Cognitive stimulation therapy (CST) is widely used with people with dementia, but there is no evidence of its efficacy in mild cognitive impairment or dementia in Parkinson's disease (PD-MCI; PDD) or dementia with Lewy bodies (DLB). We aimed to explore the impact of 'CST-PD', which is home-based, individualized CST adapted for this population. In a single-blind, randomized controlled exploratory pilot trial (RCT), we randomized 76 participant-dyads [PD-MCI ( = 15), PDD ( = 40), DLB ( = 21) and their care partners] to CST-PD or treatment as usual (TAU). CST-PD involves home-based cognitively stimulating and engaging activities delivered by a trained care partner. Exploratory outcomes at 12 weeks included cognition (Addenbrooke's Cognitive Evaluation; ACE-III), neuropsychiatric symptoms and function. In care partners, we assessed burden, stress and general health status. Relationship quality and quality of life were assessed in both dyad members. At 12 weeks, the ACE-III showed a nonstatistically significant improvement in the CST-PD group compared with the TAU group, although neuropsychiatric symptoms increased significantly in the former. In contrast, care partners' quality of life ( = 0.16) and relationship quality ('satisfaction', = 0.01; 'positive interaction', = 0.55) improved significantly in the CST-PD group, and care burden ( = 0.16) and stress ( = 0.05) were significantly lower. Qualitative findings in the CST-PD recipients revealed positive 'in the moment' responses to the intervention, supporting the quantitative results. In conclusion, care-partner-delivered CST-PD may improve a range of care-partner outcomes that are important in supporting home-based care. A full-scale follow-up RCT to evaluate clinical and cost effectiveness is warranted.
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http://dx.doi.org/10.1177/1756286419852217 | DOI Listing |
Neurochem Res
January 2025
College of Pharmacy, Guangxi Medical University, Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
To study the neuronal protective effect and its potential mechanism of C16 against gp120-induced cognitive impairment in vitro and in vivo. The NORT method was used to evaluate the short-term memory abilities of rats, the morphological changes in hippocampus were observed by Nissl staining. Cell viability and damage degree were detected by MTT and LDH.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Queen's University, Kingston, ON, Canada; D'OR Institute for Research and Education, Rio de Janeiro, Rio de Janeiro, Brazil.
Background: Physical exercise improves overall brain health, cognition, and stimulates the release of extracellular vesicles (EVs) in humans. Exercise upregulates irisin, a myokine derived from fibronectin type III domain-containing protein 5 (FNDC5) previously shown to mediate the beneficial actions of exercise on memory in mouse models of Alzheimer's disease (AD). Here, we investigated if physical exercise upregulates EVs.
View Article and Find Full Text PDFCerebellum
January 2025
Department of Neurology, Kailuan General Hospital, No. 57 Xinhua East Road, Lubei District, Tangshan City, 063000, Hebei Province, China.
This study aims to evaluate cognitive impairments in patients with acute cerebellar infarction using event-related potentials (ERP) and electrophysiological source imaging (ESI). Thirty patients with acute cerebellar infarction and 32 healthy volunteers were selected. Cognitive potentials were recorded and measured using a visual Oddball paradigm.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand.
Background: Microglia play an important role in immune memory. Lipopolysaccharide (LPS) triggers immune memory and primes microglia, resulting in brain pathologies and brain dysfunction following a second stimulus (1, 2). An increase in the C1q/ PSD95 expressions within microglia and excessively synaptic pruning were observed in mouse model of Alzheimer's disease (3).
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Albany Medical College, Albany, NY, USA.
Background: Stress is a common modifiable risk factor for AD, which increases dementia risk 2-fold. During the stress response, the hypothalamic-pituitary adrenal (HPA) axis is activated which stimulates the release of stress hormones called glucocorticoids into the blood stream. Studies on early-life stress have shown a glucocorticoid dependent vulnerability towards late-life inflammation.
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