The preliminary results of a clinical trial for a disease of "premature aging" are hopeful and inspiring, though they cannot directly inform the development of rejuvenation biotechnologies.

Recent studies show the potential -- and the limits -- of inducing telomerase expression in aging mice. We place these results in context and explore their implications for new treatments targeting age-related degeneration in humans.

UCLA Researchers have exploited a recently-discovered mammalian system for the mitochondrial import of nuclear-encoded RNA to import, express, and demonstrate functional protein translation from engineered mRNA and tRNA constructs. They used this system, with modifications for mitochondrial targeting and orthotopic translation, to rescue respiration in human mitochondriopathy cells. While further characterization and extension is clearly needed, this approach appears offer great promise for the correction of age-related mitochondrial DNA mutations.

As discussed previously,

"Senescent" cells progressively restrict the body's capacity for tissue renewal and secrete factors that disrupt local tissue homeostasis. A new study provides proof-of-concept that ablation of these cells can delay -- and potentially contribute to the reversal of -- age-related tissue dysfunction and disease.

To develop an unbreachable defense against cancer, SENS Foundation is pursuing the WILT (Wholebody Interdiction of Lengthening of Telomeres, or OncoSENS) strategy of preemptively deleting genes essential to the cellular telomere-maintenance mechanisms (TMM) from all somatic cells, while ensuring ongoing tissue repair and maintenance through periodic re-seeding of somatic stem-cell pools with autologous TMM-deficient cells whose telomeres have been lengthened ex vivo.

As we have previously reviewed, a comprehensive suite of rejuvenation biotechnologies must include the removal of extracellular aggregates from aging cells and tissues.

Efficient, safe methods of gene therapy will be essential enabling technologies for the repair or obviation of several of the cellular and molecular lesions driving age-related disease and dysfunction, notably the accumulations of mutations in mitochondrial and nuclear DNA (including the medium-term obviation of the latter through WILT), as well as the introductio

It has been an exciting period ever since Dr. Doris Taylor of the University of Minnesota's Center for Cardiovascular repair outlined her results prior to publication in 2008 at the Foundation's Understanding Aging: Biomedical and Bioengineering Apporoaches conference at UCLA.

I'm delighted to be able to share with you our research report, prepared for the first 10 months of 2010, by Tanya Jones (our Director of Research Operations), working with our researchers and my CSO Team.  I thought it would be of interest to our supporters, and serve as a precursor to our 2010 Year End Report, which is currently under production as part of our finalizing our 2010 accounts.

The often-mooted question of whether "aging itself" is or is not a "disease" has long been mooted in biogerontological circles, with a long-held rhetorical preference for asserting that it is not, but rather, that it is a risk factor for the specific diseases of aging.(1) By contrast, the same fundamental semantic dispute was initially resolved in the opposite direction with regard to age-related cognitive decline and dementia, beginning in the early decades after Alois Alzheimer and Emil Kraepelin first identified the pathological basis of the Alzheimer's disease (AD) until the ea

As we reviewed in a previous posting on a recent advance in genetic engineering with zinc finger nucleases (ZFNs),

The intrinsic biological aging process is driven by the accumulation of damage to the cellular and molecular structures in tissues and organs, resulting from the biochemical side-effects of essential metabolic processes. In turn, this rising decay of cellular and molecular structures drives the age-related rise in disability, disease, dependence, dementia, and ultimate risk of death.

SENS Foundation's CSO, Dr Aubrey de Grey, was first featured in Wired magazine in 2008, shortly before the Methuselah Foundation's initial USA-based conferences. Two years on, he's now returned in a more candid and detailed interview, discussing how the tactics involved in bringing rejuvenation biotechnologies to the attention of mainstream science have evolved and begun to bear fruit.

Neurofibrillary tangles (NFT -- cytoplasmic inclusions composed of phosphorylated and abnormally-cleaved species of  tau protein) accumulate in the aging brain, and at higher levels in Alzheimer's disease and in vulnerable regions in a range of other neurodegenerative diseases; they are closely associated with neuronal death and with onset of clinical dementing disease.

In addition to its widely-anticipated potential to provide highly-effective therapies for genetic disorders, somatic gene therapy is an essential enabling technology for the repair or obviation of several  of the cellular and molecular lesions driving age-related disease and dysfunction (notably the accumulations of mutations in mitochondrial and nuclear DNA).

Age-related accumulation of mutations in mitochondrial DNA (mtDNA) are widely suspected to play an important role in the degenerative aging process, albeit that controversy remains as to the mechanism(s) linking the two.

Last summer, California-based LifeStar Institute assembled a panel of leaders in the science of aging to ask them the question at the core of their research. How far can the potential of new biomedical therapies to slow, arrest, or even reverse the damage of aging be brought to bear against the challenge of global graying?

A variety of extracellular aggregates accumulate in the aging body, and strong evidence exists for their contribution to age-related morbidity and pathology. This makes them targets for regenerative engineering: the rescue of youthful tissue function through the restoration of structure from such damage. In the case of extracellular aggregates, the most promising biomedical approach is their clearance with targeted immunotherapy.

In late 2008, we reviewed then-unpublished work by Dr. Mark Pepys, who was working on an ambitious project anticipated to allow for the disaggregation of nearly all disease-associated amyloids. Dr. Pepys subsequently accepted an invitation to present those early results at the fourth SENS scientific conference(1).

Aggregates of beta-amyloid (Aß) and other malformed proteins accumulate in brain aging and neurodegenerative disease, leading progressively to neuronal dysfunction and/or loss. The regenerative engineering solution to these insults is therapeutic clearance of aggregates, extracellular (such as Aß plaques) and intracellular (such as soluble, oligomeric Aß).

Progress toward the goal of tissue rejuvenation via stem cells and tissue engineering ("RepleniSENS")  is badly hampered by the surprising fragility of human embryonic stem cells (hESC) relative to mouse ESC (mESC). Unlike their murine counterparts, hESC undergo extensive cell death following  enzymatic single-cell dissociation; as a result, researchers are forced to rely on laborious mechanical microdissection, or on narrowly-control enzymatic dissociation that ensures that hESC remain above a minimum cluster size.

At the core of SENS Foundation's strategy to comprehensively cure the diseases and disabilities of aging is a new biomedical heuristic: regenerative engineering.(1-3) To date, the dominant therapeutic strategy for both specific age-related diseases and (to the extent that it has been contemplated) the degenerative biological aging process itself, has been based on altering metabolic pathways.

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, and thereby rescued a respiratory defect: ATPase6^1,2, ND4³, and ND1⁴.