The results have come to light in the GRAPHIC study, funded by the British Heart Foundation. Over 450 families in Leicestershire took part in the study.

High blood pressure affects around three in ten adults in the UK and is one of the main causes of strokes and heart attacks. Risk factors for high blood pressure include being overweight and having too much salt in your diet. Genes are also important factors. The GRAPHIC study showed that variations in a gene called WNK1, which produces a protein in the human kidney, also affects blood pressure levels in the population at large.

The team of researchers at the University of Leicester was led by Professor Nilesh Samani and co-researchers Professor Paul Burton and Dr Martin Tobin. Professor Samani, British Heart Foundation Professor of Cardiology at the University of Leicester, commented: "High blood pressure is a common health problem that raises the risk of developing heart disease and stroke. For effective prevention and treatment we need to understand the root causes. The findings of our research represent an important step towards this goal. It implicates a gene that can now be a target for further analysis. This particular gene may interact with other factors such as a salt intake and could be a specific target for drug therapy. "

Professor Samani added: "I should like to express our sincere thanks to the families who have taken part, to the general practitioners who have assisted with the study and to the British Heart Foundation. Without their support, this work would not have been possible."

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Undaunted by the size of the LRRK2 gene and protein, Andrew West, Ph.D., a postdoctoral fellow and co-first author of the paper, spent months extracting the full-length gene from human brain samples and developing reliable experiments to test how mutations affected LRRK2's activity. Co-first author Darren Moore, Ph.D., also a postdoctoral fellow, built the tools to get bacteria to make mounds of LRRK2 protein and two mutant versions and also tracked down the LRRK2 protein's location inside cells.

The research team's experiments showed that the LRRK2 protein, in addition to its role as a kinase, actually sits on mitochondria, cells' energy-producing factories, where it likely interacts with a complex of proteins whose failure has also been implicated in Parkinson's disease.

Mutations in LRRK2 were first tied to Parkinson's disease in 2004 and to date explain perhaps 5 percent to 6 percent of familial Parkinson's disease (specifically so-called autosomal dominant cases, in which inheriting a single faulty copy of the gene results in disease) and roughly 1 percent of Parkinson's disease in which there is no family history. But few of the gene's genetic regions have been analyzed in depth.

"As researchers comb through the rest of the LRRK2 gene, it seems likely that more mutations will be found and that it will be tied to more varieties of the disease," says Dawson. What's known about LRRK2 so far suggests that it might connect diseases long thought to be distinct, particularly Parkinson's disease and conditions known as "diffuse Lewy body disease," named for the bundles of certain proteins that build up inside cells in the brain in affected people. As a result, studying LRRK2 might improve understanding of and eventually treatment for more than just Parkinson's disease itself, Dawson says.

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