Alzheimer's Disease and Related Dementias
New studies on the risk factor's for ADRD, as well as the protective factors which can help gaurd against these diseases, are now being published on a regular basis. These studies are reavealing more and more about the inner working's of this of diseases. A sampling of this research is collected below.
Risk Factors for ADRD
Many of the risk factors for Alzheimer's disease and related dementia's are the same familiar risks associated with the development of other chronic diseases:
A study by the Kaiser Permanente Division of Research shows a dementia risk from carrying a lot of weight in the abdominal area. The study found that normal weight individuals who have a big belly in their 40s are 89% more likely to develop dementia later in life. While obesity at middle age had already been linked to later dementia, this is the first research to suggest that people who are not overweight also increase their risk if they are “apple-shaped” rather than “pear-shaped.” The reason is not yet clear, but it’s suspected that abdominal fat may pump out higher levels of insulin. High levels of belly fat have previously been linked to a higher risk of developing diabetes, heart attack, and stroke.
Experts expect the number of people with Alzheimer’s to soar as a result of the obesity epidemic. Evidence is mounting that dementia, like heart attack and stroke, has lifestyle causes. “If you are overweight at 60, you are twice as likely to have Alzheimer’s by the time you are 75,” said Clive Ballard, director of research at Britain’s Alzheimer’s Society.
A new study suggests that depression, rather than being an early sign of Alzheimer’s, is actually a risk factor for the disease. In other words, Alzheimer’s does not cause the depression – the depression may cause the Alzheimer’s. Study participants were followed for up to 13 years. Those who developed Alzheimer’s showed no increase in depressive symptoms during the three or four years preceding clinical diagnosis. However, participants with more depressive symptoms at the start of the study were more likely to later develop Alzheimer’s.
An earlier study found that individuals scoring very high on a personality test’s pessimism scale had a 30% increased risk of developing dementia several decades later. Those scoring very high on the test’s depression scale likewise had a 30% higher risk of developing dementia. The risk was even higher – 40% - for those who scored very high on both the depression and anxiety scales. The study was designed to test more rigorously the findings of an earlier, exploratory study conducted at Mayo Clinic that suggested pessimism, depression, anxiety, and social introversion could be risk factors for Alzheimer’s disease.
The inflammation theory of Alzheimer’s disease led to a study of the preventive effect of non-steroidal anti-inflammatory drugs (NSAIDs) such as Celebrex and Aleve on cognitive decline in older people who did not have Alzheimer’s disease. While the study was halted early due to adverse cardiovascular events now known to be linked to some of the drugs used, researchers said it was already clear that the drugs provided no protective effect against mental decline.
Scientists have known for years that the ApoE-4 variation of the Apo-E gene is linked to Alzheimer’s disease. Now they’ve found that the 25% of the population that carries this genetic variant is more vulnerable to the herpes simplex virus, the virus that causes cold sores, and that the activity of herpes in the brain is greater than in people carrying other forms of the gene. People with the ApoE-4 gene who are infected with herpes are more likely to get Alzheimer’s disease than people infected with herpes who have a different form of the ApoE gene or than people who have the ApoE-4 gene but don’t have herpes. While the mechanism for this connection is not yet well understood, one possibility is that the body’s immune response against herpes somehow damages the brain, and that such damage is worse in people with ApoE-4. Inflammation is the earliest change that can be detected in a brain affected by Alzheimer’s disease, before any plaques and tangles and long before any behavioral changes are seen. Such inflammation is often a byproduct when the immune system fights an infection.