Sometimes there's just too much interesting research out there to link to one by one: inroads against age-related disease; uncovering new and important mechanisms of metabolism; progress in promising classes of future therapy. The list is endless. So sometimes, I throw together these roundups of diverse topics. Let's start with some promising gene therapy work for Parkinson's disease, and move on to Alzheimer's and cancer:

PET scans show gene therapy normalizes brain function in Parkinson's patients:

Brain scans used to track changes in a dozen patients who received an experimental gene therapy show that the treatment normalizes brain function - and the effects are still present a year later.

...

The patients only received the viral vector-carrying genes to the side of the brain that controls movement on the side of their body most affected by the disease. ... The gene makes an inhibitory chemical called GABA that turns down the activity in a key node of the Parkinson’s motor network. The investigators were not expecting to see changes in cognition, and the scans confirmed that this did not occur.

Position emission tomography (PET) scans were performed before the surgery and repeated six months later and then again one year after the surgery. The motor network on the untreated side of the body got worse, and the treated side got better. The level of improvements in the motor network correlated with increased clinical ratings of patient disability, added Dr. Feigin.

A novel way found to prevent protein plaques implicated in Alzheimer's:

Both studies used mice that were genetically engineered to produce human cystatin C as well as abundant amounts of amyloid beta plaques in their brains. The cystatin C bound to the soluble, non-pathological form of amyloid beta in these mice and inhibited the aggregation and deposition of amyloid beta plaques in the brain.

The research shows that cystatin C binds soluble amyloid beta also in the human brain, and suggests that this binding inhibits its aggregation into insoluble plaques in humans, says Dr. Levy. Cystatin C production and body fluid levels vary among healthy individuals and can be influenced by certain hormones, aging, and certain pathological conditions, she says. Furthermore, it was recently demonstrated that a genetic variation in the cystatin C gene in human populations is linked to a greater risk of developing Alzheimer’s disease during aging.

These findings suggest, says Dr .Levy, that even subtle modifications of cystatin C protein levels could affect amyloid beta accumulation and deposition in the brain, thereby modifying disease progression.

I seem to recall research indicating that the rate of turnover of amyloid is very fast, on the order of days. Alzheimer's is not a slow buildup of a compound that can just be removed, but rather a slow increase in the difference between generation and clearance rates. The best answer would be to determine where the fault lies and fix it; some work is aimed in that direction, but the majority aims to introduce new ways to clear amyloid without doing anything to repair the underlying issue. This is, alas, the dominant path in present day medical research.

But on to cancer:

Immune system can drive cancers into dormant state:

Like the older theory, cancer immunoediting suggests that conflict between cancers and the immune system naturally takes place but proposes that three very different outcomes can result. The immune system can eliminate cancer, destroying it; the immune system can establish equilibrium with cancer, checking its growth but not eradicating it; or the cancer can escape from the immune system, likely becoming more malignant in the process.

Until this latest study, evidence for the second outcome was lacking.

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"We don't think the immune system has evolved to handle cancers," Schreiber notes. "Cancer is typically a disease of the elderly, who have moved beyond their reproductive years, so there probably was no evolutionary pressure for the immune system to find a way to fight cancer."

Schreiber, Smyth and Old speculate that from the immune system's point-of-view, a cancerous cell may look like a cell infected by an invading microorganism. To overcome the safeguards that prevent the immune system from attacking the body's own tissues, the tumor has to have a high level of immunogenicity, or ability to provoke an immune reaction. Cancer cells can reduce their immunogenicity by changing the materials they present to the immune system to more closely resemble those presented by normal tissue. This enables the third outcome of the immunoediting theory: escape.

Equilibrium sometimes may be a more common outcome of tumor-immune encounters than elimination. According to the researchers' theory, some of us may harbor dormant tumors that either developed spontaneously or from exposure to carcinogens. They propose that these quiescent tumors are unleashed only as we age or are exposed to environmental, infectious or physical stresses that cause a breakdown of the immune system.

Greater understanding of the tools already present in our body will be a real boost to fighting cancer, coming in the midst of a revolution in our capacity to alter and make use of those biochemical tools. Improving, retraining and redirecting the mechanisms of the immune system to attack specific cells is a very promising field of research. A good thing too, as we need effective, reliable cures for cancer if we're going to benefit from other strands of healthy life extension research.

Posted by Reason at November 19, 2007 8:46 PM | TrackBack (0)