Опубликована: Янв. 1, 2024
Язык: Английский
Biomolecules, Год журнала: 2024, Номер 14(2), С. 163 - 163
Опубликована: Янв. 30, 2024
Migraine is a highly prevalent neurological disorder. Among the risk factors identified, psychiatric comorbidities, such as depression, seem to play an important role in its onset and clinical course. Patients with migraine are 2.5 times more likely develop depressive disorder; this becomes even higher patients suffering from chronic or aura. This relationship bidirectional, since depression also predicts earlier/worse of migraine, increasing chronicity and, consequently, requiring healthcare expenditure compared alone. All these data suggest that may share overlapping biological mechanisms. Herein, review explores topic further detail: firstly, by introducing common epidemiological for comorbidity; secondly, focusing on providing cumulative evidence aspects, particular emphasis serotoninergic system, neuropeptides calcitonin-gene-related peptide (CGRP), pituitary adenylate cyclase-activating polypeptide (PACAP), substance P, neuropeptide Y orexins, sexual hormones, immune system; lastly, remarking future challenges required elucidate etiopathological mechanisms updated information regarding new key targets pharmacological treatment entities.
Язык: Английский
Процитировано
9
Journal of Affective Disorders, Год журнала: 2025, Номер 375, С. 75 - 85
Опубликована: Янв. 21, 2025
Язык: Английский
Процитировано
1
Communications Biology, Год журнала: 2024, Номер 7(1)
Опубликована: Янв. 9, 2024
Abstract Our previous work has shown that d -ribose (RIB)-induced depressive-like behaviors in mice. However, the relationship between variations RIB levels and depression as well potential participation depressive disorder is yet unknown. Here, a reanalysis of metabonomics data from depressed patients model rats performed to clarify whether increased level positively correlated with severity depression. Moreover, we characterize intestinal epithelial barrier damage, gut microbial composition function, microbiota-gut-brain metabolic signatures RIB-fed mice using colonic histomorphology, 16 S rRNA gene sequencing, untargeted metabolomics analysis. The results show caused impairment axis dysbiosis. These modules are consistently enriched peripheral (fecal, colon wall, serum) central (hippocampus) glycerophospholipid metabolism. In addition, three differential genera (Lachnospiraceae_UCG-006, Turicibacter, Akkermansia) two types glycerophospholipids (phosphatidylcholine phosphatidylethanolamine) have greater contributions overall correlations glycerophospholipids. findings suggest disturbances microbiota by may contribute onset via regulating metabolism, providing new insight for understanding function
Язык: Английский
Процитировано
8
Journal of Affective Disorders, Год журнала: 2024, Номер 362, С. 62 - 74
Опубликована: Июнь 29, 2024
Язык: Английский
Процитировано
8
Scientific Reports, Год журнала: 2024, Номер 14(1)
Опубликована: Март 28, 2024
Abstract Major depressive disorder (MDD) is accompanied by activated neuro-immune pathways, increased physiosomatic and chronic fatigue-fibromyalgia (FF) symptoms. The most severe MDD phenotype, namely major dysmood (MDMD), associated with adverse childhood experiences (ACEs) negative life events (NLEs) which induce cytokines/chemokines/growth factors. To delineate the impact of ACE + NLEs on FF symptoms in first episode (FE)-MDMD, examine whether these effects are mediated immune profiles. ACEs, NLEs, symptoms, 48 factors were measured 64 FE-MDMD patients 32 normal controls. Physiosomatic, gastro-intestinal belong to same factor as depression, anxiety, melancholia, insomnia. extracted from seven domains labeled physio-affective phenome depression. A part (59.0%) variance explained independent interleukin (IL)-16 IL-8 (positively), CCL3 IL-1 receptor antagonist (inversely correlated). (46.5%) (IL)-16, TNF-related apoptosis-inducing ligand (TRAIL) (positively) combined activities immunoregulatory cytokines associated). Partial least squares analysis shows that exert a substantial influence partly an network composed interleukin-16, CCL27, TRAIL, macrophage-colony stimulating factor, stem cell growth factor. caused immune-associated neurotoxicity due T helper (Th)-1 polarization M1 macrophage activation relative lowered compensatory protection.
