Monthly Archives: май 2018

Enhanced lifestyle counselling prevents cognitive decline even in people who are carriers of the APOE4 gene, a common risk factor of Alzheimer’s disease, according to a new study published in JAMA Neurology.

The two-year FINGER trial involved 60–77 year-old people living in Finland with risk factors for memory disorders. The study participants were divided into two groups: one of the groups was given regular lifestyle counselling and the other enhanced lifestyle counselling. Enhanced counselling involved nutrition counselling, physical and cognitive exercises and support in managing the risk of cardiovascular diseases.

Earlier findings from the FINGER trial have shown that the regular lifestyle counselling group had a significantly increased risk of cognitive and functional impairment compared to the intervention group, i.e. the group receiving enhanced counselling.

Now the researchers analysed whether the presence of the APOE4 gene affected the intervention results. The analysis included 1,109 persons of whom 362 were carriers of the APOE4 gene.

The findings show that enhanced lifestyle counselling prevented cognitive decline despite the presence of the risk gene. Analyses carried out within the groups also indicate that the intervention results might even be better in carriers of the APOE4 gene.

Paper: “Effect of the Apolipoprotein E Genotype on Cognitive Change During a Multidomain Lifestyle Intervention

Reprinted from materials provided by the University of Eastern Finland

New research sheds light on how a breakdown in the brain’s vascular system predates the accumulation of toxic plaques and tangles in the brain that bring about Alzheimer’s disease.

Nearly 50 percent of all dementias, including Alzheimer’s, begins with the breakdown of the smallest blood vessels in the brain and their protective “gatekeeper cells,” according to the study, published in Nature Medicine.

That catastrophe causes a communications failure called small vessel disease. Many people with that disease also have white matter disease, the wearing away of fatty myelin that allows neurons to transfer messages within the brain network. In an animal model, researchers found that brain deterioration associated with dementia may start as early 40 in humans.

For more than 25 years, scientists have known that white matter disease impedes a person’s ability to learn or remember new things, slows thinking and causes people to fall more often due to balance issues. They identified a link between crippled small blood vessels in the brain and white matter disease but didn’t know what started that process until now.

The study explains that pericytes, gatekeeper cells that surround the brain’s smallest blood vessels, play a critical role in white matter health and disease via fibrinogen, a protein that circulates in blood. Fibrinogen develops blood clots so wounds can heal. When gatekeeper cells are compromised, an unhealthy amount of fibrinogen slinks into the brain and causes white matter and brain structures, including axons (nerve fibers) and oligodendrocytes (cells that produces myelin), to die.

In a mouse model, the researchers used an enzyme known to reduce fibrinogen in blood and the brain. White matter volume in the mice returned to 90 percent of their normal state, and white matter connections were back to 80 percent productivity, the study found.

Paper: “Pericyte degeneration causes white matter dysfunction in the mouse central nervous system”

Reprinted from materials provided by USC.