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NRO’s domestic-policy blog, by Reihan Salam.

Why Brain Science Matters



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As Newt Gingrich surges in the polls, I thought I’d draw attention to his call for more investment in brain science, which features prominently in his “21st Century Contract with America“:

Maximize the speed and impact of medical breakthroughs by removing unnecessary obstacles that block new treatments from reaching patients and emphasizing research spending towards urgent national priorities, like brain science with its impact on Alzheimer’s, autism, Parkinson’s, mental health and other conditions knowledge of the brain will help solve. 

He elaborates on the potential impact of breakthroughs in brain science later on:

 

As Americans now live longer than ever, one of the greatest fiscal threats in health is the rising cost of treating Alzheimer’s patients. The current estimate is that the combined public and private cost of Alzheimer’s between today to 2050 will be $20 trillion.  That is one and a half times the current total federal debt.

But a smart emphasis on brain science and innovation today can change this projection for the better.

Brain scientists note that because Alzheimer’s is largely (but not entirely) a disease of older citizens you can have an enormous effect simply by postponing the onset of the disease by five years. The Alzheimer’s Association believes this could save between $5 and $10 trillion in the next four decades.  

In addition, investments in brain science hold enormous potential to improve the lives of those who struggle with Autism, Parkinson’s, and mental health trouble. Intensified research in this area could make untold contributions to understanding learning, cognition, and other important aspects of life. 

A strategy of maximizing the speed with which new science can be developed and implemented to help the patient has a greater potential to pay off in brain science than in any other area.

This happens to be one of my pet causes, and I’m immensely gratified to see Gingrich bring this issue to the attention of the wider public.

My interest in the subject was first sparked by an article by S. Jay Olshansky, Daniel Perry, Richard A. Miller, and Robert N. Butler. The authors explain that we’ve already since impressive increases in healthy lifespan for mice:

An extension of disease-free lifespan of approximately 40% has already been achieved repeatedly in experiments with mice and rats. These examples provide powerful new systems to study how aging processes influence disease expression and will yield clues about where to look for interventions that can slow down aging in people in a safe and effective way. Since many of aging’s biological pathways are conserved also in simple invertebrate species such as fruit flies, it should be possible to experimentally evaluate candidate intervention strategies rapidly.

Some people, including a proportion of centenarians, live most of their lives free from frailty and disability. Genetics play a critical role in their healthy survival. Identifying variation in these subgroups of humans holds great potential for improving public health. For example, Microsomal Transfer Protein (MTP) on Chromosome 4 has been identified as a longevity modifier in a sample of centenarians;17 there is strong evidence linking a common variant of KLOTHO, the KL-VS allele, to human longevity;18 and it has been demonstrated that lipoprotein particle sizes promote a healthy aging phenotype through codon 405 valine variation in the cholesteryl ester transfer protein (CETP) gene.19

Given the speed at which the study of aging has advanced and the ability to obtain research results quickly from the study of short-lived species, scientists have reason to be confident that a Longevity Dividend is a plausible outcome of aging research.

And so the authors advance a relatively modest goal:

If we succeed in slowing aging by seven years, the age-specific risk of death, frailty, and disability will be reduced by approximately half at every age. People who reach the age of 50 in the future would have the health profile and disease risk of today’s 43-year-old; those aged 60 would resemble current 53-year-olds, and so on. Equally important, once achieved, this seven-year delay would yield equal health and longevity benefits for all subsequent generations, much the same way children born in most nations today benefit from the discovery and development of immunizations. 

The economic benefits would be considerable, as the Alzheimer disease population alone is expected to quadruple to 16 million from now until 2050. To achieve the Longevity Dividend, the authors call for $3 billion in annual spending: 

 

The National Institutes of Health is funded at $28 billion in 2006, but less than 0.1% of that amount goes to understanding the biology of aging and how it predisposes us to a suite of costly diseases and disorders expressed at later ages. We are calling on Congress to invest 3 billion dollars annually to this effort; or about 1% of the current Medicare budget of $309 billion; and to provide the organizational and intellectual infrastructure and other related resources to make this work.

Specifically, we recommend that one-third of this budget ($1 billion) be devoted to the basic biology of aging with a focus on genomics and regenerative medicine as they relate to longevity science. Another third should be devoted to age-related diseases as part of a coordinated trans-NIH effort. One sixth ($500 million) should be devoted to clinical trials with proportionate representation of older persons (aged 65+) that include head-to-head studies of drugs or interventions including lifestyle comparisons, cost effectiveness studies, and the development of a national system for post-marketing surveillance. The remaining $500 million should go to a national preventive medicine research initiative that would include studies of safety and health in the home and workplace and address issues of physical inactivity and obesity as well as genetic and other early-life pathological influences. This last category would include studies of the social and economic means to effect positive changes in health behaviors in the face of current health crises – obesity and diabetes – that can lower life expectancy. Elements of the budget could be phased in over time, and it would be appropriate to use funds within each category for research training and the development of appropriate infrastructure. We also strongly encourage the development of an international consortium devoted to this task, as all nations would benefit from securing the Longevity Dividend.

With this effort, we believe it will be possible to intervene in aging among the baby boom cohorts, and all generations after them would enjoy the health and economic benefits of delayed aging. Such a monetary commitment would be small when compared to that spent each year on Medicare alone, but it would pay dividends an order of magnitude greater than the investment. And it would do so for current and future generations.

While many of Newt Gingrich’s ideas are profoundly flawed, this one strikes me as sensible. My guess is that Gene Healy would disagree. His latest column criticizes Gingrich for having big government instincts, and there is something to that charge. One can make a reasonable case that while an investment in brain science is an attractive proposition, so are many other investments that government shouldn’t be making. My rejoinder, and it’s hardly bulletproof, is that the federal government has already taken on the obligation of providing a health safety net for over-65s, and so taxpayers bear a disproportionately large share of the cost of meeting the needs of future AD sufferers. Investing in interventions that will sharply lower the cost of care thus seems like a good way to keep spending and taxes lower than they would be otherwise. 

Recently, Nicholas Wade of the New York Times reported on how purging senescent cells seems to have mitigated the impact of aging on mice:

 

Senescent cells accumulate in aging tissues, like arthritic knees, cataracts and the plaque that may line elderly arteries. The cells secrete agents that stimulate the immune system and cause low-level inflammation. Until now, there has been no way to tell if the presence of the cells is good, bad or indifferent.

The answer turns out to be that the cells hasten aging in the tissues in which they accumulate. In a delicate feat of genetic engineering, a research team led by Darren J. Baker and Jan M. van Deursen at the Mayo Clinic in Rochester, Minn., has generated a strain of mouse in which all the senescent cells can be purged by giving the mice a drug that forces the cells to self-destruct.

Rid of the senescent cells, the Mayo Clinic researchers reported online Wednesday in the journal Nature, the mice’s tissues showed a major improvement in the usual burden of age-related disorders. They did not develop cataracts, avoided the usual wasting of muscle with age, and could exercise much longer on a mouse treadmill. They retained the fat layers in the skin that usually thin out with age and, in people, cause wrinkling.

This is all very encouraging, and it will create enormous economic opportunities for entrepreneurs in the life sciences. 



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