Scientists are hoping to discover exactly how oily fish can protect against Alzheimer’s disease.
It is known that eating fish such as salmon, sardines and mackerel appears to cut the risk of developing dementia, BBC News website said.
But now, Cardiff University researchers Professor John Harwood, who is leading the research, said: “We put the mice through a maze, and the ones with normal brain functions learn quickly when to turn left and right, but the Alzheimer’s mice are absolutely hopeless at remembering.
It is suggested that the omega 3 oils contained in the fish could prevent the build-up of a protein called amyloid, which grows like a plaque on the brain of Alzheimer’s sufferers, and slows down brain functions.
Professor Harwood added: “There have already been a number of studies showing that people who consume a significant amount of oily fish or fish oil capsules seem to have a smaller incidence of Alzheimer’s disease.
Harriet Millward, of the Alzheimer’s Research Trust, said “We are funding 25 research projects in all, but the oily fish study looks very promising.
“We hope the research into the biology of Alzheimer’s disease will give us a greater understanding of how the disease develops and lead to other new treatments.“
In the meantime, the researchers say people should eat oily fish at least twice a week.
The three-year study will be carried out on mice which have been genetically designed to have an Alzheimer’s-like disease.
Researchers will monitor the effects of different diets on the mice.
Preliminary research has shown that feeding the mice oily fish improved their brain function.

Three-dimensional structure of the conserved pseudoknot found in human telomerase RNA, determined by UCLA biochemists using NMR spectroscopy.

UCLA biochemists have determined the three-dimensional structure of a major domain of telomerase, the enzyme that helps maintain telomeres--small pieces of DNA on the ends of chromosomes that act as protective caps--allowing DNA ends to be copied completely when cells are replicated, according to Science Daily online.
This is the first major piece of telomerase for which the structure is known. Telomerase plays a key role in most cancers, and this work ultimately may lead to targets for drug intervention, the scientists said. The discovery is the cover story in the March 4 issue of the journal Molecular Cell.
“Knowledge of the structure should provide insights into how telomerase works,“ said Juli Feigon, professor of chemistry and biochemistry at UCLA, who led the research group. Every time a cell divides, telomeres, which act like the plastic tips on the ends of shoelaces, get shorter. In the natural aging process, the telomeres eventually get so short that cells can no longer divide, and they die. While telomerase is turned off in most types of healthy cells in our bodies, it is active in the vast majority of cancer cells, Feigon said.
Because cancer cells divide rapidly, their telomeres should get shorter more quickly than normal cells. However, because cancer cells have high levels of telomerase activity, which rebuilds the telomeres, cancer cells can maintain the length of their telomeres indefinitely. Although it is not known whether telomerase activation is just a marker for cancer cells or involved in causing it, telomerase is an attractive target for development of anti-cancer drugs by pharmaceutical companies.
Mutations in the RNA are associated with the inherited diseases aplastic anemia and dyskeratosis congenita, which frequently are manifested by progressive bone-marrow failure.
For telomerase to be active, it needs the telomerase RNA and a protein called human telomerase reverse transcriptase, which is related to the reverse transcriptase protein that is important for replicating the AIDS virus. Feigon’s laboratory has been working on the RNA.
The structure reveals a “pseudoknot“ that is required for telomerase activity, at whose core three strands of RNA come together to form a triple helix. All vertebrate animals investigated so far have nearly the identical sequence of nucleotides through the triple helix, Theimer said.

Being financially comfortable appears to ease the woes of disability, at least in the short term, reports a University of Michigan study.
“When you get a major new problem in your life, you are likely to get over it--people are amazingly resilient--but it is easier and faster with financial resources,“ said study author Dr. Peter Ubel, a professor of internal medicine and psychology at the University of Michigan in Ann Arbor.
According to Yahoo, in an eight-year study of 478 people over the age of 50 experiencing temporary or chronic disability, 167 people whose income was above the median net worth of those in the study reported being substantially happier, less lonely and less sad than those whose income fell below the median.
However, two years later, those with lower median incomes reported an increase in happiness, closing the gap between the differing rates of the two groups, report the researchers.
For the study, researchers used data from the University of Michigan’s Health and Retirement study to track people’s emotional responses to being disabled.
After controlling for health, age and education, the researchers found those with higher incomes were about 10 percent more likely to report being happier than those with lower incomes, and less likely to report sadness or loneliness in the two years following the start of their disability.