"The best way to avoid Alzheimer's disease is to become a lawyer, scientist or doctor, according to a study. Having a stimulating job offers protection later in life - and researchers say those three careers come out top...People with challenging jobs may have to work hard, but the payoff could be some protection against Alzheimer's disease later in life, new research suggests.

In a study of more than 10,000 older Swedish adults who were part of a twin registry, researchers found that people with a history of "complex" work had a lower risk of Alzheimer's disease. The same held true even among twin pairs in which one was affected by Alzheimer's but the other was not — a situation that factors in the influence of genes and upbringing.

The findings suggest that complex jobs may "provide some mental exercise" that helps delay the onset of dementia later in life, said the study's lead author, Dr. Ross Andel of the University of South Florida in Tampa. And that does not mean you need to be a rocket scientist, Andel told Reuters Health.

The study found that the complexity of a worker's interactions with other people - with teaching as an example of higher complexity — showed the strongest link to a lower Alzheimer's risk. Men and women with the most challenging jobs in this regard were 22 percent less likely to develop the disease compared with those with the least complex work.

These individuals also had a slightly lower risk of all forms of dementia, according to findings published in the Journal of Gerontology: Psychological Sciences.

The findings fit in with other research that has linked higher education, as well as mentally stimulating leisure activities like reading and doing crossword puzzles, to a lower risk of Alzheimer's disease.

Although it's not clear that these are cause-and-effect relationships, scientists speculate that people who stay mentally engaged throughout their lives may have a greater "cognitive reserve" that allows them to withstand more of the brain damage seen in Alzheimer's disease before symptoms begin.

The physical-fitness principle of "use it or lose it" may apply, in a fashion, to the brain as well, Andel said."ABC News: Complex work may help ward off Alzheimer's

"OBJECTIVE: Caregiver input is important in the assessment of depression in Alzheimer disease (AD), but depression and subjective burden can bias this input. METHODS: In a 12-week, controlled, clinical trial of sertraline in depressed AD patients, authors correlated caregiver mood and subjective burden on several patient mood measures, incorporating varied degrees of caregiver input. RESULTS: Caregiver variables accounted for up to 33% of the variance in patient mood ratings. Caregiver depression and burden decreased regardless of treatment assignment. CONCLUSION: Caregiver depression and burden affect their rating of AD patients' mood, but the majority of variance is due to patient characteristics."National Library of Medicine

Research reported in the American Academy of Neurology has found that the more vascular risk factors someone has the greater the risk of developing Alzheimer's disease. 'Vascular' means vessels that carry or circulate fluids, such as blood.
Vascular risk factors were defined as high blood pressure, diabetes, hypertension, heart disease, and current smoking.

The researchers from Columbia University followed up 1,138 people (average age mid 70's) over 5 years. None of them had dementia when the study began. Their findings showed that;

The risk of Alzheimer disease increased with the number of vascular risk factors

Diabetes and current smokers were the strongest risk factors by themselves.
Four risk factors i.e. diabetes, hypertension, heart disease, and current smoking, were associated with a higher risk of Alzheimer's Disease

People with 3 or more vascular risk factors had nearly three-and-one-half times the risk of developing Alzheimer’s as those with none.
Research Implications
These research findings have implications for minimizing vascular health risks through;

Preventative health screening

Appropriate medical control of any symptoms of vascular disorders and /li]
Having a healthy lifestyle that includes a good balanced diet, not smoking and taking regular exercise.alzheimers.about.com

An ingredient in green tea has prevented Alzheimer's disease-like brain damage in mice, researchers report. The compound, called epigallocatechin-3-gallate (EGCG), decreased production of the protein beta-amyloid, which accumulates in the brains of Alzheimer's patients and causes nerve damage and memory loss. "The findings suggest that a concentrated component of green tea can decrease brain beta-amyloid plaque formation," senior researcher Dr. Jun Tan, director of the Neuroimmunology Laboratory at the the University of South Florida's Silver Child Development Center, said in a prepared statement. Reporting in the Sept. 21 issue of the Journal of Neuroscience, the research team worked with mice genetically programmed to develop a disease mimicking human Alzheimer's.more

"Silencing Alzheimer's: targeting a key enzyme with gene therapy reversed course of disease in mouse models...In mice, that had been genetically engineered to develop Alzheimer's disease, scientists were able to reverse the rodents' memory loss by reducing the amount of an enzyme that is crucial for the development of Alzheimer's disease.
"What we are showing is a proof of principle that stopping the synthesis of a protein that is necessary for the formation of the telltale plaques reverses the progression of the disease, and more importantly, the cognitive function of these mice, which had already been impaired, has now recovered," says Inder Verma, professor in the Laboratory for Genetics at the Salk Institute for Biological Studies.

The findings, which are the result of a close collaboration between researchers at the Salk Institute and scientists at the University of California in San Diego, are reported in an advance on-line publication of Nature Neuroscience.

In the past, gene therapy has been mainly used to deliver normal genes into cells to compensate for defective versions of the gene causing disease. In their study, the researchers used gene therapy to silence a normally functioning gene. Exploiting a mechanism called RNA interference, they were able to turn down the gene that helps produce the characteristic amyloid plaques that are one of the hallmarks of Alzheimer's disease.

"Within a month of treatment, mice that had already suffered memory deficits could learn and remember how to find their way through a water maze," says co-author Robert Marr, a post-doctoral researcher in Verma's lab.

"It appears that these mice can come back from a very severe level of disease progression," adds first author Oded Singer, also at the Salk. "This is a very important finding because humans are usually diagnosed when the disease has already progressed relatively far."

But he warns that it is too early to make direct comparisons with the human disease, since mice ordinarily don't develop the symptoms of the disease unless they are genetically engineered to do so.

Amyloid plaques, which are insoluble protein clumps in the brain, can precede the onset of dementia by many years. These plaques are formed when enzymes cleave the amyloid precursor protein (APP) releasing the toxic beta amyloid fragments that clump together to form the sticky plaques. One of the enzymes doing the cleaving is called beta secretase or BACE1.

And although the production of beta amyloid occurs in all brains, healthy brains are able to clear away excess amounts. Brains of people with Alzheimer's disease, on the other hand, are unable to control beta amyloid accumulation.

For several years now, drug companies have been trying to find a drug that inhibits BACE1 and thus prevent beta amyloid from building up in brains of people with Alzheimer's disease. But so far, the goal has remained elusive.

Instead of looking for chemical compounds to inhibit BACE1, Oded Singer, collaborating with the laboratories of Fred H. Gage at the Salk Institute and lead author Eliezer Masliah at UCSD, resorted to small biological molecules, called short interfering RNA, or siRNA, which derail the process of translating genes into proteins. They work like a dimmer switch, reducing the amount of available gene product, in this case the enzyme BACE1.

A modified lentivirus, which has been developed in Verma's lab, delivered the siRNAs into the brain cells of the transgenic mice that were producing vast amounts of human beta-amyloid and whose brains where littered with plaques.

"When you compare the brains of treated and untreated mice, the difference is striking. Silencing BACE1 reduced the number and size of plaques by two thirds within a month, which is incredibly fast," says Singer.

Co-authors of this work also include Edward Rockenstein and Leslie Crews, both at UCSD.

Alzheimer's disease is a progressive neurodegenerative disorder and the most common cause of dementia among the elderly in the United States, affecting 4.5-5 million adults - 10 times more than those affected by Parkinson's disease. Starting with mild memory problems and ending with severe brain damage, Alzheimer's usually begins after the age of 60, the risk increasing with age."eurekalert.org