Category: Blog

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.

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.

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.

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.

To date, three of the thirteen OXPHOS genes still encoded in the mitochondria have been allotopically expressed (AE) in human cells with mutated versions of the same gene, thereby rescuing a respiratory defect. Now we have the first report of a new gene, COX2, being allotopically expressed in yeast, by mutating the gene to overcome the hydrophobicity of the mitochondrial membrane; a similar mutation has been shown to underlie the ability of the unusual case of the soybean COX2, which is a case of a native nuclear-encoded COX2 gene.

Intravenously delivered immunoglobulin G (IVIgG) is a mixture of antibodies extracted from human blood which has demonstrated promising preliminary results in clearing the beta-amyloid (Abeta) deposits that drive the pathogenesis of Alzheimer’s disease. A recent study compares multiple commercial sources of IVIgG and finds significant differences in their Abeta-binding activity, suggesting that results from impending clinical trials are likely to be highly dependent on the specific “brand” of IVIgG in use.