Selina Wray

Professor of Molecular Neuroscience

UCL Institute of Neurology, University College London

United Kingdom

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Professor Selina Wray is a distinguished faculty member at UCL Queen Square Institute of Neurology in the United Kingdom. Her research primarily focuses on molecular neuroscience, with recent contributions exploring Alzheimer's disease, the mechanobiology of the blood-brain barrier, and the roles of microglia and astrocytes in neuroinflammation. She has published influential articles addressing the impacts of genetic mutations on neurological disorders and the potential of induced pluripotent stem cells in research.

Articles (19)

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2025

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2020

Collaborators (14)

Olga Kopach

Lecturer

City St George's University

UNITED KINGDOM

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Claudia Manzoni

Lecturer in Translational Neuroscience

University College London

UNITED KINGDOM

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Zhongbo Chen

UNITED KINGDOM

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Dmitri Rusakov

Professor of Neuroscience

University College London

UNITED KINGDOM

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Lauren Byrne

University College London

UNITED KINGDOM

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Jennifer Pocock

University College London

UNITED KINGDOM

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John S H Danial

University of St Andrews

UNITED KINGDOM

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Michela Alessandra Denti

University of Trento

ITALY

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Ross W. Paterson

UNITED KINGDOM

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Lucy Granat

King's College London

UNITED KINGDOM

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Johan Jakobsson

Lund University

SWEDEN

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Emad Moeendarbary

University College London

UNITED KINGDOM

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Tatiana Alvarez Giovannucci

Karolinska Institutet

SWEDEN

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Filip Tomczuk

Institute of Psychiatry and Neurology

POLAND

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Selina Wray

Research Interests

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About

Articles (19)

Mechanobiology of the blood-brain barrier during development, disease and ageing

Mutations in PSEN1 predispose inflammation in an astrocyte model of familial Alzheimer’s disease through disrupted regulated intramembrane proteolysis

Reconstructing Alzheimer’s disease one cell type at a time using in vitro tricultures

The annotation of GBA1 has been concealed by its protein-coding pseudogene GBAP1

CSF neurofilament light chain profiling and quantitation in neurological diseases

The presenilin 1 mutation P436S causes familial Alzheimer's disease with elevated Aβ43 and atypical clinical manifestations

Selective suppression of oligodendrocyte-derived amyloid beta rescues neuronal dysfunction in Alzheimer’s disease

Antibody-mediated degradation of 4R-tau restores mitochondrial membrane polarization in human induced pluripotent stem cell-derived neurons with the MAPT 10+16 mutation

Microglia contribute to the production of the amyloidogenic ABri peptide in familial British dementia.

Generation of an induced pluripotent stem cell line (BIORTCi001-A) from a healthy adult indigenous Nigerian participant.

Differential Stimulation of Pluripotent Stem Cell-Derived Human Microglia Leads to Exosomal Proteomic Changes Affecting Neurons

Mass spectrometry analysis of tau and amyloid‐beta in iPSC‐derived models of Alzheimer’s disease and dementia

Genetically engineered MAPT 10+16 mutation causes pathophysiological excitability of human iPSC-derived neurons related to 4R tau-induced dementia

MIR-NATs repress MAPT translation and aid proteostasis in neurodegeneration.

Plasma amyloid-β ratios in autosomal dominant Alzheimer's disease: the influence of genotype.

The role of SQSTM1 (p62) in mitochondrial function and clearance in human cortical neurons.

Familial Alzheimer's Disease Mutations in PSEN1 Lead to Premature Human Stem Cell Neurogenesis.

Modelling frontotemporal dementia using patient-derived induced pluripotent stem cells.

Maturation and phenotype of pathophysiological neuronal excitability of human cells in tau-related dementia.

Collaborators (14)

Olga Kopach

Claudia Manzoni

Zhongbo Chen

Dmitri Rusakov

Lauren Byrne

Jennifer Pocock

John S H Danial

Michela Alessandra Denti

Ross W. Paterson

Lucy Granat

Johan Jakobsson

Emad Moeendarbary

Tatiana Alvarez Giovannucci

Filip Tomczuk

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