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Annette Karmiloff Smith - What could babies possibly tell us about dementia
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THE 17TH ANNUAL MALCOLM JEEVES LECTURE
Professor Annette Karmiloff Smith Birkbeck Centre for Brain & Cognitive Development University of London
It may seem paradoxical to study babies in order to understand Alzheimer’s dementia (AD) which only occurs in adults! And why Down syndrome (DS)? Babies born with DS have an extra copy of chromosome 21, and one of the genes implicated in the AD brain pathology (the APP gene) in the general population is located on chromosome 21 and thus over-expressed throughout DS development. Thus, DS is an excellent model for AD. Moreover, despite 100% of individuals with DS getting the brain pathology of Alzheimers by about early adulthood, not all go on to develop dementia. What protects those who do not? What are the risk factors for those who do? Because we believe in tracing adult outcomes back to their developmental roots in infancy, we are studying babies with DS to ascertain whether we can identify early markers at the genetic, cellular, neural, cognitive, behavioural or environmental levels of risk and protective factors for subsequent AD, that we could then target for intervention in early development. We’ve joined forces with a group at University College London who are studying adults with DS, with and without dementia, with colleagues examining the cell biology and genetics of our DS populations, as well as with colleagues at St.Thomas Hospital, London who are imaging the brains of foetuses with Down syndrome who, after birth, will join our project. This talk will focus on the DS infant studies of memory, attention, and sleep, using behavioural, eye-tracking and electrophysiological measures of brain activity, arguing for a developmental approach to an adult phenotypic outcome.
Professor Annette Karmiloff Smith Birkbeck Centre for Brain & Cognitive Development University of London
It may seem paradoxical to study babies in order to understand Alzheimer’s dementia (AD) which only occurs in adults! And why Down syndrome (DS)? Babies born with DS have an extra copy of chromosome 21, and one of the genes implicated in the AD brain pathology (the APP gene) in the general population is located on chromosome 21 and thus over-expressed throughout DS development. Thus, DS is an excellent model for AD. Moreover, despite 100% of individuals with DS getting the brain pathology of Alzheimers by about early adulthood, not all go on to develop dementia. What protects those who do not? What are the risk factors for those who do? Because we believe in tracing adult outcomes back to their developmental roots in infancy, we are studying babies with DS to ascertain whether we can identify early markers at the genetic, cellular, neural, cognitive, behavioural or environmental levels of risk and protective factors for subsequent AD, that we could then target for intervention in early development. We’ve joined forces with a group at University College London who are studying adults with DS, with and without dementia, with colleagues examining the cell biology and genetics of our DS populations, as well as with colleagues at St.Thomas Hospital, London who are imaging the brains of foetuses with Down syndrome who, after birth, will join our project. This talk will focus on the DS infant studies of memory, attention, and sleep, using behavioural, eye-tracking and electrophysiological measures of brain activity, arguing for a developmental approach to an adult phenotypic outcome.