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Projects funded by the Dementia Consortium

Modulation of CSF1R: a promising strategy to control neuroinflammati

Target - CSF1R-IL34

The contribution of ARUK, CRO and Industry partners was optimal. We were lucky to form a very productive collaboration… As a collaboration with a translational objective, this has been the most positive and productive experience I’ve had so far.
The contribution of ARUK, CRO and Industry partners was optimal. We were lucky to form a very productive collaboration… As a collaboration with a translational objective, this has been the most positive and productive experience I’ve had so far.

Dr Diego Gomez-Nicola, University of Southampton

The project validated IL34 as a target for controlling microglial proliferation in the brain and aimed to develop and optimise small molecule inhibitors and antibodies to block the interaction between CSFR1 and its ligand IL34.

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ALS disease models and therapeutic drug screen

Target - TDP-43

The Dementia Consortium has been essential in bringing my academic research to a level that would now be considered by companies working in early drug discovery. This has been done not only by providing the funding but as importantly creating and facilitating a network of collaborators that have contributed with ideas, expertise and project management
The Dementia Consortium has been essential in bringing my academic research to a level that would now be considered by companies working in early drug discovery. This has been done not only by providing the funding but as importantly creating and facilitating a network of collaborators that have contributed with ideas, expertise and project management

Dr Marco Baralle, International Centre for Genetics Engineering and Biotechnology, Italy

The project identified compounds that reduced or cleared aggregates of TDP-43 and restored TDP-43 function. A series of novel small molecule compounds were identified that prevented TDP43 inclusions.

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The role of P2Y6R in mice in cognition, neuronal loss and tauopathy

Target - P2Y6

The Dementia Consortium project provided…invaluable expertise and advice in translation and drug development…[the] hands-on expertise of the Dementia Consortium team was invaluable
The Dementia Consortium project provided…invaluable expertise and advice in translation and drug development…[the] hands-on expertise of the Dementia Consortium team was invaluable

Prof Guy Brown, University of Cambridge

The project validated P2Y6R as a novel dementia drug target and examined inhibition of the P2Y6 receptor expressed in microglia, a target that plays a critical role in excessive neuronal phagocytosis during neurodegeneration.

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Developing novel small molecules as effective inhibitors of the NLRP3 inflammasome

Target - NLRP3

The grant employed a postdoc in Manchester for a short period. We were able to achieve a publication which helps career development
The grant employed a postdoc in Manchester for a short period. We were able to achieve a publication which helps career development

Prof David Brough, University of Manchester

The aim of this project was to test and optimise novel small molecule inhibitors of the NLRP3 inflammasome. The project developed and characterised a small molecule tool kit/assay for interrogating and validating NLRP3 inflammasome-dependent responses in cells.

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Validating TTBK1 as a target for AD: TTBK1 knock-down and small molecule inhibitor approaches

Target - TTBK1

We would like to express our sincere gratitude for the opportunity to participate in the Dementia Consortium collaboration. The input of the funding partners based on their experience in drug discovery is very important and will be a benchmark for us in the future
We would like to express our sincere gratitude for the opportunity to participate in the Dementia Consortium collaboration. The input of the funding partners based on their experience in drug discovery is very important and will be a benchmark for us in the future

Prof Tsuneya Ikezu, Boston University

The project tested the hypothesis that supressing TTBK1 could prevent progression of AD through suppression of pTau accumulation and associated neuroinflammation.

CLPP-dependent activation of mitochondria quality control signalling in neurodegenerative diseases

Target - CLPP

The project benefited from the DC framework by regular meetings with ARUK and the research partner and updates with the industry partners. These meetings facilitate thorough analysis of the data and support decision making for follow-up steps
The project benefited from the DC framework by regular meetings with ARUK and the research partner and updates with the industry partners. These meetings facilitate thorough analysis of the data and support decision making for follow-up steps

Dr Nicoleta Moisoi, De Montfort University

The project tested the hypothesis that activating the mitochondrial peptidase CLPP, enhances mitochondrial quality control signalling which has a neuroprotective action in models of Parkinson’s disease.

ER-mitochondria signalling as a new target for Dementia (VAPB-PTPIP51 tethering)

Target - VAPB-PTPIP51

The input from members was intrinsic in developing the core structure of the project. Moreover, the expertise in drug discovery by consortium members and by EVOTEC scientists has been essential for progress on this crucial component of the project. We do not have such skills with our academic collaborators.
The input from members was intrinsic in developing the core structure of the project. Moreover, the expertise in drug discovery by consortium members and by EVOTEC scientists has been essential for progress on this crucial component of the project. We do not have such skills with our academic collaborators.

Prof Chris Miller, King’s College London

The aim of this project is to confirm the hypothesis that damage to the endoplasmic reticulum (ER) mitochondria signalling via loss of the interaction between the VABP and PTPIP51 (ER-mitochondrial tethers), is a driver of early pathology in FTD/ALS with relevance also to Alzheimer’s disease and Parkinson’s disease.

Identification of tool compounds targeting the SRSF1-dependent nuclear export of pathological C9ORF72-repeat transcripts

Target - C9ORF72

This model of bringing in industry partners to complement academic work has many benefits. [It allows]… independent validation of project by industrial and academic researchers. This is especially critical in this time where data reproducibility is at an all-time low.
This model of bringing in industry partners to complement academic work has many benefits. [It allows]… independent validation of project by industrial and academic researchers. This is especially critical in this time where data reproducibility is at an all-time low.

Dr Tennore Ramesh & Guillaume Hautbergue,

University of Sheffield

The aim of the project is to demonstrate that inhibiting the interaction between SRSF1 and C9orf72 prevents the build up of pathogenic dipeptide repeat proteins in FTD/ALS. C9orf72 genetic mutations cause the majority of familial and sporadic ALS and FTD.