Biomarkers.

Background: Alzheimer disease (AD) related cognitive decline occurs at relatively young ages in individuals with Down syndrome (DS, early-mid 50s) and in those with autosomal dominant mutations (ADAD, 40-50s). Both groups show similar patterns of amyloid accumulation. We examined if brain volumes are similarly affected by AD pathology in individuals with DS and ADAD.

Public Health.

Background: Population dementia prevalence is traditionally estimated using cohort studies, surveys, routinely-collected administrative data, and registries. Hospital Electronic Health Records (EHRs) are comprised of rich structured and unstructured (text) clinical data that are underutilised for this purpose. We aimed to develop a suite of algorithms using routinely-collected EHR data to reliably identify cases of dementia, as a key step towards incorporating such data in prevalence estimation.

Developing Topics.

Background: Late-life depression (LLD) often coincides with cognitive decline, impacting antidepressant treatment outcomes. Investigating the genetic profile of cognitive function and its association with antidepressant response in individuals with LLD is crucial.

Method: In the Incomplete Response in Late-Life Depression: Getting to Remission (IRL-GRey) study, 307 older adults with major depressive disorder underwent 12-week venlafaxine treatment.

IL-1β-driven NF-κB transcription of ACE2 as a Mechanism of Macrophage Infection by SARS-CoV-2.

Coronavirus disease 2019 (COVID-19), caused by infection with the enveloped RNA betacoronavirus, SARS-CoV-2, led to a global pandemic involving over 7 million deaths. Macrophage inflammatory responses impact COVID-19 severity; however, it is unclear whether macrophages are infected by SARS-CoV-2. We sought to identify mechanisms regulating macrophage expression of ACE2, the primary receptor for SARS-CoV-2, and to determine if macrophages are susceptible to productive infection.

Cartilage Injuries of the Ankle.

Osteochondral lesions of the talus involve injury to the articular cartilage and underlying subchondral bone. These lesions are difficult to treat because of the poor blood supply and poor regenerative capacity of the talar articular cartilage. It is important to provide a comprehensive overview of the clinical presentation, diagnostic tools, and nonsurgical and surgical treatment strategies for osteochondral lesions of the talus.