Michael Duchen

Professor of Physiology

University College London

United Kingdom

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Research Interests

Biochemistry

100%

Cell Biology

80%

Metabolic Biology

80%

Mitochondrial Biology

80%

Oxidative Stress

60%

Neuroprotection

30%

Neurochemistry

30%

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Recent Grants

Grant: Open

Role of microvascular dysfunction in mitochondrial disease: impact of mtDNA mutations on microvascular function as a cause of multisystem mitochondrial disease

Open Date: 2023-08-01

Close Date: 2026-07-01

Grant: Close

Targeting Mitochondrial Dysfunction in iPSc-Derived Neurons from Vici Syndrome Patients: Towards Novel Treatments

Open Date: 2023-03-01

Close Date: 2026-02-01

Grant: Close

causes and consequences of impaired metabolism in GBA1 related Parkinson’s Disease

Open Date: 2021-11-01

Close Date: 2024-10-01

Grant: Close

Exploring novel treatment strategies for primary mitochondrial disease. Collaboration with Nannatherapeutics

Open Date: 2020-09-01

Close Date: 2023-12-01

Grant: Close

Targeting pathways to metabolic dysfunction in Down syndrome-associated Alzheimer’s disease using iPSC derived neurons as a platform for drug discovery

Open Date: 2020-01-01

Close Date: 2023-01-01

Michael Duchen

Professor of Physiology

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Research Interests

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Recent Grants

Articles17

The mitochondrial ATP synthase as an ATP consumer—a surprising therapeutic target

Nrf2 regulates glucose uptake and metabolism in neurons and astrocytes

PolyQ length-dependent metabolic alterations and DNA damage drive human astrocyte dysfunction in Huntington's disease.

NAD(P)H binding configurations revealed by time-resolved fluorescence and two-photon absorption.

The PERKs of mitochondria protection during stress: insights for PERK modulation in neurodegenerative and metabolic diseases

Paradoxical neuronal hyperexcitability in a mouse model of mitochondrial pyruvate import deficiency

Polymerogenic neuroserpin causes mitochondrial alterations and activates NFκB but not the UPR in a neuronal model of neurodegeneration FENIB.

A Plate Reader-Based Measurement of the Cellular ROS Production Using Dihydroethidium and MitoSOX.

Analysis of Organization and Activity of Mitochondrial Respiratory Chain Complexes in Primary Fibroblasts Using Blue Native PAGE.

Assessing the Redox Status of Mitochondria Through the NADH/FAD<sup>2</sup><sup>+</sup> Ratio in Intact Cells.

Constitutive activation of the PI3K-Akt-mTORC1 pathway sustains the m.3243 A > G mtDNA mutation

Allosteric activation of Hsp70 reduces mutant huntingtin levels, the clustering of N-terminal fragments, and their nuclear accumulation

Rewiring cell signalling pathways in pathogenic mtDNA mutations

Selective mitochondrial antioxidant MitoTEMPO reduces renal dysfunction and systemic inflammation in experimental sepsis in rats

The spectrum of neurodevelopmental, neuromuscular and neurodegenerative disorders due to defective autophagy

Activation of the Integrated Stress Response and ER Stress Protect from Fluorizoline-Induced Apoptosis in HEK293T and U2OS Cell Lines

Excitotoxicity Revisited: Mitochondria on the Verge of a Nervous Breakdown

Collaborators8

Manolis Fanto

Jorge Oliveira

Albena Dinkova-Kostova

Rodolfo Lavilla

Pablo M. Garcia-Roves

Angus Bain

Dr Olga Baron

Andreas Neueder

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