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Mendeley: Cite Smarter Not Harder
No full textTired of manually formatting bibliographies and struggling to keep your research organized? This class introduces you to Mendeley, the free, powerful reference manager that will revolutionize how you handle citations. Learn how to quickly capture and organize references, generate bibliographies in various citation styles (e.g., APA, MLA, Chicago), and deduplicate your results. Join us to save time, reduce errors, and focus on your research, not your formatting
Tau in Alzheimer’s Disease: Shaping the Future Patient Journey
No full textAlzheimer\u27s disease is a complex and multifactorial disease characterized by two key pathological hallmarks: amyloid-beta plaques and tau neurofibrillary tangles. Recent progress has led to the development and approval of disease-targeted therapies for Alzheimer\u27s disease in the form of anti-amyloid-beta monoclonal antibodies. However, findings suggest that amelioration of multiple pathological drivers may be required to maximize clinical effect. An increasing body of evidence suggests that tau is a critical player in Alzheimer\u27s disease pathophysiology, contributing significantly to neurodegeneration and cognitive decline. There are now several tau-targeting drugs in clinical development. In this review, we build on research and advancements in the field of tau to envision how an increasing focus on tau could shape the future Alzheimer\u27s disease patient journey. We highlight the potential of tau as both a promising therapeutic target and a valuable biomarker, with the potential to inform treatment decisions and provide insight into disease trajectories. We also consider what a greater focus on tau may bring to an already evolving patient care pathway characterized by an increased influx of patients presenting earlier in the disease continuum, changes in workflow and infrastructural requirements, and increased complexity in treatment decision-making, treatment administration, treatment monitoring, and patient tracking. This review underscores the critical changes that may be required and knowledge gaps to be elucidated to ensure healthcare system preparedness for additional classes of disease-targeted therapy to move toward a next-generation, individualized treatment approach to Alzheimer\u27s disease diagnosis and care
Fall Prevention in a Medical Intermediate Care Unit (MIMU) Through Use of a Collaborative Fall Bundle
Full text linkPURPOSE
This DNP project focused on reducing the fall rate in a medical intermediate care unit by half, from 1.81 falls per 1000 patient days to 0.91 falls per 1000 patient days.
BACKGROUND
The number of patient falls poses a significant concern in a medical intermediate care unit. The fall rate goal is zero.
METHODOLOGY
The Collaborative Fall Bundle includes implementing the Fall TIPS Toolkit, an 11 x 17 bedside poster informing patients and staff of their fall risk factors and interventions to counteract; an alarm buddy system pairing two nurses to answer each other\u27s call lights and assist with ambulation-required tasks; and a zoning approach requiring nurses to complete charting at an assigned zone, enabling timely responses to bed alarms. The project was guided by the Plan-Do-Study- Act model. Anonymous electronic surveys evaluated staff opinions of each element. The primary project measure was the fall rate.
RESULTS
The fall rate decreased from 1.81 to 0.89 falls per 1000 patient days. Surveys revealed non- compliance with certain elements of the bundle such as zoning staff within the unit and the alarm buddy system, while the Fall TIPS toolkit was widely favored.
