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APBs – protein complexes associated with telomeric DNA in ALT (Alternative Lengthening of Telomeres) cancer cells – are the leading candidates for the sub-cellular site at which the ALT mechanism occurs. Recent work involving the generation of artificial APBs has shed light on their composition and function, providing hints as to how ALT might be disabled.

Parkinson’s disease is characterised by the loss of dopaminergic neurons from the substantia nigra, and cell therapy is being actively pursued as a means to replace the losses. Most trials to date have used fetal tissue, an approach that although transiently effective is unscalable and prone to immune rejection. Human dopaminergic neurons differentiated from stem cells have historically had poor therapeutic efficiency, but a new study using an improved differentiation protocol has shown much more positive results.

Aggregates of beta-amyloid protein (Abeta) and other malformed proteins accumulate in both “normal” brain aging and neurodegenerative disease, leading to neuronal loss. Their removal by immunotherapy is a central plank of the SENS platform, and the most clinically advanced. Gantenerumab, a new fully human anti-Abeta monoclonal antibody, has just completed a Phase I trial.

The elimination from the body of telomerase, the enzyme used by most cancer cells to maintain their DNA through unlimited numbers of cell divisions, is the central component of the WILT (Whole-body Interdiction of Lengthening of Telomeres) strategy proposed by SENS Research Foundation as a universal and unbreachable defence against all forms of cancer. Concerns have been raised, however, that telomerase may have other biologically important functions, making its elimination dangerous or impossible. Fortunately, recent work by Nobel laureate Carol Greider indicates a lack of any such activity.