Differences in the Neurophysiology of Infants with Down Syndrome May Predict Protective/Risk Markers for Subsequent Alzheimer’s Disease
Poster Feb 01, 2016
Esha Massand1,2, Hana D’Souza1,2, George Ball1,2, Maria Eriksson1, Charlotte Dennison1, Joanna Ball1 & Annette Karmiloff-Smith1,2
Background;
Most individuals with DS: AD brain pathology by middle age but not all get dementia
Amyloid precursor protein (APP) gene on Hsa21 over-expressed from infancy onwards
Signs of amyloid plaque build-up already present in some infants at 20 months (Gyure et al., 2011).
Still not understood why some do/don’t go on to develop AD dementia
Only way to fully understand phenotypic endpoint at neural, cognitive or behavioural levels: trace it back to its developmental origins (Karmiloff-Smith 1998)
This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License
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When there is a need to quickly analyze samples using a number of different PCR assays, it is likely that optimal conditions for each assay will not be the same. First, different assays often will require different annealing temperatures for their primers. In addition, amplicons may be designed to be of different lengths and therefore require varying durations of the extension step.
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