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:Cognitive impairment is a frequent outcome of chronic viral infections linked to premature aging, including HIV. The mechanisms underlying this decline remain poorly understood. Here, we identify pro-inflammatory glycan degradation, characterized by loss of sialic acid and galactose, alterations that are hallmarks of premature aging, as key contributors to HIV-associated cognitive impairment (HIV-CI). In two independent cohorts of people living with HIV, these degradative changes were enriched in individuals with cognitive impairment, particularly women, and correlated with worse neurocognitive performance. In both a humanized mouse model of HIV and Eco-HIV, a complementary model that allows behavioral testing, pharmacological inhibition of glycan degradation with sialidase inhibitors prevented virally induced inflammation, immune activation, accelerated aging, and memory deficits. These findings implicate glycan degradation as a contributor to inflammation and neurocognitive impairment in HIV and highlight glycan-preserving therapies as a promising strategy to mitigate inflammation, premature aging, and cognitive decline during viral infections.
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.