The Developing Brain: There is no final, optimal state

To reflect the ongoing structural changes in the adolescent and twenty-something brain, many journalists and scientists use words and phrases like “unfinished,” “work in progress,” “under construction” and “half-baked.”

Such language implies that the brain eventually reaches a kind of ideal state when it is “done.” But there is no final, optimal state.

The human brain is not a soufflé that gradually expands over time and finally finishes baking at age 30.

Yes, we can identify and label periods of dramatic development—or windows of heightened plasticity—but that should not eclipse the fact that brain changes throughout life.

Whether we can, at this moment in time, meaningfully link this life stage to neuroscience seems a tenuous proposition at best. By itself, brain biology does not dictate who we are.

The members of any one age group are not reducible to a few distinguishing structural changes in the brain.

Ultimately, the fact that a twenty-something has weaker bridges between various brain regions than someone in their thirties is not hugely important—it’s just one aspect of a far more complex identity.

Leukoaraiosis: 'Harmless' condition shown to alter brain function in elderly

Researchers at the Mayo Clinic say a common condition called leukoaraiosis, made up of tiny areas in the brain that have been deprived of oxygen.

They appear as bright white dots on MRI scans, is not a harmless part of the aging process, but rather a disease that alters brain function in the elderly.

Results of their study are published online in the journal Radiology. "There has been a lot of controversy over these commonly identified abnormalities on MRI scans and their clinical impact," said Kirk M. Welker, M.D., assistant professor of radiology in the College of Medicine at Mayo Clinic in Rochester, Minn.

"In the past, leukoaraiosis has been considered a benign part of the aging process, like gray hair and wrinkles."

 Leukoaraiosis, also called small vessel ischemia and often referred to as unidentified bright objects or "UBOs" on brain scans, is a condition in which diseased blood vessels lead to small areas of damage in the white matter of the brain.

The lesions are common in the brains of people over the age of 60, although the amount of disease varies among individuals.

"We know that aging is a risk factor for leukoaraiosis, and we suspect that high blood pressure may also play a role," Dr. Welker said.

Dr. Welker's team performed functional MRI (fMRI) scans on cognitively normal elderly participants recruited from the Mayo Clinic Study of Aging between 2006 and 2010.

In 18 participants, the amount of leukoaraiosis was a moderate 25 milliliters, and in 18 age-matched control participants, the amount of disease was less than five milliliters.

The patients were imaged in an MRI scanner as they performed a semantic decision task by identifying word pairs and a visual perception task that involved differentiating straight from diagonal lines.

fMRI is a special type of magnetic resonance imaging that measures metabolic changes in an active part of the brain.

Although both groups performed the tasks with similar success, the fMRI scans revealed different brain activation patterns between the two groups.

Compared to members of the control group, patients with moderate levels of leukoaraiosis had atypical activation patterns, including decreased activation in areas of the brain involved in language processing during the semantic decision task and increased activation in the visual-spatial areas of the brain during the visual perception task.

"Different systems of the brain respond differently to disease," Dr. Welker explained. "White matter damage affects connections within the brain's language network, which leads to an overall reduction in network activity."

He pointed out that identifying leukoaraiosis in the brain is important, both for individual patients undergoing brain mapping for surgery or other treatments and for research studies.

 For improved neurological health, Dr. Welker said efforts should be taken to prevent leukoaraiosis from occurring.

"Our results add to a growing body of evidence that this is a disease we need to pay attention to," he said.

"Leukoaraiosis is not a benign manifestation of aging but an important pathologic condition that alters brain function."

Gene switch rejuvenates failing mouse brains

Gene switch rejuvenates failing mouse brains

Step aside, Sudoku. A genetic switch that causes memory impairment in ageing mice when it goes into "off" mode has been flicked on, restoring failing brains to a more youthful state.

If a similar switch can be found in people, it might provide a new way to keep ageing human brains young.
Cognitive decline, particularly memory impairment, is a normal part of ageing in humans and animals. Yet why this happens, and how we can prevent it, is largely unknown, says David Sweatt at the University of Alabama, Birmingham, who was not involved in the new work.

André Fischer of the European Neuroscience Institute in Göttingen, Germany, and colleagues forced 3-month-old mice to find their way around a new environment and assessed them on their ability to associate an electric shock with a particular environment.

New neurons
The result was increased activity of a cluster of over 1500 genes which are known make proteins that are needed for the creation of new neurons – a process that is necessary for learning in humans and mice.

This boost in gene expression did not occur in 16-month-old mice given the same tasks: the activity of their genes changed only slightly. The mice also did worse than the young ones at spatial learning and memory tasks.

To uncover what prevents elderly mice getting this genetic boost, Fischer analysed the DNA found in neurons in the hippocampus of both old and young mice.

They found that when young mice are learning, a molecular fragment known as an acetyl group binds to a particular point on the histone protein that DNA wraps itself around – with the result that the cluster of learning and memory genes on the surrounding DNA ends up close to the acetyl group.

DNA 'on' switch
This acetyl "cap" was missing in the older mice that had been set the same tasks. From this, the team concludes that the cap acts as an "on" switch for the cluster of learning and memory genes: removing the cap switches off the genes.

Next, by injecting an enzyme known to encourage caps to bind to any kind of histone molecule, Fischer's team artificially flipped the switch to the on position in old mice. The acetyl group returned to the histone molecule and the mice's learning and memory performance became similar to that of 3-month-old mice.