Public Health.

Background: People living in diverse rural areas have shown higher rates of Alzheimer's disease and related dementias (ADRD) compared with their urban counterparts. Further, individuals in rural areas have higher rates of modifiable risk factors for ADRD, such as physical inactivity and alcohol misuse, that account for up to 40% of dementia cases. This study aimed to investigate the efficacy of a novel public health initiative to reduce dementia incidence in both urban and rural settings in Australia's island state: Tasmania.

Public Health.

Background: Previous research has focused on early-life education to reduce dementia risk, yet there is great potential for enhancing cognitive reserve in later-life through educational interventions, even for people with low early-life educational attainment. In 2019, we launched ISLAND (Island Study Linking Ageing and Neurodegenerative Disease) Campus, offering free university study to participants, with flexible in-person/online learning models removing educational, socioeconomic and geographical barriers. After four years, here we investigate our core hypothesis: that engagement in later life education leads to improvements in modifiable risk factors for dementia, cognition and plasma biomarkers.

Developing Topics.

Background: TANGO was a Phase 2 clinical study designed to assess the safety and efficacy of gosuranemab, an anti-tau monoclonal antibody, in participants with mild cognitive impairment due to Alzheimer's disease (AD) or with mild AD dementia. Despite robust target engagement of unbound N-terminal tau, the clinical efficacy endpoint was not met. In this exploratory analysis of TANGO participants, we examine plasma p-tau217 levels to assess the feasibility of using this biomarker to identify patients with AD pathology and predict disease progression.

Drug Development.

Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by the formation of amyloid-beta (Aβ) plaques and neurofibrillary tangles (NFTs) composed of tau aggregates. Research in animal models has generated hypotheses on the underlying mechanisms of the interaction between Aβ and tau pathology. In support of this interaction, results from clinical trials have shown that treatment with anti-Aβ monoclonal antibodies (mAbs) affects tau pathology.