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1.
Front Neurol ; 12: 608188, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33763012

RESUMO

Background: Screening for post-stroke cognitive impairment (PSCI) is necessary because stroke increases the incidence of and accelerates premorbid cognitive decline. The Quick Mild Cognitive Impairment (Qmci) screen is a short, reliable and accurate cognitive screening instrument but is not yet validated in PSCI. We compared the diagnostic accuracy of a Chinese version of the Qmci screen (Qmci-CN) compared with the widely-used Chinese versions of the Montreal Cognitive Assessment (MoCA-CN) and Mini-Mental State Examination (MMSE-CN). Methods: We recruited 34 patients who had recovered from a stroke in rehabilitation unit clinics in 2 university hospitals in China: 11 with post-stroke dementia (PSD), 15 with post-stroke cognitive impairment no dementia (PSCIND), and 8 with normal cognition (NC). Classification was made based on clinician assessment supported by a neuropsychological battery, independent of the screening test scores. The Qmci-CN, MoCA-CN, and MMSE-CN screens were administered randomly by a trained rater, blind to the diagnosis. Results: The mean age of the sample was 63 ± 13 years and 61.8% were male. The Qmci-CN had statistically similar diagnostic accuracy in differentiating PSD from NC, an area under the curve (AUC) of 0.94 compared to 0.99 for the MoCA-CN (p = 0.237) and 0.99 for the MMSE-CN (p = 0.293). The Qmci-CN (AUC 0.91), MoCA-CN (AUC 0.94), and MMSE-CN (AUC 0.79) also had statistically similar accuracy in separating PSD from PSCIND. The MoCA-CN more accurately distinguished between PSCIND and normal cognition than the Qmci-CN (p = 0.015). Compared to the MoCA-CN, the administration times of the Qmci-CN (329s vs. 611s, respectively, p < 0.0001) and MMSE-CN (280 vs. 611s, respectively, p < 0.0001) were significantly shorter. Conclusion: The Qmci-CN is accurate in identifying PSD and separating PSD from PSCIND in patients post-stroke following rehabilitation and is comparable to the widely-used MoCA-CN, albeit with a significantly shorter administration time. The Qmci-CN had relatively poor accuracy in identifying PSCIND from NC and hence may lack accuracy for certain subgroups. However, given the small sample size, the study is under-powered to show superiority of one instrument over another. Further study is needed to confirm these findings in a larger sample size and in other settings (countries and languages).

2.
Neurol Res ; 43(5): 349-357, 2021 May.
Artigo em Inglês | MEDLINE | ID: mdl-33393454

RESUMO

Objectives: To investigate the effect on vascular dementia of involuntary exercise induced by functional electrical stimulation and of forced and voluntary exercise, focusing on the recovery of cognitive function and using a rat model of dementia.Methods: A demential model was created in Wistar rats who were then given forced exercise, allowed voluntary exercise (wheel running) or had exercise induced through functional electrical stimulation. Their responses were quantified using a Morris water maze and by measuring long-term potentiation in the hippocampus. Immunohistochemical staining was used to evaluate neurogenesis in the hippocampus and Nissl staining was applied to visualize viable neuron loss in the DG sector. In addition, the levels of NMDAR1, AMPAR1, pAMPAR1, pCaMKII, CaMKII, Bcl-2 and Bax in the hippocampus were assessed by western blotting.Results: All of the exercise groups showed a recovery of cognitive performance and improved long-term potentiation. The three modes of exercise all increased the number of DCX immunopositive cells and reduced losses of intact-appearing neurons in the hippocampal DG zones roughly equally. All proved about equally effective in increasing the levels of NMDAR1, pAMPAR1 and pCaMKII and increasing the Bcl-2/Bax ratio to protect neurons from apoptosis.Conclusion: Exercise induced by electrical stimulation has beneficial effects comparable to those of other types of exercise for alleviating the cognitive deficits of vascular dementia.


Assuntos
Proteína Quinase Tipo 2 Dependente de Cálcio-Calmodulina/metabolismo , Disfunção Cognitiva/fisiopatologia , Demência Vascular/fisiopatologia , Hipocampo/metabolismo , Atividade Motora/fisiologia , Receptores de AMPA/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo , Animais , Modelos Animais de Doenças , Estimulação Elétrica , Masculino , Teste do Labirinto Aquático de Morris , Neurogênese/fisiologia , Condicionamento Físico Animal , Ratos , Ratos Wistar , Proteína X Associada a bcl-2/metabolismo , Proteína de Morte Celular Associada a bcl/metabolismo
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