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Background: To improve clinical translatability of non-clinical in-vivo Alzheimer's disease (AD) models, a humanized APP knock-in mouse model (APP) was recently created (Xia, D. et al., 2022).
View Article and Find Full Text PDFBackground: Participant retention is a key determinant for a successful clinical trial. In Alzheimer's disease (AD) trials, participants are typically required to enroll with a study partner, which adds barriers to retention. Previous analyses of North American trial data found that most study partners were spouses and that such dyads had higher study completion rates than other study partner types.
View Article and Find Full Text PDFBackground: The advent of disease-modifying therapies in Alzheimer's disease (AD) necessitates a nuanced understanding of how therapies impact disease processes. Over the past decades, AD clinical trials have primarily relied on classical statistical analysis methodology such as the mixed model for repeated measures (MMRM) to estimate treatment effects. These conventional treatment effect quantifications are given as group differences in clinical outcome measures at a single visit.
View Article and Find Full Text PDFBackground: TAR-DNA-binding protein 43 (TDP43), is a pathologic marker in neurodegenerative diseases including frontotemporal lobar degeneration and amyotrophic lateral sclerosis. The aggregation of TDP-43, a crucial RNA-binding protein, is a consequence of post-translational modifications (PTMs) that disrupt its normal function. PTMs such as phosphorylation and ubiquitination contribute to the aberrant accumulation of TDP-43 aggregates, leading to neurodegenerative disorders like amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD).
View Article and Find Full Text PDFBackground: Neuroinflammation is a critical factor of Alzheimer's Disease (AD). Dysregulation of complement leads to excessive inflammation, direct damage to self-cells and propagation of injury. This is likely of particular relevance in the brain where inflammation is poorly tolerated and brain cells are vulnerable to direct damage by complement.
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