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.
The discovery of natural antibodies against beta-amyloid, the major component of the plaques that characterise Alzheimer's disease, is a promising suggestion as to the potential effectiveness of a relatively straightforward immunotherapy.
Affibodies are artificial, antibody-like proteins generated through protein engineering techniques. ZAβ3, an affibody that targets amyloid-beta (Abeta), has been shown to prevent plaque formation and neurotoxicity in animal models of Alzheimer's disease. Affibodies like ZAβ3 might have important practical advantages over antibody-based Abeta-clearing agents, making this a promising new approach.
Daniel Kimbel joined our SENS Foundation Research Center team this week as a lab technician. Daniel will be assisting Lorenzo Albanello with our LysoSENS projects already in progress. Coming to us with a BA in Biological Sciences from Rice University, Daniel has demonstrated his commitment to pursuing the SENS objectives, by volunteering both at the research center (while it was still in Tempe) and at Arizona State University's Biodesign Institute.
Widespread optimism about the life-extension potential of calorie restriction (CR) is tempered by doubt that any significant number of people will ever adopt it as a lifestyle. However, thus far the search for "CR mimetics" – drugs that convey the same benefits on a normal calorie intake - has been fruitless. Here we review some of the prominent examples.
Unlike mouse embryonic stem cells (ESCs), human ESCs are highly prone to death after enzymatic dissociation from a growing cell cluster; as a result, researchers are forced to rely on far more laborious methods for their expansion. New research at the Scripps Institute has revealed the molecular basis for this frustrating limitation, and also uncovered two small-molecule drugs able to greatly improve the cells' survival.
Abeta Epitope DNA and Peptide Vaccination: Bridging the 'Therapeutic Threshold' for Cognitive Aging and Alzheimer's DiseasePosted by Michael Rae on April 26, 2010 | Chief Science Officer's Team
Immunotherapeutic clearance of beta-amyloid is the preferred regenerative medicine approach to the treatment and prevention of Alzheimer's disease (AD), but existing attempts to develop such therapies have been fraught with side-effects and limited efficacy, as well as concerns about clinical translatability. A new approach using DNA vaccines is showing great promise, and has the potential to be safe and cheap enough for deployment in pre-clinical AD - before any irreversible memory loss can occur.
Biomedical research has traditionally focused on identifying and correcting the abnormalities in metabolic pathways that lead to disease states. However, this approach suffers numerous side-effects due to the complexity of metabolism. It is also inappropriate to treating many age-related diseases, which arise as a result of damage accumulated over decades of normal function. Regenerative engineering, by focusing instead on the removal of this damage, largely avoids both of these chronic problems.
In addition to telomerase, some cancer cells become immortalised via the phenomenon known as ALT ("Alternative Lengthening of Telomeres"). A new paper published in Nature suggests that Zscan4, a gene essential for telomere maintenance in embryonic stem cells, may be the driver of the ALT mechanism.
The SENS Foundation Research Center would like to welcome Anne Corwin, an electrical engineer with a long-time interest in biotech and regenerative medicine, and Kelsey Moody, SENS Foundation's Academic Coordinator, to our growing team of in-house researchers.