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BRAIN REPEATS

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Repeat polymorphisms as genetic modifiers of brain function in healthy subjects...

Repeat polymorphisms as genetic modifiers of brain function in healthy subjects and Huntington disease mutation carriers Neuropsychiatric disorders such as dementia and depression are among the leading causes of disability and exert a dramatic burden on Europe’s healthcare systems. In order to devise more effective therapies it is essential to eluci... ver más

30/09/2017

UNIVERSITY COLLEGE...

98K€

Presupuesto del proyecto: 98K€

Líder del proyecto

UNIVERSITY COLLEGE LONDON No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2017-09-30

MSCA-IF-2015-EF: Marie Skłodowska-Curie Individual F...

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1 Participantes

UNIVERSITY COLLEGE LONDON

97.73K€ | Lider

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Duración del proyecto: 18 meses Fecha Inicio: 2016-03-07
Fecha Fin: 2017-09-30

Líder del proyecto

UNIVERSITY COLLEGE LONDON No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 98K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Neuropsychiatric disorders such as dementia and depression are among the leading causes of disability and exert a dramatic burden on Europe’s healthcare systems. In order to devise more effective therapies it is essential to elucidate their genetic basis. However, to date genetic association studies have only identified a small fraction of the genetic determinants, possibly due to neglect of some important genomic variations, especially DNA repeat expansions. Expanded DNA repeats above a certain threshold are associated with various neurological disorders, the most common of which are polyglutamine diseases caused by exonic triplet (cytosine-adenine-guanine (CAG)) repeat expansions leading to a range of cognitive and psychiatric abnormalities. Emerging findings indicate that even CAG repeat length variations in the normal range in polyglutamine disease-associated genes (PDAGs) can affect mental health and cognition. Nevertheless, virtually nothing is known about the biological mechanisms through which these genetic variations affect brain structure and function. Therefore, the key objective of this proposal is to evaluate the effects of CAG repeat polymorphisms in PDAGs on brain structure and function, both in healthy controls and carriers of the mutation for Huntington disease (HD), the most common polyglutamine disease. To this end I will: 1) Systematically assess the association between these genetic polymorphisms and mental health, cognition and brain morphometric and functional MRI imaging in a large cohort of well-characterized control subjects and HD mutation carriers, and 2) Perform pathway analysis using gene expression data already available from these participants in order to elucidate the underlying molecular pathways. This proposal is unique as it translates novel insights into the pathophysiology of polyglutamine diseases to those of more common, complex disorders, thereby accelerating development of effective therapies for all patient groups.

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