Mice have been cured of the functional symptoms of Alzheimer’s while retaining the pathological symptoms. Human trials of the molecular-level treatment, which involved modifying a single protein, are at least two years away, but the exciting thing is that this represents a new approach to understanding and treating the disease.

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Johns Hopkins University hopes to be at the forefront of what the US National Science Foundation predicts will be a $1 trillion nanotechnology industry during the next decade, by means of its recently opened Institute for NanoBioTechnology. The institute is one of dozens of similar initiatives cropping up at universities and organizations across the country, says an article in the Baltimore Sun, joining the Nanobiotechnology Center — a five-university consortium (including Howard and Princeton) on Cornell’s New York campus, Northwestern University’s US $34 million nano-manufacturing facility, and the University of Maryland’s two-year-old NanoCenter.

“Our mission is world domination, literally, to be the world leader in nanobiotechnology,” the institute’s director told the Sun. Funded with $6 million, which includes seed money for research proposals, the Hopkins institute is “virtual.” It has no office, but instead functions as a network of over 100 multidisciplinary faculty and staff.

Molecular Approach to Alzheimer’s

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The modification of a single amino acid out of 695 has prevented memory loss and dementia in lab mice that had all the pathological signs of a human strain of Alzheimer’s, including plaque buildup. Whether the same modification would work in humans is at least two years away from being tested, but in any event the research is important in shedding new light on the progression of Alzheimer’s, providing a completely different view of the disease and pointing in the direction of a new way to treat it.

Even at the “old age” of 18 months, mice that received the treatment were symptom-free. Those that did not get the treatment showed symptoms of Alzheimer’s by age 3 months. “Our mice all had the same Alzheimer’s disease, but we simply changed one amino acid.”