Язык: Английский
Процитировано
5
Brain Behavior and Immunity, Год журнала: 2024, Номер 122, С. 75 - 94
Опубликована: Авг. 9, 2024
Язык: Английский
Процитировано
4
Journal of Psychosomatic Research, Год журнала: 2024, Номер 187, С. 111951 - 111951
Опубликована: Окт. 10, 2024
Язык: Английский
Процитировано
4
Life, Год журнала: 2025, Номер 15(2), С. 135 - 135
Опубликована: Янв. 21, 2025
Background: Cervical cancer (CC) is the fourth most common diagnosis in women worldwide. Infection with high-risk human papillomavirus (HPV) a critical but not determinative condition for CC development, as several co-factors modulate progression of HPV-associated cervical lesions. Interleukin-8 (IL-8) and Interleukin-16 (IL-16) are chemokine-like interleukins involved pathogenesis various cancers. Singular studies Asian populations have suggested potential role IL-8 rs4073 (−251 A>T) IL-16 rs1131445 (3′UTR T>C) carcinogenesis. Methods: A case-control study was conducted European cohort 339 women, including 126 patients 213 controls. Four SNPs, A>T), rs2227306 (+781 C>T), rs1126647 (+2767 rs2227543 (+1633 four polymorphism, rs4778889 (−295 T>C), rs11556218 (3441 T>G), rs4072111 (1300 were assessed using RFLP-PCR analyzed under seven inheritance models. Subgroup analyses stratified by menopausal status (age threshold 51 years), disease stage, histological subtype. Results: significantly associated an increased risk premenopausal co-dominant (p = 0.038), dominant 0.022), heterozygote 0.045) models, identifying T allele (OR 2.31, CI95% 1.17–4.56; p 0.017). In aged over 51, 0.048) overdominant 0.042) models model 0.092). None SNPs entire cohort. Specifically, neither nor rs4073, previously reported factors populations, this Conclusions: These findings highlight age stage immunity susceptibility, suggest that may function differently carcinogenesis compared other cancers, emphasize importance ethnic background risk, warranting further research.
Язык: Английский
Процитировано
0
medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2025, Номер unknown
Опубликована: Март 3, 2025
Abstract Background Major depressive disorder (MDD) is associated with neuro-immune – metabolic oxidative (NIMETOX) pathways. Aims To examine the connections among NIMETOX pathways in outpatient MDD (OMDD) and without syndrome (MetS); to determine prevalence of aberrations a cohort OMDD patients. Methods We included 67 healthy controls 66 patients we assessed various Results successfully identified subgroup individuals pathways, including diminished lecithin-cholesterol acyltransferase (LCAT), paraoxonase 1 (PON1) activity, reverse cholesterol transport (RCT) activities, elevated atherogenicity, differentially expressed immune networks, advanced oxidation protein products (AOPP). A large part variance (around 44%) atherogenicity indices was AOPP, fasting blood glucose (FBG), PON1 activation. LCAT activity positively correlated negatively FBG, AOPP RCT related R/R 192 genotype FBG larger overall severity (50.4%), suicidal behaviors (27.7%), neuroticism (42.1%) adverse childhood experiences immune-related neurotoxicity, insulin, inversely neuroprotection. Conclusions Many (78.8%) show The features OMDD, illness, neuroticism, behaviors, are caused by intertwined that may exert additional effects depending on whether MetS present or not.
Язык: Английский
Процитировано
0
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2759 - 2759
Опубликована: Март 19, 2025
It is known that the effectiveness of drug treatment for depression, ammine deficit based, largely unsatisfactory. In this review, we examine proposal a precision therapy has emerged and received strong push by identification role inflammation in depression. However, psychiatry risks being caught reductionist trap searching molecular switch resets whole system switches off disease. This an illusion since human complex depression systemic variable disorder. study, show inadequacy paradigm, and, at same time, illustrate superiority paradigm centered on psychoneuroendocrineimmunology (PNEI). According to PNEI disease being, caused different sources working together: psychological, biological, behavioral. means knowing biological psychological history subject, identifying relational crisis factors, building personalized treatments targeting those factors with tools medicine psychology, which are not reducible combination drugs psychotherapy. Our presents shift both theoretical practical, enables clinicians assess patients experiencing unified way treat them integrated manner.
Язык: Английский
Процитировано
0