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High blood pressure could affect memory

A new research has found that high blood pressure in middle age plays a critical role in whether blood pressure in old age may affect memory and thinking.

“Our findings bring new insight into the relationship between a history of high blood pressure, blood pressure in old age, the effects of blood pressure on brain structure, and memory and thinking,” study author Lenore J Launer, PhD, of the National Institute on Aging in Bethesda, Md., and a member of the American Academy of Neurology, said.

For the study, 4,057 older participants free of dementia had their blood pressure measured in middle-age, (average age of 50). In late life (an average age of 76) their blood pressure was remeasured and participants underwent MRIs that looked at structure and damage to the small vessels in the brain.

They also took tests that measured their memory and thinking ability. The study found that the association of blood pressure in old age to brain measures depended on a history of blood pressure in middle age. Higher systolic (the top number on the measure of blood pressure) and diastolic (the bottom number on the measure of blood pressure) blood pressure were associated with increased risk of brain lesions and tiny brain bleeds.

This was most noticeable in people without a history of high blood pressure in middle age. For example, people with no history of high blood pressure in middle age who had high diastolic blood pressure in old age were 50 percent more likely to have severe brain lesions than people with low diastolic blood pressure in old age.However, in people with a history of high blood pressure in middle age, lower diastolic blood pressure in older age was associated with smaller total brain and gray matter volumes.

Blame four new genes for increased breast cancer risk

Researchers have added four new genes to the growing list of those known to cause increased breast cancer risk when mutated.

Sean Tavtigian, Ph.D., an HCI investigator, professor in the Department of Oncological Sciences at the University of Utah (U of U), and one of three joint-principal investigators on the study, said BRCA1 and BRCA2 aren’t the whole story when it comes to inherited breast cancer risk. We’ve known for a long time that more genes had to be responsible and several have since been discovered, by us and by others.

Tavtigian said originally, the gene we are currently studying, called RINT1, was not considered a human cancer susceptibility gene. But then we discovered there was a two- to three-fold increase in risk for breast cancer in families that carry a mutation in that gene. Surprisingly, RINT1 was also found to increase risk for a broad spectrum of gastrointestinal and gynecological cancers in these families.

In another study led by Tavtigian, mutations in three other genes—MRE11A, RAD50, and NBN—were also confirmed to increase breast cancer risk, as reported in the journal Breast Cancer Research on June 3.
New gene involved in Parkinson’s disease

Researchers have identified a new gene involved in Parkinson’s disease, a finding that may one day provide a target for a new drug to prevent and potentially even cure the debilitating neurological disorder.

A handful of genes have been identified in inherited cases of Parkinson’s disease. The research team of Dr Ming Guo, the study team leader, associate professor of neurology and pharmacology and a practicing neurologist at UCLA was one of two groups worldwide that first reported in 2006 in the journal Nature that two of these genes, PTEN-induced putative kinase 1 (PINK1) and PARKIN, act together to maintain the health of mitochondria – the power house of the cell that is important in maintaining brain health. 

Mutations in these genes lead to early-onset Parkinson’s disease.

In this study, the team found that the new gene, called MUL1 (also known as MULAN and MAPL), plays an important role in mediating the pathology of the PINK1 and PARKIN. 

The study, performed in fruit flies and mice, showed that providing an extra amount of MUL1 ameliorates the mitochondrial damage due to mutated PINK/PARKIN, while inhibiting MUL1 in mutant PINK1/PARKIN exacerbates the damage to the mitochondria. 

In addition, Guo and her collaborators found that removing MUL1 from mouse neurons of the PARKIN disease model results in unhealthy mitochondria and degeneration of the neurons.

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