Severe Persistent Urinary Retention Following Treatment With Intravenous Lecanemab: Urinary Retention With IV Lecanemab.

Lecanemab is an amyloid-targeted antibody indicated for treating patients with amyloid-confirmed early Alzheimer's Disease in mild dementia or mild cognitive impairment stages. We report here a case of a subject with early stage of Alzheimer's Disease dementia, amyloid positive, who developed severe acute urinary retention following his first dose of intravenous lecanemab. His urinary retention resolved after a week but recurred following the second intravenous dose 2 weeks later.

Crossword puzzle training and neuroplasticity in mild cognitive impairment (COGIT-2): 78-week, multi-site, randomized controlled trial with cognitive, functional, imaging and biomarker outcomes.

Background: Cognitive training represents an important potential therapeutic strategy for mild cognitive impairment (MCI). In our recently completed trial, crossword puzzles were superior to computerized cognitive training on Alzheimer's disease assessment scale-cognitive subscale-11 (ADAS-Cog11) and function, correlating with decreased brain atrophy over 78 weeks.

Methods: COGIT-2 is a 78-week, multicenter, clinical trial comparing home-based, high-dose crosswords (4 puzzles per week) to low-dose crosswords (1 puzzle per week) and a health education control group in 240 MCI subjects.

AI-Assisted Detection of Amyloid-related Imaging Abnormalities (ARIA): Promise and Pitfalls.

The advent of anti-amyloid therapies (AATs) for Alzheimer's disease (AD) has elevated the importance of MRI surveillance for amyloidrelated imaging abnormalities (ARIA) such as microhemorrhages and siderosis (ARIA-H) and edema (ARIA-E). We report a literature review and early quality assurance experience with an FDA-cleared assistive AI tool intended for detection of ARIA in MRI clinical workflows. The AI system improved sensitivity for detection of subtle ARIA-E and ARIA-H lesions but at the cost of a reduction in specificity.

Data-Driven Modeling of Amyloid-beta Targeted Antibodies for Alzheimer's Disease.

Alzheimer's disease (AD) is caused by the build-up of amyloid beta (A$\beta$) proteins in the brain, leading to memory loss and cognitive decline. Despite the approval of monoclonal antibodies targeting A$\beta$, optimizing treatment strategies while minimizing side effects remains a challenge. This study develops a mathematical framework to model A$\beta$ aggregation dynamics, capturing the transition from monomers to higher-order aggregates, including protofibrils, toxic oligomers, and fibrils, using mass-action kinetics and coarse-grained modeling.