Periodic leg movements during sleep (PLMS) may have crucial consequences in adults. This study aimed to identify baseline characteristics, symptoms, or questionnaires that could help to identify sleep-disordered breathing patients with significant PLMS. Patients aged 20-80 years who underwent polysomnography for assessing sleep disturbance were included. Various factors such as sex, age, body measurements, symptoms, apnea-hypopnea index (AHI), and sleep quality scales were analysed to determine the presence of PLMS. The study included 1480 patients with a mean age of 46.4 ± 13.4 years, among whom 110 (7.4%) had significant PLMS with a PLM index of 15 or higher. There were no significant differences observed in terms of sex or BMI between patients with and without significant PLMS. However, the odds ratios (OR) for PLMS were 4.33, 4.41, and 4.23 in patients who were aged over 50 years, had insomnia, or had an ESS score of less than 10, respectively. Notably, the OR increased up to 67.89 times in patients who presented with all three risk factors. Our analysis identified significant risk factors for PLMS: age over 50, self-reported insomnia, and lower daytime sleepiness levels. These findings aid in identifying potential PLMS patients, facilitating confirmatory examinations and managing associated comorbidities.
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http://dx.doi.org/10.1111/jsr.14198 | DOI Listing |
Alzheimers Dement
December 2024
GSK R&D, Stevenage, Hertfordshire, United Kingdom.
Background: Genetic variants in GRN, the gene encoding progranulin, are causal for or are associated with the risk of multiple neurodegenerative diseases. Modulating progranulin has been considered as a therapeutic strategy for neurodegenerative diseases including Frontotemporal Dementia (FTD) and Alzheimer's Disease (AD). Here, we integrated genetics with proteomic data to determine the causal human evidence for the therapeutic benefit of modulating progranulin in AD.
View Article and Find Full Text PDFBackground: The autophagy lysosomal pathway (ALP) and the ubiquitin-proteasome system (UPS) are key proteostasis mechanisms in cells, which are dysfunctional in AD and linked to protein aggregation and neuronal death. Autophagy is over activated in Alzheimer's disease brain whereas UPS is severely impaired. Activating autophagy has received most attention, however recent evidence suggests that UPS can clear aggregate proteins and a potential therapeutic target for AD and protein misfolding diseases.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Alzheimer Center Amsterdam, Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc, Amsterdam, North Holland, Netherlands.
The lack of an in-vivo pathology marker for synuclein pathology has been a long standing challenge for dementia for Lewy bodies (DLB) research. This issue is critically important for phase II trials, which are often small, requiring the precise measurement of the biological effects, whether disease modifying or symptomatic. Recent advances have enabled the determination of alpha-synuclein pathology status with CSF measurements, using aggregation assays [RT-QUIC].
View Article and Find Full Text PDFBackground: There is an urgent need for new therapeutic and diagnostic targets for Alzheimer's disease (AD). Dementia afflicts roughly 55 million individuals worldwide, and the prevalence is increasing with longer lifespans and the absence of preventive therapies. Given the demonstrated heterogeneity of Alzheimer's disease in biological and genetic components, it is critical to identify new therapeutic approaches.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is the most common cause of dementia worldwide. It is characterized by dysfunction in the U1 small nuclear ribonucleoproteins (snRNPs) complex, which may precede TAU aggregation, enhancing premature polyadenylation, spliceosome dysfunction, and causing cell cycle reentry and death. Thus, we evaluated the effects of a synthetic single-stranded cDNA, called APT20TTMG, in induced pluripotent stem cells (iPSC) derived neurons from healthy and AD donors and in the Senescence Accelerated Mouse-Prone 8 (SAMP8) model.
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