7Tesla MRI Scanning in Alzheimer’s disease and Frontotemporal Lobar Degeneration

Study ID: 31477
Short Title: 7Tesla MRI Scanning in AD and FTLD
Organisation: University Hospital Southampton NHS Foundation Trust
Location: Southampton General Hospital
Condition: Dementia
Main Specialty: Dementias
Expected End Date: 01/10/2021
Postcode: SO16 6YD
Contact Name: R&D department
Contact Email: R&Doffice@uhs.nhs.uk
Active: Yes

Inclusion Criteria

Either pathological, genetic or biomarker evidence to suggest a disease in the FTLD pathological spectrum or Alzheimer’s disease, or a clinical diagnosis consistent with the same. FTLD includes the following clinical diagnoses: - Frontotemporal dementia (behavioural variant, semantic variant, non-fluent variant, progressive apraxia of speech). - Progressive supranuclear palsy - Corticobasal degeneration - poorly differentiated Tauopathy with features of FTLD Alzheimer’s disease includes the following clinical diagnoses: - Amnestic (classic) Alzheimer’s disease - Posterior cortical atrophy - Logopenic or mixed primary progressive aphasia - Frontal variant Alzheimer’s disease

Exclusion Criteria

Pregnancy The presence of non-MRI safe metal implants Implanted medical devices not certified as compatible with ultrahigh-field MRI (e.g.cardiac pacemakers) Lack of mental capacity to consent to study involvement Severe claustrophobia

Study summary:

There is a long history of research precisely describing the thinking difficulties that occur in different types of dementia. Recently there have been exciting discoveries about how this is caused by changes in brain cells as they become damaged, by malfunction and shrinkage in different parts of the brain. We will use a cutting edge brain scanning technology called “7T MRI” to measure in intricate detail what is going wrong in the brain of people with dementia - including the way that groups of cells in different brain areas are damaged, how they are activated during different tasks, and how they communicate with each other across the brain. We will link these changes to patients’ symptoms and, where possible, to the underlying damage to brain cells. The results of this work will increase our knowledge of the causes of dementia, and allow us to explain the causes of symptoms of dementia. It may also improve animal models of dementia, by testing in patients the predictions made from laboratory scientists elsewhere in the world. In the longer term, by studying how these problems change over time, we aim to develop tools that will allow us to assess the effectiveness of new drug treatments.

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