IMPLICATIONS
The project duration limited the sample size. While the project yielded positive results, a year-long project may better assess the impact of the Fall TIPS toolkit alone in reducing falls. This project effectively reduced falls by 50%, and with the staff’s satisfaction with the Fall TIPS toolkit, improvements appear sustainable
Get into a \u27Back to School\u27 State of Mind with the TMC Library
No full textYou might not need a new lunchbox, but everyone needs a refreshed set of resources! We are taking it Back to School to showcase how the TMC Library supports every stage of your career.Come to learn about:For the Faculty: Curriculum support and copyright navigation.For the Researcher: Advanced data management and evidence synthesis tools.For Everyone: The latest tech, quiet spaces, and hidden perks of your library card.Let’s make this your most efficient year yet
Enhancing Research Communication with Visual Tools
No full textUnderstand the role of visual communication in medical research. Distinguish between data visualizations, infographics, and visual abstracts. Identify best practices and some resources and tools for creating effective visuals
Neuronal Subtype Governs Amyloid Structure, Cellular Response, and Cognitive Outcome in Genetically Targeted App Mouse Models
No full textPathological heterogeneity is increasingly appreciated in Alzheimer’s disease, yet we do not know how distinct aggregate conformations arise or influence cognitive outcomes. In an amyloid mouse model, we found that different brain regions formed structurally distinct Aβ deposits, prompting us to test whether neuronal subtypes shape aggregate conformation. To address this, we created transgenic mice expressing the same APP construct in either glutamatergic or GABAergic neurons. APP expression in GABAergic neurons resulted in diffuse plaques with high Aβ42/Aβ40 ratios and minimal gliosis, while glutamatergic expression produced neuritic plaques with activated glia. Despite similar Aβ levels, only mice with neuritic plaques exhibited cognitive deficits. These results show that the neuronal source of APP shapes Aβ plaque structure, influencing both cellular response and behavioral outcome. Our findings affirm that amyloid conformation and gliosis—rather than total Aβ load—drive disease progression, and suggest that regional differences in neuronal composition may govern vulnerability
Primary Cortical Neurons Precipitate and Extrude Large Mitochondria-Associated Calcium-Phosphate Sheets With a Bone-Precursor-Like Ultrastructure
No full textCalcium-phosphate (CaP) is a ubiquitous inorganic compound that plays an important structural role in healthy bone and teeth formation, but its pathologic buildup can occur in dyshomeostatic calcium disorders like Alzheimer\u27s disease and Leigh syndrome. The nexus of pathologic extracellular CaP in the nervous system is not well understood, but prior evidence suggests mitochondria could be a source. We have observed mitochondria-sized sheet-like CaP aggregates within functional wild type cortical neuron cultures at 1 and 20 days in vitro. Neurons were extracted from embryonic day 18 (E18) rat embryos following standard protocols to study neuronal structure and function. We have used a combination of cryo-ET, cryo-CLEM, and LDSAED to demonstrate that these aggregates are octacalcium phosphate-like, are associated with mitochondria, and that at least a portion are extruded via migrasomes. Visually similar aggregates were previously observed in Huntington\u27s disease model neurons, but in that study they were not observed in WT controls. These findings show that this CaP aggregation process occurs routinely in WT neurons and may reveal an important link for how mitochondria may participate in calcification, highlighting them as potential therapeutic targets in neurological disorders characterized by pathological calcification, such as Alzheimer\u27s disease
The Biomedical Landscape of Genomic Structural Variation in the Qatari Population
No full textWe present a large-scale study of structural variation (SV) in the Qatari population, based on short-read whole-genome sequencing (WGS) of 6,141 individuals, identifying 153,946 variants across 5 classes reflecting the region\u27s diversity and evolutionary history. Leveraging consanguinity and biobank phenotypes, we identify \u3e180 putative gene knockouts, and use proteomics to show functional consequences in homozygotes. Conversely, 52 genes show significant depletion of homozygous deletions, eight of which cause severe pediatric disease or murine embryonic lethality. Examining phenotypic extremes uncovers several non-exonic homozygous deletions with large effect, including in SPIRE2 (creatinine), MAGI2 (leanness) and a chr19 microRNA cluster (extreme obesity). Further, SV-GWAS reveals gene-trait associations independent of SNPs, including at ACY1 (acetylation), SLC2A9 (uric acid), UGT1A8 (bilirubin) and ZNF251 (alanine aminotransferase). Notably, 3.2% of Qataris carry findings in medically actionable genes, one-third attributable to SVs. Our findings offer a rich SV reference for a globally understudied population, and demonstrate the utility of consanguineous biobanks for studying SVs in health and disease. All common SVs and tag-SNPs are provided as imputation resource