RESUMO
BACKGROUND: The role of comprehensive geriatric assessment (CGA) in screening for mild cognitive disorders was not known. AIM: To evaluate the role of CGA in screening for mild cognitive disorders. METHODS: A total of 100 elderly people who underwent health examinations in our hospital and community between January 2020 and December 2021 were included for analysis. Using Petersen as the diagnostic gold standard, healthy individuals were included in the control group and patients with mild cognitive impairment were assigned to the study group. The correlation between the cognitive function of the patients and their baseline clinical profiles was analyzed. Patients' Montreal Cognitive Assessment (MoCA) and CGA screening results were compared, and the sensitivity and specificity were calculated to assess the screening role of CGA. RESULTS: CGA assessment yielded higher diagnostic accuracy than MoCA. The results of the multivariate regression analysis showed no correlation of gender, age, body mass index and literacy with cognitive function. Patients with mild cognitive impairment obtained significantly lower MoCA scores than healthy individuals (P < 0.05). In the CGA scale, patients with mild cognitive impairment showed significantly lower Mini-mental State Examination, Miniature Nutritional Assessment and Berg Balance Scale scores, and higher Activity of Daily Living, Instrumental Activities of Daily Living Scale and Frailty Screening Inventory scores than healthy individuals (P < 0.05), whereas the other assessment scales showed no significant differences (P > 0.05). The CGA provides higher diagnostic sensitivity and specificity than the MoCA (P < 0.05). CONCLUSION: CGA allows accurate identification of mild cognitive impairment with high sensitivity and specificity, facilitating timely and effective intervention, and is thus recommended for clinical use.
RESUMO
Heat shock protein 90 (HSP90) is widely found in brain tissue. HSP90 inhibition has been proven to have neuroprotective effects on ischemic strokes. In order to study the role of HSP90 in traumatic brain injury (TBI), we carried out the present study. A novel inhibitor of the HSP90 protein, 17-dimethylaminoethylamino-17-demethoxygeldanamycin (17-DA), has been investigated for its function on the blood-brain barrier (BBB) damage after traumatic brain injury (TBI) in mouse models. These C57BL/6 mice were used as a TBI model and received 17-DA (0.1 mg/kg/d, intraperitoneally) until the experiment ended. To find out whether 17-DA may protect against TBI in vitro, bEnd.3 cells belonging to mouse brain microvascular endothelium were used. The HSP90 protein expressions were raised after TBI at the pericontusional area, especially at 3 d. Our study suggested that 17-DA-treated mice improved the recovery ability of neurological deficits and decreased brain edema, Evans blue extravasation, and the loss of tight junction proteins (TJPs) post-TBI. 17-DA significantly promoted cell proliferation and alleviated apoptosis by inhibiting the generation of intracellular reactive oxygen species (ROS) to downregulate cleaved caspase-3, matrix metallopeptidase- (MMP-) 2, MMP-9, and P-P65 in bEnd.3 cells after the injury. As a result, we assumed that the HSP90 protein was activated post-TBI, and inhibition of HSP90 protein reduced the disruption of BBB and improved the neurobehavioral scores in a mouse model of TBI through the action of 17-DA, which inhibited ROS generation and regulated MMP-2, MMP-9, NF-κB, and caspase-associated pathways. Thus, blocking HSP90 protein may be a potential therapeutic strategy for TBI.