The brain was previously believed to be an “immune privileged” organ without an immune system. However, recent discoveries have shown a connection between the peripheral lymphatic system and the brain. This review article provides an overview of the three distinct lymphatic systems within the brain - the glymphatic, meningeal, and parenchymal systems - with a focus on the recently discovered deep brain parenchymal lymphatic vessels. The article also discusses how these lymphatic systems are regulated by various pathological conditions, including Alzheimer’s disease, Parkinson’s disease, and other neurological disorders. By shedding light on the link between these diseases and the brain lymphatic systems, the article emphasizes the importance of understanding these systems for potential therapeutic interventions to treat neurodegenerative and psychiatric disorders.
Endogenous retroviruses (ERVs), remnants of ancient viral invasions, make up a significant part of the mammalian genomes. ERVs are typically held in check by complex epigenetic mechanisms, which serve to limit their expansion and potential adverse effects on the genome. However, ERVs can become aberrantly activated in response to stressful challenges, contributing to progression in pathological conditions, including cancer, inflammation, auto-immune disorders, and aging, through various mechanisms. Notably, ERV activation is also detected in the brain and is increasingly recognized as an important factor in neuropsychiatric disorders. In this review, we encapsulate the general understanding of ERVs in both physiological and pathological states and compiled evidence for ERV activation across a spectrum of neuropsychiatric disorders, along with current studies exploring the underlying mechanisms. Despite the accumulating body of evidence, research in this field remains in its infancy and faces substantial challenges. Further studies are warranted to enhance our understanding of ERV activation mechanisms and their roles in neuropsychological conditions, potentially contributing to the development of innovative therapeutic interventions.
Sleep disruption is common in older adults and has been linked to many negative health outcomes, including impaired cognitive, emotional, and interpersonal functioning and maladaptive metabolic changes. Sleep disturbance is the most common symptom in depressive patients, and it was formerly thought to be a major secondary manifestation of depression. Many longitudinal studies have identified insomnia as an independent risk factor for the development of emerging or recurrent depression in older adults, with bidirectional relationships between sleep quality and depression. This narrative review summarizes recent research or evidence on the sleep–depression association in older adults, as well as the potential common mechanisms underlying the comorbidity of sleep and depression disorders, focusing on the clock system, neurochemical substrates, and neurocircuits. A better understanding of the pathophysiological mechanisms underlying sleep disturbance and depression can assist psychiatrists in better managing this comorbidity.
Purpose We aimed to explore the relationship between thyroid peroxidase antibody (TPO-Ab) and suicidal and aggressive behaviors in patients with major mental disorders. Methods We enrolled 812 inpatients with major mental disorders (schizophrenia, bipolar disorder, and major depressive disorder) in this retrospective study. Baseline interviews were conducted by two psychiatrists. The patients’ suicidal and aggressive behaviors were recorded in the electronic medical record system and these patients were evaluated in terms of violence and suicide behaviors according to the risk assessment form formulated in the Work Code for the Management and Treatment of Severe Mental Illness by the Ministry of Health of China. We calculated the incidence rates of positive TPO-Ab, the suicidal and aggressive behaviors. Furthermore, we explored the relationships among risk factors for suicidal and aggressive behaviors using logistics regression analysis. Results Among the 812 patients, 42.6% (n = 346) had TPO-Abs and were defined as the positive group. Rates of suicide and aggression among the enrolled patients were 12.7% (n = 103) and 10.2% (n = 83) respectively. The percentage of patients with aggressive behaviors (13%, n = 45) was higher than that in the negative group (8.2%, n = 38). In contrast, the incidence (9.5%) of suicidal behaviors in the positive group was lower than that (15.0%) in the negative group. TPO-Ab was found to increase the risk of aggressive behavior (odd ratio (OR) = 1.64, 95%CI (1.04, 2.59), P = 0.03) and this effect was still evident after we adjusted for thyroid function (OR = 1.65, 95%CI (1.03, 2.64), P = 0.04). Furthermore, subclinical hypothyroidism (OR = 2.64, 95%CI (1.19, 5.85), P = 0.02) and subclinical hyperthyroidism (OR = 7.03, 95%CI (2.23, 22.20), P = 0.001) were found to be risk factors of aggressive behavior but not for suicide behaviors. Conclusion TPO-Abs can affect aggressive behavior but do not affect suicidal behaviors, in patients with major mental disorders. Thus, antibody testing is necessary for psychiatric patients with aggressive behavior. The TPO-Ab test helped the psychiatric staff to determine aggressive behavior in advance.
The ten-eleven translocation 2 (Tet2) protein, a member of the Tet family, acts as an α-ketoglutarate- and Fe2+-dependent dioxygenase that catalyzes the iterative oxidation of 5-methylcytosine. Tet2 is widely recognized for its involvement in diverse physiological and pathological processes. Herein, we focused on Tet2 changes in stress-related disease models, behavioral changes in response to mutant forms of Tet2, and potential mechanisms underlying the involvement of Tet2 in psychiatric symptoms. This information can contribute to the comprehensive understanding of the role of Tet2 in stress-related disorders and its potential as a therapeutic target.
