FLAIR-AD: Functional Landscape Analysis of Inflammatory Regulation in Alzheimer's Disease

FLAIR-AD: An Interactive Public Engagement Website for Functional Landscape Analysis of Inflammatory Regulation in Alzheimer's Disease

Description: 

FLAIR-AD is an interactive, scrollytelling web application designed to communicate the scientific rationale and methodology of a PhD research project investigating the role of microglial immunogenetics in Alzheimer's disease risk.
The website presents a five-stage narrative journey through the key evidence linking brain immune cells (microglia) to Alzheimer's disease, drawing on published GWAS data, single-cell RNA-sequencing cell-type enrichment analyses, and transcription factor binding studies centered on IRF1. Visitors are guided from foundational concepts—the paradigm shift away from the amyloid hypothesis—through the genetic, transcriptomic, and epigenomic evidence converging on microglia as the primary cell type mediating Alzheimer's disease risk, culminating in an explanation of the CETCh-seq experimental strategy being developed to map IRF1 binding genome-wide in human microglia.

The site includes a procedural SVG animation system that illustrates microglial state transitions (ramified healthy microglia to disease-associated microglia, DAM), interactive D3.js data visualisations of GWAS loci, EWCE cell-type enrichment scores and differentially expressed genes, a public community forum with upvote/downvote functionality powered by Firebase Firestore, and a structured "Share Your Thoughts" portal collecting visitor reflections and usability feedback.

Scientific context:

Genome-wide association studies have identified over 80 loci associated with late-onset Alzheimer's disease risk. Expression-weighted cell-type enrichment analysis demonstrates that these risk variants are disproportionately active in microglia. IRF1, a master transcription factor in interferon-mediated immune activation, is among the most differentially expressed regulators in disease-associated microglia and its binding motifs overlap with known Alzheimer's risk loci. Existing commercial antibodies against IRF1 fail ChIP-seq quality control, leaving its genome-wide binding landscape in human microglia unmapped. This PhD project addresses that gap using Prime Editing (CETCh-seq) to endogenously tag IRF1 and generate the first high-resolution atlas of its binding sites in microglia.

Institution: Skene Lab, UK Dementia Research Institute, Imperial College London
Technologies: HTML5, CSS3, JavaScript (ES6), D3.js v7, Scrollama, Firebase Firestore, procedural SVG