GLP-1's role in neuroprotection: a systematic review.

Glucagon-like peptide 1 (GLP-1) is a target for treatment of diabetes; however, its function in the brain is not well studied. In this systematic review, we aimed to analyze the neuroprotective role of GLP-1 and its defined mechanisms. Methods: We searched 'Web of Science' and 'Pubmed' to identify relevant studies using GLP-1 as the keyword. Two hundred and eighty-nine clinical and preclinical studies have been included. Data have been presented by grouping neurodegenerative, neurovascular and specific cell culture models. Results: Recent literature shows that GLP-1 and its agonists, DPP-4 inhibitors and combined GLP-1/GIP molecules are effective in partially or fully reversing the effects of neurotoxic compounds, neurovascular complications of diabetes, neuropathological changes related with Alzheimer's disease, Parkinson's disease or vascular occlusion. Possible mechanisms that provide neuroprotection are enhancing the viability of the neurons and restoring neurite outgrowth by increased neurotrophic factors, increasing subventricular zone progenitor cells, decreasing apoptosis, decreasing the level of pro-inflammatory factors, and strengthening blood-brain barrier. Conclusion: Based on the preclinical studies, GLP-1 modifying agents are promising targets for neuroprotection. On the other hand, the number of clinical studies that investigate GLP-1 as a treatment is low and further clinical trials are needed for a benchside to bedside translation of recent findings.

Association Between Mood Disorder Severity, Treatment Response and Systemic Inflammatory Markers: Exploring the Role of NLR, PLR, MLR, and SII.

Background: In this study, the relationship between treatment response, clinical features of episodes such as psychosis, suicidal behavior, and agitation, duration of hospitalization, and systemic inflammation markers Systemic Inflammatory Index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-lymphocyte ratio (MLR) in bipolar affective disorder manic episode (BAD-M), bipolar affective disorder-depressive episode (BAD-D), and major depressive disorder (MDD) were investigated. Methods: TheNLR, MLR, PLR, and log SII were measured using parameters from a complete blood count. Admission and discharge Young Mania Rating Scale and Hamilton Depression Rating Scale scores were evaluated. This is a retrospective study conducted with a total of 451 inpatients, 122 (27.10%) of whom were diagnosed with BAD-M, 60 (13.20%) with BAD-D, and 269 (56.60%) with MDD. Results: The patients with manic episodes have higher levels of NLR (P = .019), MLR (P = .002), and log SII (P = .007). In the bipolar depression and mania groups, the patients with and without treatment responses did not differ in terms of inflammation markers; the log PLR value was found to be higher in the unipolar depression group in the patients who did not reach remission (P = .048). Conclusion: This study reveals associations between inflammation markers and different types of mood episodes. Higher NLR, MLR, and log SII levels in bipolar mania and lower NLR levels in agitated unipolar depression provide clues about changes in inflammation across different episodes. Studies with larger samples are needed to evaluate the relationship between inflammatory markers, the severity of mania and depression, and the response to treatment.

Can Incidental Vascular Calcifications at Mammography be Used as a Screening Biomarker for Heart and Kidney Disease?

Mammography is a screening test with extensive international application and financial infrastructure promoting accessibility and affordability. Designed specifically to detect microcalcifications, mammography is powered to detect calcifications in vessel walls. Breast arterial calcifications (BAC) are one of the most common incidental findings documented by mammography. This review considers the literature regarding BAC in relation to cardiovascular disease (CVD) and its risk factors. The aim is to assess the possibility of using BAC as an early surrogate imaging biomarker of CVD.