Project description:Alzheimer's disease (AD) is a neurodegenerative disease and is the most common form of dementia, cognitive dysfunction is a pre-AD manifestation, followed by progressive deterioration in behavior and mood, CK has good pharmacological activity, inhibit neuronal damage associated with Aβ and improve learning memory in mice through its antioxidative properties. We used microarrays to detail the regulation of brain tissue genes in cognitively impaired mice by ginsenoside CK.
Project description:We investigated mRNA expression levels in fibroblast-like synoviocytes (FLS) from rheumatoid arthritis (RA) patients, after no treatment, or after ginsenoside CK or dexamethasone treatment. The aim of the study was to determine the differences in the effects of ginsenoside CK and dexamethasone on mRNA levels in RA-FLS. Both ginsenoside CK and dexamethasone regulate some of the same inflammatory genes.
Project description:We studied hepatic mRNA expression levels in normal Wistar rats, adjuvant arthritic (AA) rats, and AA rats administered by gavage (ginsenoside CK or dexamethasone). The aim of the study was to determine the differences in the effects of ginsenoside CK and dexamethasone on hepatic mRNA levels in AA rats. The dexamethasone group may have a greater effect on mRNA in the liver.
Project description:To validate the protection effect of physical exercises on age-related cognitive impairment, aged male C57BL/6J mice (12 months old, 12M) were subjected to treadmill running or standard housing for 4 weeks, and comparing with young (2 months old, 2M) male mice.
Project description:Alzheimer case-control samples originate from the EU funded AddNeuroMed Cohort, which is a large cross-European AD biomarker study relying on human blood as the source of RNA. The design is case-control. Cases are either Alzheimer's disease patients, subjects with mild cognitive impairment or age and gender matched controls.
Project description:<p>Parkinson's disease (PD) is a common neurodegenerative disorder. It is marked by motor dysfunction and cognitive decline. In recent years, scientific studies have found that PD's pathogenesis may be tied to an imbalance in the gut microbiota. This offers new perspectives for PD treatment. Modulating the gut microbiota is recognized as a potential way to enhance PD symptoms. While aerobic exercise can positively influence the gut microbiota, research on how the gut microbiota mediates aerobic exercise's effects on PD cognitive impairment is still limited. Thus, this study aimed to explore the potential mechanisms by which aerobic exercise improves cognitive impairment in PD patients. It does so by modulating the gut microbiota's structure and, in turn, improving cognitive function. Through this study, we hope to offer new strategies and a theoretical basis for treating PD cognitive impairment.</p>
Project description:It is important to maintain cognitive integrity during underwater operations, which may also trigger cognitive alterations. Cognitive effect of underwater operations and the underlying mechanism remain elusive. Here, we found a single underwater operation affects cognition in a time-dependent model. Prolonged exposure elicits significant cognitive impairment and hippocampal dysfunction, which was accompanied by activation of microglia and upregulation of pro-inflammatory cytokines. RNA-sequencing supported the involvement of neuroinflammation and indicated the critical role of CCR3. Knockdown of CCR3 significantly rescued cognitive impairment and hippocampal dysfunction. Furthermore, the upregulation of pro-inflammatory cytokines was also reversed. Mechanistically, CCR3 knockdown switched the activated microglia from a pro-inflammatory to neuroprotective phenotype. Taken together, these results highlighted the time-dependent effects of a single underwater operation on cognitive function. Knocking down CCR3 can attenuate neuroinflammation by regulating polarization of activated microglia, thereby alleviating prolonged underwater operation-induced cognitive impairment.
Project description:Persistent central nervous system (CNS) immune dysregulation and consequent dysfunction of multiple neural cell types is central to the neurobiological underpinnings of a cognitive impairment syndrome, colloquially referred to as “brain fog”, that can occur following traditional cancer therapies or certain infections. Immunotherapies have revolutionized cancer care for many tumor types, but the potential long-term cognitive sequelae are incompletely understood. Here, we demonstrate in mouse models that chimeric antigen receptor (CAR) T-cell therapy for both CNS and non-CNS cancers can impair cognitive function and induce a persistent CNS immune response characterized by white matter microglial reactivity, microglial chemokine expression, and elevated cerebrospinal fluid (CSF) cytokines and chemokines. Consequently, oligodendroglial homeostasis and hippocampal neurogenesis are disrupted. Single nucleus sequencing studies of human frontal cortex and subcortical white matter from brain tumor patients with or without previous CAR T-cell therapy confirm reactive states of microglia and oligodendrocytes in patients treated with CAR T cell therapy. In mice, transient microglial depletion or CCR3 chemokine receptor blockade rescues oligodendroglial deficits and cognitive performance in a behavioral test of attention and short-term memory function following CAR T-cell therapy. Taken together, these findings illustrate similar mechanisms underlying immunotherapy-related cognitive impairment (IRCI) and cognitive impairment following traditional cancer therapies and other immune challenges.