). Supplementation may adjust gene expression through efficient DNA methylation. To verify this, we measured the expression and methylation of the kynureninase gene (Kynu), whose product metabolizes neurotoxic metabolites often accumulated in PD as kynurenine. Supplementation prevented the decrease in Kynu expression induced by rotenone in the substantia nigra (p < 0.05), corroborating the behavioral data. No differences were observed concerning the methylation analysis of two CpG sites in the Kynu promoter. Instead, we suggest that folic acid and vitamin B12 increased global DNA methylation, reduced the expression of Kynu inhibitors, maintained Kynu-dependent pathway homeostasis, and prevented the memory impairment induced by rotenone. Our study raises the possibility of adjuvant therapy for PD with folic acid and vitamin B12.

Introduction: Atherosclerosis is a central element in the pathogenesis of contemporary cardiovascular diseases. Atherosclerosis can be defined as a slowly progressive inflammatory process associated with several causal factors. The pathophysiological process is characterized by a complex inflammatory cascade, initiated by vascular endothelial injury, leading to vascular narrowing and hardening. Objective: To review the presence of a systemic inflammatory process through the analysis of interleukin-6 and tumor necrosis factor alpha (TNF-a) markers in the inflammatory tissue manifestations in different segments of the aorta. Method: An integrative review was carried out in the PubMed and Scielo databases. The search used the following keywords: "inflammation, atherosclerosis, type 2 diabetes mellitus, CD68, IL-6, THFa, endothelium" and their English versions. Inclusion criteria included review articles, experimental studies, and preclinical and clinical research, written in Portuguese and English and available in full text. The selected articles were analyzed based on the technologies discussed, future prospects and challenges mentioned, and diseases related to the article's central idea. Result: 63 articles were evaluated. Conclusion: Pro-inflammatory cytokines are examples of inflammatory markers with serological expression. Tissue inflammatory markers, such as CD68, the macrophage activation glycoprotein, identified through immunohistochemical analysis, can allow the assessment of the vascular inflammatory process, especially in the context of atherosclerosis.