Exercising to improve our cardiovascular strength may protect us from cognitive impairment as we age, according to a new study by researchers at the University of Montreal and its affiliated Institut universitaire de gératrie de Montréal Research Centre. “Our body’s arteries stiffen with age, and the vessel hardening is believed to begin in the aorta, the main vessel coming out of the heart, before reaching the brain. Indeed, the hardening may contribute to cognitive changes that occur during a similar time frame,” explained Claudine Gauthier, first author of the study. “We found that older adults whose aortas were in a better condition and who had greater aerobic fitness performed better on a cognitive test. We therefore think that the preservation of vessel elasticity may be one of the mechanisms that enables exercise to slow cognitive aging.”
The researchers worked with 31 young people between the ages of 18 and 30 and 54 older participants aged between 55 and 75. This enabled the team to compare the older participants within their peer group and against the younger group who obviously have not begun the aging processes in question. None of the participants had physical or mental health issues that might influence the study outcome. Their fitness was tested by exhausting the participants on a workout machine and determining their maximum oxygen intake over a 30 second period. Their cognitive abilities were assessed with the Stroop task. The Stroop task is a scientifically validated test that involves asking someone to identify the ink colour of a colour word that is printed in a different colour (e.g. the word red could be printed in blue ink and the correct answer would be blue). A person who is able to correctly name the colour of the word without being distracted by the reflex to read it has greater cognitive agility.
The participants undertook three MRI scans: one to evaluate the blood flow to the brain, one to measure their brain activity as they performed the Stroop task, and one to actually look at the physical state of their aorta. The researchers were interested in the brain’s blood flow, as poorer cardiovascular health is associated with a faster pulse wave,at each heartbeat which in turn could cause damage to the brain’s smaller blood vessels. “This is first study to use MRI to examine participants in this way,” Gauthier said. “It enabled us to find even subtle effects in this healthy population, which suggests that other researchers could adapt our test to study vascular-cognitive associations within less healthy and clinical populations.”
The results demonstrated age-related declines in executive function, aortic elasticity and cardiorespiratory fitness, a link between vascular health and brain function, and a positive association between aerobic fitness and brain function. “The link between fitness and brain function may be mediated through preserved cerebrovascular reactivity in periventricular watershed areas that are also associated with cardiorespiratory fitness,” Gauthier said. “Although the impact of fitness on cerebral vasculature may however involve other, more complex mechanisms, overall these results support the hypothesis that lifestyle helps maintain the elasticity of arteries, thereby preventing downstream cerebrovascular damage and resulting in preserved cognitive abilities in later life.”
A little dirt trails with Lana…^_^ #bike4life #biketillupuke #bikelife #bike #adventures
Out of the shower haha #workout #sweaty #workoutface
"One’s mind, once stretched by a new idea, never regains its original dimensions."- Oliver Wendell Holmes
(Image Caption: Human neurons differentiated from induced pluripotent stem cells, with cell nuclei shown in blue and synapses in red and green. Credit: Credit: Zhexing Wen/Johns Hopkins Medicine)
A genetic variation linked to schizophrenia, bipolar disorder and severe depression wreaks havoc on connections among neurons in the developing brain, a team of researchers reports. The study, led by Guo-li Ming, M.D., Ph.D., and Hongjun Song, Ph.D., of the Johns Hopkins University School of Medicine and described online Aug. 17 in the journal Nature, used stem cells generated from people with and without mental illness to observe the effects of a rare and pernicious genetic variation on young brain cells. The results add to evidence that several major mental illnesses have common roots in faulty “wiring” during early brain development.
“This was the next best thing to going back in time to see what happened while a person was in the womb to later cause mental illness,” says Ming. “We found the most convincing evidence yet that the answer lies in the synapses that connect brain cells to one another.”
Previous evidence for the relationship came from autopsies and from studies suggesting that some genetic variants that affect synapses also increase the chance of mental illness. But those studies could not show a direct cause-and-effect relationship, Ming says.
One difficulty in studying the genetics of common mental illnesses is that they are generally caused by environmental factors in combination with multiple gene variants, any one of which usually could not by itself cause disease. A rare exception is the gene known as disrupted in schizophrenia 1 (DISC1), in which some mutations have a strong effect. Two families have been found in which many members with the DISC1 mutations have mental illness.
To find out how a DISC1 variation with a few deleted DNA “letters” affects the developing brain, the research team collected skin cells from a mother and daughter in one of these families who have neither the variation nor mental illness, as well as the father, who has the variation and severe depression, and another daughter, who carries the variation and has schizophrenia. For comparison, they also collected samples from an unrelated healthy person. Postdoctoral fellow Zhexing Wen, Ph.D., coaxed the skin cells to form five lines of stem cells and to mature into very pure populations of synapse-forming neurons.
After growing the neurons in a dish for six weeks, collaborators at Pennsylvania State University measured their electrical activity and found that neurons with the DISC1 variation had about half the number of synapses as those without the variation. To make sure that the differences were really due to the DISC1 variation and not to other genetic differences, graduate student Ha Nam Nguyen spent two years making targeted genetic changes to three of the stem cell lines.
In one of the cell lines with the variation, he swapped out the DISC1 gene for a healthy version. He also inserted the disease-causing variation into one healthy cell line from a family member, as well as the cell line from the unrelated control. Sure enough, the researchers report, the cells without the variation now grew the normal amount of synapses, while those with the inserted mutation had half as many.
“We had our definitive answer to whether this DISC1 variation is responsible for the reduced synapse growth,” Ming says.
To find out how DISC1 acts on synapses, the researchers also compared the activity levels of genes in the healthy neurons to those with the variation. To their surprise, the activities of more than 100 genes were different. “This is the first indication that DISC1 regulates the activity of a large number of genes, many of which are related to synapses,” Ming says.
The research team is now looking more closely at other genes that are linked to mental disorders. By better understanding the roots of mental illness, they hope to eventually develop better treatments for it, Ming says.
The majesty of the outdoors :) #adventures