Dr. Lawrence A. Hansen has a double life he is proud to publicize in his writings and interviews.

On one hand, he is a neuroscientist at one of the finest institutions in the country — the University of California at San Diego. On the other hand, he is a member and a mouthpiece for People for the Ethical Treatment of Animals.

PeTA, of course, is an animal rights organization that holds the view that all living beings have the same basic right to life and freedom. A corollary of this position is that animals cannot be used by humans in any way, including their use in scientific research designed to advance human health and medical knowledge.

Dr. Lawrence Hansen regularly attends the Society for Neuroscience Annual Meeting, where he joins his PeTA colleagues in order to protest the “organization’s stated goal of broadening support for animal research.”

He has written numerous opinion pieces (for example, here, here and here) asserting with confidence that animal research will not lead to any advancements in human health, that the experiments are unnecessary because they can be conducted in human volunteers, and that the treatment of the animals in our nation’s laboratories amount to torture.

Dr. Hansen is wrong on all counts.

Animal research has contributed widely to human health. Multiple layers ensure the welfare of animals during experimentation. Methods do not exist today that would allow scientists to study the cellular and molecular mechanisms underlying disease in human volunteers non-invasively. This is what is really required to understand the evolution of a disease in a living organism and how we can interfere with its development. Indeed, a recent poll by the journal Nature revealed that nearly 92% of scientists agree with the statement “animal research is essential to the advancement of biomedical science.” The fact is that there are no current alternatives — otherwise, they would be used. This is the reason the scientific consensus on the topic is nothing short of overwhelming.

Being wrong is just one problem with Dr. Hansen. The other is the level of hypocrisy required for a scholar like him to criticize animal research while simultaneously being involved in the work. Specifically, Dr. Hansen is a co-author in animal studies that use transgenic mice to model Alzheimer’s disease in humans: here, here, here and here.

Justification for all these studies relies on the notion that one can model the disease in mice in ways that might be relevant to human patients — an idea that Dr. Hansen rejects vociferously. Was authorship on these studies forced upon him?

Perhaps Dr. Hansen will argue that he played a minor role in these studies, merely providing resources and reagents for the studies? This seems unlikely, as at least in one instance Dr. Hansen’s role is listed as having “conceived and designed the experiments.”

All these articles list the Neuropathology Core grant (NIH P50 AG005131), of which Dr. Hansen is the responsible Principal Investigator, as partly funding them. In other words, Dr. Hansen’s own federal grant has funded the animal research he presumably opposes. (Incidentally, as far as we can tell, the Aims of the grant do not include any animal research.)

Perhaps Dr. Hansen approves only of work with mice but not in other species? If so, it seems he fails to understand the concept of “animal rights.” The notion that all living beings have a right to live free from all human intervention would render his own work ethically wrong as well. Or does PeTA make an exception for his mice work? Maybe membership has its privileges?

Perhaps Dr. Hansen thinks that for some magic reason his work with mice is guaranteed to translate to humans, while findings in other species will not? One wonders if there something magical about the biology of mice? If mice can be used to model human disease, why couldn’t other animals? However, it doesn’t seem that Dr. Hansen holds mice work in high regard. Last year, in an interview, he stated:

“the amoral scientific problem with using rodents as models for neurodegenerative diseases is that rodents do not naturally develop Alzheimer disease or Parkinson`s disease. The only way to get what looks even a little like AD or PD pathology in rats and mice is to make them transgenic — that is, to insert human disease causing genes into the rodents. This does create a Frankenstein-like mutant model with some expression of AD or PD pathology which can be manipulated to make it go away. But reversing artificially induced AD or PD changes in animals that never naturally develop them is a far cry from curing the human diseases. The “cures” that work in the rodents have never worked when applied to humans. […] The species differences that have evolved over millions of years make animal models largely useless, except for the purposes of enhancing scientific careers and attracting lots of grant money.”

If this represents his scientific opinion, why in the world would he participate and fund the very same “unnecessary” experiments that create “Frankenstein-like” animals? Perhaps Dr. Hansen thinks his transgenic animals are under good care and condition, while the other ones down the hall that belong a colleague are being tortured instead?

Perhaps Dr. Hansen believes his studies are restricted to some basic biological process of Alzheimer’s that has no consequence for the human condition? But then, how would he justify the use of animals? And why would he write that his work “supports the possibility that modulators of the autophagy pathway might provide potential therapeutic effects.” Therapeutic effect for mice but not humans? Again this seems unlikely, as stated that mice do not develop AD or PD pathology naturally, and thus are not in need of any therapeutics.

The fact is that the justification behind his work can be found in the Introduction and Discussion sections within the very same articles he co-wrote. Dr. Hansen and his co-authors explain, for example, that:

It is important to note that neurogenesis persists in the aged brain; however, its rate declines with increasing age, as revealed by previous studies in rodents (Kuhn et al., 1996; Kempermann et al., 1998), nonhuman primates (Gould et al., 1999), and humans (Cameron and McKay, 1999). Despite this natural decline with age, previous studies have shown that the adult brain remains responsive to therapeutic interventions that enhance neurogenesis (Jin et al., 2003; Wise, 2003). Understanding the molecular mechanisms involved in AD-related alterations in neurogenesis might help guide the development of new therapies in this direction.

This is one of several passages illustrating the synergy between human, mouse and in vitro techniques in biomedical research, and highlights the similarities between development of the human disease and its recapitulation in animals models of AD. These are the very same scientific facts he denies and renounces in his interviews, OpEds, and PeTA demonstrations.

It would be worth for Dr. Hansen to dedicate some effort in justifying his own work with animals, studying a little bit more about the contributions of animal research to human health, and dedicating less of his time demonizing his colleagues for the wrong reasons.

Speaking of Research

Update: There is more discussion going on at DrugMonkey’s blog as well.