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Deanna Z. Macek, MD
Wayne, NJ

Arch Ophthalmol. 1995;113(2):138-139.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

In the Editorial in the July 1993 issue of the ARCHIVES, Zack¹ maintains that genetic studies with mice will "surely lead to increased understanding and new treatments for ophthalmic disease." I do not share his optimism. Even closely analogous genetic defects in humans and animals tend to have markedly different phenotypic expressions and responses to treatment, owing to profound genetic and physiological differences. This severely compromises the utility of animal models.

Philosophers Hugh LaFollette and Niall Shanks have helped clarify the potential uses and limitations of animal models.² For an animal model to provide insights into a human disease, it must share the same causes as the analogous human disease. Superficial similarity is not enough to warrant extrapolating animal data to humans.

Even in the uncommon cases in which the causes are well understood and are very similar in humans and animals, animal models are undermined by "systemic . . . [Full Text PDF of this Article]

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