Professor J rgen G?¶tz and Dr Lars Ittner are based at Sydney University's Alzheimer's and Parkinson's Disease Laboratory at the Brain and Mind Research Institute, having moved from the University of Zurich/Switzerland three years ago.

In the article they review what we have learned from disease models of Alzheimer's and related dementias, and in particular how they have contributed to the early diagnosis and the prospect of a treatment strategy. They also discuss their groundbreaking work, together with research by others that has led to the identification of novel players and promising drug targets.

"At present, neither Alzheimer's nor related dementias can be cured," said Professor G?¶tz. "Current treatment approaches include vaccination, anti-inflammatory drugs, and modulators for formation, aggregation and clearance of toxic proteins that accumulate in the brains of Alzheimer patients. Many of the new therapeutic strategies have their foundation in disease models as the work of J rgen G?¶tz and Lars Ittner highlights," he said.

The Alzheimer's and Parkinson's Disease Laboratory headed by Professor G?¶tz works to identify the mechanisms that lead to progressive neurodegeneration and dementia, and study the effects of genetics, aging and associated disorders such as diabetes, as well as dietary aspects.

The researchers are convinced that by adopting a healthier lifestyle and introducing early diagnosis and a targeted therapy, Alzheimer's disease can be successfully treated in the near future.

The article appears in the current issue of Nature Reviews Neuroscience (Vol. 9, Issue 7, 532-544, July 2008).

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They found that in almost one-third of individuals, methylation changed over that 11-year span, but not all in the same direction. Some individuals gained total methylation in their DNA, while others lost. "What we saw was a detectable change over time, which showed us proof of the principle that an individual's epigenetics does change with age," says M. Daniele Fallin, Ph.D., an associate professor of epidemiology at the Johns Hopkins Bloomberg School of Public Health. "What we still didn't know was why or how, but we thought 'maybe this, too, is something that's heritable' and could explain why certain families are more susceptible to certain diseases."

The team then measured total methylation changes in a different set of DNA samples collected from Utah residents of northern and western European descent. These DNA samples were collected over a 16-year span from 126 individuals from two- and three-generation families.

Similar to the Icelandic population, the Utah family members also showed varied methylation changes over time. But they found that family members tended to have the same kind of change-if one individual lost methylation over time, they saw similar loss in other family members.

"We still haven't concretely figured out what this means for health and disease, but as an epidemiologist, I think this is very interesting, since epigenetic changes could be an important link between environment, aging and genetic risk for disease," Fallin says.

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