Why do teenagers sleep so late?

Almost half of all adolescents in the United States are sleep deprived. Why is this such a widespread problem? The authors argue in this review that besides societal pressures and schoolwork, changes in sleep regulation during puberty lead to delayed sleep and later bedtimes. This is incompatible with early school start times and other societal pressures, but delayed sleep during puberty is likely common to mammals and not just humans.

Hagenauer MH et al. Adolescent Changes in the Homeostatic and Circadian Regulation of Sleep. Dev Neurosci 2009;31:276-284.

Zapping the brain to treat severe depression in human patients

severe depression

Severe Depression by Zapping the Brain

Chances are that you know somebody, perhaps a family member, friend, or acquaintance, who has had severe depression or at least some kind of depression before.

It’s a hugely prevalent mental disorder, with up to 17% of people in the US suffering from it at some point in their lives.

In a small subset of severe depression cases, even strong medication or electroconvulsive brain therapy don’t help.

To treat these patients, a group of psychiatrists and neurosurgeons in Mannheim and Heidelberg, Germany, have successfuly conducted an initial deep brain stimulation study.

Deep brain stimulation is a surgical procedure where a thin metal wire, an electrode, is implanted into a certain part of the brain to stimulate it. The electrode has to be placed in a very, very specific area (millimeters in size) of the brain and thus the patient’s head is fixed in place with a ‘stereotactic rig,’ which is a precisely machined device that can guide the electrode to a precise coordinate within the head.

The scientists in this most recent study implanted the electrode into the habenula, which is a small group of neurons that is thought to be involved in reward processing and many other functions. They found that habenular stimulation was able to successfuly treat a 64-year-old woman who had intractable, severe depression since the age of 18!

The researchers and clinicians are now attempting to expand on this severe depression success with a larger clinical study of severely depressed patients all over Germany.

Human babies aren’t that special after all

human babies

Human babies take a long time to start walking

The onset of walking for human babies is thought to represent a critical milestone in development of the nervous system, when neuronal systems mature enough to coordinate the complex movements of multiple limbs and prevent the animal from falling over.

How long it takes for human babies to start walking is one area that scientists originally thought that humans differ from other mammals.

A human baby only starts to walk on shaky legs around a year after birth, but a foal can get up almost immediately and rodents like mice only require a few hours to start moving around. In a new study published in PNAS, a group from Lund University in Sweden has found why this difference exists – and surprisingly, it’s not because humans are uniquely different.

Most mammals start walking around the same developmental time!
They showed that human babies actually start walking at the same brain developmental stage as most other mammals that walk. If you look at progression of brain development after conception, and not birth, humans start walking at the same relative point in time.

This shows that the neural mechanisms that underlie the ability to walk are very similar across animals and the neural building blocks of human brains come together in a similar manner as even lower mammals that diverged in evolution many millions of years ago.

Analyzing brain development data from other animals allowed them to predict quite accurately when humans would start to walk. Though humans may be different in many ways, motor development of the brain is not one of them.

These findings shed new light on how developmental paths in early life could have been conserved evolutionarily from lower organisms all the way up to humans, and they lead to better understanding of the developmental clock and what events occur at what stage of development, which may have relevance for treating developmental disorders in the future.

“Human babies” Photo by Photostock.

Your appetite might be linked to risk of Alzheimer’s disease

Alzheimer's disease

Alzheimer’s disease – Appetite might be linked to risk of Alzheimer’s

The hormone leptin controls your appetite
Leptin is a potent and important appetite-regulating hormone – if you’ve just polished off a couple plates of food at a buffet, your blood leptin levels will rise and signal to your brain that you’re full.

The picture to the right shows an obese mouse that is missing the leptin gene and thus doesn’t produce leptin in its body. When it starts eating, it doesn’t stop and becomes obese.

The same thing happens in a small population of humans who are missing the leptin gene. They can’t control their appetite and get fat. But as always in biology, the story is more complicated. Some obese people have exactly the opposite effect – higher leptin levels than normal.

This might be because they have a genetic defect that makes them resistant to the effects of the hormone – when their bodies detect that the existing leptin in the bloodstream isn’t working, more leptin is pumped out, leading to higher levels.

Higher leptin = less risk of Alzheimer’s disease
A group of researchers based in Boston University have just finished an epic 12-year study of over 750 elderly people, where they tracked leptin levels and brain function (with brain scans). In short, they found that people with overall higher leptin levels at the start of the study ended up with less Alzheimer’s disease and healthier brains.

This is exciting because it would be extremely powerful to find a way to predict whether somebody is going to get Alzheimer’s disease later in their life, allowing early intervention and treatment – this study shows that leptin might be a useful predictive biomarker.

Now you might be thinking, if people with lower leptin levels get more Alzheimer’s disease, why don’t we give them some more leptin? Great minds think alike, because that’s exactly what Dr. J. Wesson Ashford and the Stanford/VA Alzheimer’s Center received $3M from the NIH (National Institute of  Health) to look into.

Of course, any clinical application of this leptin / Alzheimer’s disease work is still many years away, but it’s good to see progress being made in understanding risk factors for Alzheimer’s disease.