Alzheimer's disease (AD) is the most common cause of dementia in the Western world, accounting for up to 50-60% of all late-onset dementia cases. Neuropathologically, AD is characterised by abnormal accumulations of intracellular neurofibrillary tangles and extra-cellular amyloid plaques in the brain; additional features are deficits in multiple neurotransmitter signalling systems and synaptic loss. The objectives of this proposal are to study transgenic mouse models to define molecular mechanisms leading to amyloid and tau pathology and examine at what level they impact the normal signalling pathways of cognition.
Our basic aims are to
(i) investigate proliferation, neural differentiation, cell renewal, survival and synaptic plasticity in
(ii) highly relevant single or multiple transgenic AD mouse models with amyloidoses and tauopathies,
(iii) assess cognition, learning, memory and behaviour in the same mouse models and (iv) devise therapies to improve any deficiencies.
We expect the research outlined in this proposal to:
(i) increase our understanding of amyloid and tau pathology, enabling us
(ii) to explore diagnostic biomarkers and drug targets for AD and
(iii) to contribute to the fundamental knowledge of neuro-degenerative disease.
Fields of science
Call for proposal
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