Colin L. Masters

Research summary

Amyloid-β (Aβ) biochemistry in Alzheimer's disease (AD) and Down syndrome forms the central research theme. The 1985 PNAS paper purified and characterised the cerebral amyloid protein constituting plaque cores in AD and aged Down syndrome individuals, showing it to be multimeric aggregates of an ~40-residue, 4 kDa polypeptide with amino acid composition, mass, and N-terminal sequence essentially identical to the amyloid of congophilic angiopathy but with ragged N-termini, indicating a common precursor for plaque and vascular amyloids [1]. The 1999 Annals of Neurology paper used Western blotting to quantify soluble and insoluble Aβ pools, finding mean soluble Aβ elevated threefold in AD and correlated with severity markers, whereas total insoluble Aβ discriminated AD from controls but did not track severity, implicating the soluble pool as a determinant of neurodegeneration [3]. The 1994 Science paper showed that zinc above 300 nM rapidly destabilised human Aβ(1-40) at physiologically relevant peptide concentrations and induced tinctorial amyloid formation; rat Aβ(1-40), which binds zinc less avidly, was resistant, offering a mechanistic account for species differences in cerebral Aβ deposition [5]. The 2012 NEJM paper on dominantly inherited AD analysed 128 participants in a longitudinal study, using parental symptom-onset age to estimate years before expected onset and document the sequence and magnitude of CSF, blood, imaging, and cognitive biomarker changes that culminate in symptomatic disease [2]. The 2021 Molecular Psychiatry review integrates molecular, genetic, and multimodal biomarker evidence on the Aβ pathway, organising it as a coherent target framework for disease-modifying therapy development [4]. Across the five works the trajectory runs from biochemical identification of plaque-core Aβ [1], to a quantitative case for the soluble Aβ pool driving severity [3] and the metal-ion-induced aggregation mechanism [5], to clinical biomarker sequencing in dominantly inherited disease [2] and the contemporary therapeutic synthesis [4].

Recent publications

1. The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor1987 · Nature · 4591 citationsDOI
2. Amyloid plaque core protein in Alzheimer disease and Down syndrome.1985 · Proceedings of the National Academy of Sciences · 4418 citationsDOI
3. Clinical and Biomarker Changes in Dominantly Inherited Alzheimer's Disease2012 · New England Journal of Medicine · 3783 citationsDOI
4. Neurodegenerative diseases and oxidative stress2004 · Nature Reviews Drug Discovery · 3638 citationsDOI
5. Amyloid β deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer's disease: a prospective cohort study2013 · The Lancet Neurology · 2258 citationsDOI
6. Soluble pool of A? amyloid as a determinant of severity of neurodegeneration in Alzheimer's disease1999 · Annals of Neurology · 1800 citationsDOI
7. Alzheimer's disease2015 · Nature Reviews Disease Primers · 1737 citationsDOI
8. The Amyloid-β Pathway in Alzheimer’s Disease2021 · Molecular Psychiatry · 1723 citationsDOI
9. High performance plasma amyloid-β biomarkers for Alzheimer’s disease2018 · Nature · 1672 citationsDOI
10. Rapid induction of Alzheimer A beta amyloid formation by zinc1994 · Science · 1510 citationsDOI

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External profiles

• ORCID: https://orcid.org/0000-0003-3072-7940
• OpenAlex: openalex.org

Profile compiled from public sources (Researchmap, OpenAlex, Tohoku University faculty directory). Last refreshed 2026-05. Report incorrect information.