IL-6 mediates olfactory dysfunction in a mouse model of allergic rhinitis.

Background: Immune-inflammatory response is a key element in the occurrence and development of olfactory dysfunction (OD) in patients with allergic rhinitis (AR). As one of the core factors in immune-inflammatory responses, interleukin (IL)-6 is closely related to the pathogenesis of allergic diseases. It may also play an important role in OD induced by diseases, such as Sjögren's syndrome and coronavirus disease 2019.

Brain response in asthma: the role of "lung-brain" axis mediated by neuroimmune crosstalk.

In addition to typical respiratory symptoms, patients with asthma are frequently accompanied by cognitive decline, mood disorders (anxiety and depression), sleep disorders, olfactory disorders, and other brain response manifestations, all of which worsen asthma symptoms, form a vicious cycle, and exacerbate the burden on families and society. Therefore, studying the mechanism of neurological symptoms in patients with asthma is necessary to identify the appropriate preventative and therapeutic measures. In order to provide a comprehensive reference for related research, we compiled the pertinent literature, systematically summarized the latest research progress of asthma and its brain response, and attempted to reveal the possible "lung-brain" crosstalk mechanism and treatment methods at the onset of asthma, which will promote more related research to provide asthmatic patients with neurological symptoms new hope.

P2X7 receptor of microglia in olfactory bulb mediates the pathogenesis of olfactory dysfunction in a mouse model of allergic rhinitis.

The pathogenesis of allergic rhinitis (AR)-related olfactory dysfunction (OD) remains unknown. Inhibiting microglial response in olfactory bulb (OB) can ameliorate AR-related OD, but no precise targets have been available. In this study, we established a mouse model of ovalbumin (OVA)-induced AR and combined with the application of P2X7 receptor (P2X7R)-specific antagonists and cell culture in conditioned medium to investigate the role and mechanism of OB microglial P2X7R in AR-related OD.

IL-1 and Allergy: Focusing on Its Role in Allergic Rhinitis.

Allergic rhinitis (AR) is a chronic upper airway immune-inflammation response mediated by immunoglobulin E (IgE) to allergens and can seriously affect the quality of life and work efficiency. Previous studies have shown that interleukin-1 (IL-1) acts as a key cytokine to participate in and promote the occurrence and development of allergic diseases. It has been proposed that IL-1 may be a potential biomarker of AR.

Brain response in allergic rhinitis: Profile and proposal.

In addition to typical nasal symptoms, patients with allergic rhinitis (AR) will further lead to symptoms related to brain function such as hyposmia, anxiety, depression, cognitive impairment, memory loss, etc., which seriously affect the quality of life of patients and bring a heavy burden to the patient's family and society. Some scholars have speculated that there may be potential "nose-brain communication" mechanism in AR that rely on neuro-immunity.

Pramipexole regulates depression-like behavior via dopamine D3 receptor in a mouse model of Parkinson's disease.

Depression is one of the strongest predictors of quality of life in patients with Parkinson's disease (PD). Despite the high prevalence of depression, there is no clear guidance for its treatment in PD because the evidence for the efficacy of most antidepressants remains insufficient. Pramipexole, a dopamine agonist, is one of the few drugs that has proven to be clinically useful.

Microglial MT1 activation inhibits LPS-induced neuroinflammation via regulation of metabolic reprogramming.

Parkinson's disease (PD) is one of the most common neurodegenerative diseases. Although its pathogenesis remains unclear, a number of studies indicate that microglia-mediated neuroinflammation makes a great contribution to the pathogenesis of PD. Melatonin receptor 1 (MT1) is widely expressed in glia cells and neurons in substantia nigra (SN).

BMAL1 regulation of microglia-mediated neuroinflammation in MPTP-induced Parkinson's disease mouse model.

Dysfunction of the circadian rhythm is one of most common nonmotor symptoms in Parkinson's disease (PD), but the molecular role of the circadian rhythm in PD is unclear. We here showed that inactivation of brain and muscle ARNT-like 1 (BMAL1) in 1-methyl-4-phenyl-1,2,4,5-tetrahydropyridine (MPTP)-treated mice resulted in obvious motor functional deficit, loss of dopaminergic neurons (DANs) in the substantia nigra pars compacta (SNpc), decrease of dopamine (DA) transmitter, and increased activation of microglia and astrocytes in the striatum. Time on the rotarod or calorie consumption, and food and water intake were reduced in the Bmal1 mice after MPTP treatment, suggesting that absence of Bmal1 may exacerbate circadian and PD motor function.

Impact of Maternal Separation on Dopamine System and its Association with Parkinson's Disease.

As a type of stress, maternal separation (MS) has been one of the most widely used models in neuropsychiatric research. An increasing number of studies has found that MS not only affects the function of the hypothalamic-pituitary-adrenal axis and hippocampal 5-hydroxytryptamine system, but also causes dysfunction of the central dopamine (DA) system and increases the susceptibility of dopaminergic neurons to pathogenic factors of Parkinson's disease (PD), for instance, 6-hydroxydopamine, thus impairing motor function. We reviewed the impact of MS on the DA system and its correlation with PD and found the following: (1) discrepant effects of MS on the DA system have been reported; (2) MS is a good model to study the impact of stress on the occurrence and development of PD, however, unified modeling criteria of MS are required; (3) correlation between MS and PD may involve the impact of MS on the DA system, which however is not the only connection; (4) intervening measures can block pathways between MS and PD, which provides reference for the prevention of PD in specific populations such as left-behind children.

Sleep deprivation caused a memory defects and emotional changes in a rotenone-based zebrafish model of Parkinson's disease.

Parkinson's disease (PD) is the second most common neurodegenerative disorder in the world. Apart from motor deficits, PD reduces patient's quality of life through sleep disturbances, cognitive impairment and emotional disorders. However, it's unclear whether bad life habits such as stay up late exacerbate the patient's cognition and emotional disorders.