In the study of people aged over 55, researchers found “repetitive negative thinking” (RNT) is linked to subsequent cognitive decline as well as the deposition of harmful brain proteins linked to Alzhiemer’s. The researchers say RNT should now be further investigated as a potential risk factor for dementia, and psychological tools, such as mindfulness or meditation, should be studied to see if these could reduce dementia risk. Dr. Natalie Marchant said: “Depression and anxiety in mid-life and old age are already known to be risk factors for dementia. Here, we found that certain thinking patterns implicated in depression and anxiety could be an underlying reason why people with those disorders are more likely to develop dementia.” Taken alongside other studies, which link depression and anxiety with dementia risk, we expect that chronic negative thinking patterns over a long period of time could increase the risk of dementia. We do not think the evidence suggests that short-term set backs would increase one’s risk of dementia.
The researchers suggest that RNT may contribute to Alzheimer’s risk via its impact on indicators of stress such as high blood pressure, as other studies have found that physiological stress can contribute to amyloid and tau deposition. The researchers hope to find out if reducing RNT, possibly through mindfulness training or targeted talk therapy, could in turn reduce the risk of dementia. Researchers are currently working on a large project to see if interventions such as meditation may help reduce dementia risk by supporting mental health in old age.
Early-Life Education Improves Memory in Old Age, Especially for Women
Education appears to protect older adults, especially women, against memory loss, according to a study by investigators at Georgetown University Medical Center. The results suggest that children, especially girls, who attend school for longer will have better memory abilities in old age. This may have implications for memory loss in Alzheimer’s disease and other dementia’s. The investigators found that their memory performance became progressively worse with aging. However, more years of early-life education countered these losses, especially in women. In men, the memory gains associated with each year of education were two times larger than the losses experienced during each year of aging. However, in women, the gains were five times larger. For example, the declarative memory abilities of an 80-year-old woman with a bachelor’s degree would be as good as those of a 60-year-old woman with a high school education. So, four extra years of education make up for the memory losses fom 20 years of aging. “Evidence suggests that girls often have better declarative memory than boys, so education may lead to greater knowledge gains in girls; education may particularly benefit memory abilities in women, even years later in old age.”
How toxic protein spreads in Alzheimer’s disease
Toxic versions of the protein tau are believed to cause death of neurons of the brain in Alzheimer’s disease. A new study shows that the spread of toxic tau in the human brain in elderly individuals may occur via connected neurons. The researchers could see that beta-amyloid facilitates the spread of toxic tau. “Reseach suggests that toxic tau may spread across different brain regions through direct neuronal connections, much like infectious diseases may spread to different cities through different transportation pathways. The spread is restricted during normal aging, but in Alzheimer’s disease the spread may be facilitated by beta-amyloid, and likely leads to widespread neuronal death and eventually dementia” There are two proteins that are known to be linked to Alzheimer’s disease, beta-amyloid, which forms what is known as plaque in the brain, and tau, which forms tangles within the brain cells. Previous studies have linked the spread of toxic tau, in particular, to degeneration of the brain and symptoms such as memory impairment. Intense research is ongoing to better understand how toxic tau spreads in the brain, in order to develop new therapies that can stop the spread and thereby stop the disease. Ongoing clinical trials are currently evaluating whether antibodies developed to bind to tau might stop the disease. Findings have implications for understanding the disease, but more importantly for the development of therapies against Alzheimer’s, which are directed against other bete-amyloid or tau. The results suggest that therapies that limit uptake of tau into the neurons or transportation or excretion of, could limit disease progression.