I'm not going to quote the comments, but simply add my two cents worth to this discussion.
I *really really* wish people would get off the whole telomere kick.
Telomeres and telomerase are to a large degree irrelevant to the longevity of your *mind* unless you intend to stay in your current biological body indefinately.
Telomeres are *only* important for dividing cells, that means your epithelial cells or "external" cells that are exposed to environmental wear and tear in some way (skin, gut, lung) and perhaps the endotheilial cells (on the surfaces of your blood vessels). They may also play a role in which hyperactive cell division occurs such as cancer or AIDS.
Fossel did the aging field a huge disservice when he suggested that telomeres explain relatively all aspects of aging. Brain aging is much more likely to be based on mitochondrial DNA damage leading to energy insufficiency and/or cell death and/or recombination and shortening in the repeated ribosomal DNA sequences leading to a reduction in protein synthesis. Neurons do not divide and so telomere shortening is unlikely to be involved in their "aging" (Fossel's suppositions that they effect glial cells and indirectly neurons is a real stretch).
So with regard to clones & telomeres the only question becomes what impact does shortened telomeres have on "cloned" organisms? In short it makes them less healthy and causes some organ systems to age more quickly. If you create an organism with shorter telomeres than the natural version, then those tissues that depend on dividing cells are likely wear out more quickly.
Is this significant? Not if we plan to replace those organ systems with versions grown in pigs or laboratory grown equivalents. Also irrelevant if we plan to upload.
Also *completely* irrelevant if you envision being able to augment the genome with multiple genes with a ten year time frame or completely replace the genome with an alternate program within a 20 year time frame. The telomere shortening appears to only affect genes on the ends of 2-6 chromosomes (see work by Olivia Pierra-Smith), so whatever is involved as effectors downstream from the telomeres can be replaced, adjusted, augmented, etc.) with complete disregard to the telomere length once we undertand the location and function of those genes.
So please, if you want to drag up telomeres or telomerase, drag them up with a disclaimers about *what* specifically you want to apply them to that has real significance to our evolution and long term survival. From my perspective they represent a lot of noise that actually distracts us from the real problems in aging and longevity.