Neurites - projections from a neuron's cell body - become structurally abnormal in proximity to the extracellular aggregates that occur in both neurodegenerative disease and "normal" cognitive aging. These structural abnormalities have been suggested to play a role in cognitive pathology, by disrupting normal synaptic integration. Active immunotherapy against beta-amyloid (using the AN1792 antibody) has now been shown to reverse much of this structural deformity, even in cases where plaque clearance is incomplete.
New insights into the role of AID, a DNA demethylase, in the reprogramming process that produces induced pluripotent stem (iPS) cells are expected to allow greater efficiencies and permit the elimination of clinically problematic viral vectors and proto-oncogenes.
Serum amyloid P component (SAP) is a universal constituent of amyloid deposits, apparently regardless of the disease in question (and thus the other proteins present). Although methods have been developed to eliminate SAP from the body, this approach could have potentially serious side-effects. We announce a new SENS Research Foundation-funded project to tackle amyloid accumulation via the alternative, more direct approach of catalysing degradation of the pathogenic protein components.