Study Objectives: Idiopathic REM sleep behavior disorder (iRBD) is characterized by atypical REM sleep motor activity, vivid dreams and nightmares, and dream-enacting behaviors that can result in injuries to the patient and bed partner. It is also a known predictor of Parkinson disease (PD). Alexithymia has been associated with disturbances in sleep and dreaming (e.g., nightmares) and is a non-motor symptom of PD. We assessed alexithymia and disturbed dreaming in iRBD patients with the aim of determining if these two factors are elevated and interrelated among this population.
Design: Questionnaire study of clinically diagnosed patients.
Setting: Clinical sleep disorders center.
Patients or participants: Thirty-two iRBD patients and 30 healthy age- and sex-matched control participants.
Measurements and Results: Participants completed the 20-item Toronto Alexithymia Scale (TAS-20), the Dream Questionnaire, and the Beck Depression Inventory. iRBD patients obtained higher TAS-20 total scores (62.16 ± 13.90) than did controls (52.84 ± 7.62; F1,59 = 10.44, P < 0.01), even when controlling for depressive symptoms, and more frequently attained the suggested cutoff for alexithymia than did controls (P < 0.01). iRBD patients obtained higher scores on the Difficulty Identifying Feelings alexithymia subscale. For both iRBD and control groups, the Difficulty Indentifying Feelings subscale correlated positively with the Nightmare Distress scale of the Dream Questionnaire.
Conclusions: Elevated alexithymia scores among idiopathic rapid eye movement sleep behavior disorder patients, and especially a difficulty in identifying feelings, parallels evidence of dysautonomia in this population. The higher incidence of distressing nightmares and the association of nightmares with alexithymia further extend similar findings for both clinical and non-clinical samples and suggest that an affect regulation disturbance may be common to the two sets of symptoms.
Citation: Godin I; Montplaisir J; Gagnon JF; Nielsen T. Alexithymia associated with nightmare distress in idiopathic REM sleep behavior disorder. SLEEP 2013;36(12):1957-1962.
Breaking the Brain Clock (BMAL1) Predisposes Nerve Cells to Neurodegeneration
Findings point to possible ways to fight some age-related diseases
PHILADELPHIA — As we age, our body rhythms lose time before they finally stop. Breaking the body clock by genetically disrupting a core clock gene, Bmal1, in mice has long been known to accelerate aging , causing arthritis, hair loss, cataracts, and premature death.
Synaptic degeneration and impaired functional connectivity in cortex of Bmal1 knockout. Electron micrographs show presynaptic terminals (Sy) in 6-month-old wild-type mouse (A) and Bmal1 knockout (B and C) retrosplenial cortex. In Bmal1 knockout cortex, synaptic terminals are swollen and relatively devoid of synaptic vesicles, while the presynaptic and postsynaptic membranes, synaptic cleft, and dendritic spine [D] have normal morphology. Bmal1 knockout mice showed both normal and abnormal terminals. Activated astrocytes and numerous organelle-rich astrocytic processes were seen throughout the Bmal1 KO cortical tissue. Scale bars: 500 nm. Credit: Erik Musiek, M.D., Ph.D., Journal of Clinical Investigation
New research now reveals that the nerve cells of these mice with broken clocks show signs of deterioration before the externally visible signs of aging are apparent, raising the possibility of novel approaches to staving off or delaying neurodegeneration – hallmarks of Parkinson’s and Alzheimer’s diseases. Erik Musiek, M.D., Ph.D., who was a postdoctoral fellow in the lab of Garret FitzGerald, M.D., director of the Institute of Translational Medicine and Therapeutics,Perelman School of Medicine, University of Pennsylvania, took on this project four years ago. Musiek, now an assistant professor at Washington University, completed this line of research over the last two years in the lab of David Holtzman, M.D., also at WashU. The Penn-WashU team found that the expression of certain clock genes, includingBmal1, plays a fundamental role in delaying emergence of age-related signs of decay in the brain. The clock proteins appear to do this by protecting the brain against oxidative stress – a process akin to rusting – that is normally controlled by enzymes that degrade harmful forms of oxygen generated in the course of normal metabolism. Their findings appear this week in the Journal of Clinical Investigation.
As I mentioned in an earlier post, the NIH Data Book on RePORT.nih.gov contains biomedical workforce data from NIH databases as well as data from national surveys sponsored by NSF and NIH. I thought it would be interesting to highlight the data on what’s trending for NIH-supported trainees and fellows receiving PhDs, in terms of fields of study. The chart below uses NIH trainee and fellow records and self-reported data on field of study from the Survey of Earned Doctorates, a census of all individuals receiving a research doctorate from a US university within a given academic year.
Jet lag, shift work, and even late nights staring at your tablet or smartphone may be making you sick. That’s because the body’s internal clock is set for two 12-hour periods of light and darkness, and when this rhythm is thrown off, so is the immune system. One reason may be that the genes that set the body clock are intimately connected to certain immune cells, according to a new study.
The finding “was a happy accident,” says Lora Hooper, an immunologist at the University of Texas Southwestern Medical Center in Dallas. She and her colleagues were studying NFIL3, a protein that guides the development of certain immune cells and turns on the activity of others. The gene for this protein is mutated in some human patients with inflammatory bowel disease, and mice lacking the gene for NFIL3, the team found, had more so-called TH17 cells in their intestines.
These cells are a type of immune cell known as a T cell. They get their name from a signal they produce, called interleukin 17, which tells other T cells to increase the immune response. In normal numbers, TH17 cells, which live in the intestines, help the body fight bacterial and fungal infections. But when there are too many, the immune defense begins to cause illness rather than prevent it. Boosting NFIL3 levels in T cells growing in lab cultures resulted in fewer of them turning into TH17 cells, the researchers found, suggesting that the protein’s job is to prevent T cells from going into that area of specialization. The absence of the protein, the team concluded, leads to runaway TH17 activity.
At this point, the researchers had no reason to suspect a connection to our body’s internal timekeeping system—also known as our circadian clock—which responds to daily cycles of light and dark. But as they continued to explore the connection between NFIL3 and TH17 cells, they found that some of the proteins produced by the body’s “clock genes” attach to the NFIL3 genes. What’s more, cultured cells and mice whose clock genes were experimentally tampered with produced fewer TH17 cells. The researchers surmise that a key protein in the clock network binds to the NFIL3 gene to keep the production of TH17 cells synchronized with periods of light and darkness. And the team found that normal mice produce less NFIL3, and thus more TH17 cells, during the day than at night.
In a final experiment, the researchers gave the mice jet lag. “We didn’t fly them anywhere,” Hooper jokes. Instead, the team shifted the rodents’ light/dark cycles by 6 hours every 4 days. “It would be like flying from the U.S. to Europe, India, and Japan and spending 4 days in each country,” she explains. Mice with altered light cycles had nearly twice as many TH17 cells in their spleens and intestines, compared with mice having a normal day, the team reports online today in Science. The jet-lagged mice also mounted a stronger inflammatory response to irritation by an experimental chemical—a test used to gauge immune-system sensitivity that hints the animals may be more prone to inflammatory disease.