Objective: To study the possibility of using immunological parameters for the evaluation of the activity of endogenous process in depression and quality of response to psychopharmacotherapy.
Material And Methods: Authors examined 42 patients, aged 20-55 years, with the prevalence of anxiety (n = 22) or apathy (n = 20) in the clinical picture of depression. The following immunological parameters were measured in the blood of the patients: degranulation activity of leukocyte elastase (LE), functional activity of alpha-1-proteinase inhibitor (alpha-1-PI); the level of autoantibodies to neuroantigen S-100B and myelin basic protein.
Results And Conclusion: The involvement of inflammatory and autoimmune responses in the pathophysiology of endogenous depression was confirmed. Depression associated with increased levels of autoantibodies to brain neuroantigens (an autoimmune component) had a more complicated structure and showed the tendency to prolonged course and resistance to the therapy. The results suggest that some immunological parameters may be used as markers of patient's clinical status and quality and completeness of psychopathological symptom reduction.
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http://dx.doi.org/10.17116/jnevro20151154149-53 | DOI Listing |
J Antimicrob Chemother
December 2024
Department of Virology, Sorbonne Université, INSERM, UMR-S 1136, Institut Pierre Louis d'Epidémiologie et de Santé Publique, AP-HP, Hôpitaux Universitaires Pitié Salpêtrière - Charles Foix, 83 Boulevard de l'Hôpital 39, F-75013 Paris, France.
Background: The S147G mutation is associated with high-level resistance to the integrase strand transfer inhibitor (INSTI) elvitegravir. In several poorly documented cases, it was also selected in patients on dolutegravir. Given the widespread use of dolutegravir, further studies of S147G are required.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is a progressive neurodegenerative disease with multifactorial etiology. The toxicity of senile plaques and neurofibrillary tangles is associated with changes in the clearance of tau and beta-amyloid proteins, which are closely related to inflammatory imbalances. Pro-inflammatory cytokines are present in abnormal details due to the overactivation of immunological pathways, especially toll-like receptors.
View Article and Find Full Text PDFBackground: There is increasing evidence that the pathogenesis of Alzheimer's disease (AD) involves various immunological responses. Indeed, astrocyte reactivity or astrocytosis is a pathological process that is commonly found surrounding amyloid-β plaques in the brains of AD patients. Although the exact role of astrocytosis is still unrevealed, monitoring astrocyte activity using biomarkers leads to a better understanding of the underlying mechanism of AD pathogenesis.
View Article and Find Full Text PDFBackground: PLCG2 is signal-transduction protein identified as a potential drug target for the treatment of Alzheimer's disease (AD). PLCG2 is regulated by stimulation of the TREM2 pathway in microglia, which results in phagocytosis of beta-amyloid. PLCG2 catalyzes the cleavage of PI(4,5)P2 into IP3 and diacylglycerol, resulting in increased cell motility, phagocytosis, and proliferation in microglia.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indiana University School of Medicine, Indianapolis, IN, USA.
Background: TREM2 signaling has been implicated in Alzheimer's Disease (AD). TREM2 regulates microglial states and functions such as phagocytosis. The most prominent TREM signaling adapter is DAP12, encoded by TYROBP.
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