Researchers at the University of British Columbia’s Department of Pediatrics and at Harvard University’s Center for Brain Science recently studied whether infants’ language development is altered by prenatal exposure to serotonin reuptake inhibitors (SRIs) and whether such effects differ from exposure to maternal mood disturbances. They used a control group of infants from non-SRI-treated mothers with little or no depression and compared them with infants of depressed but non-SRI-treated mothers and those of depressed mothers who were treated with SRIs.
The infants were evaluated at 36 weeks of gestation (in utero) on a consonant and vowel discrimination task; at this age, typically developing fetuses are capable of discriminating vowel sounds, but not consonant, with a change in fetal heart rate. Fetuses in the control group performed as expected, whereas the SRI-exposed fetuses showed accelerated perceptual development by discriminating both vowels and consonants. The infants were also evaluated at 6 and 10 months of age on a nonnative speech and visual language discrimination task: Infants can visually discriminate English and French at 4 and 6 months of age, but fail at 8 months unless they are raised to be bilingual. The control infants responded as expected, with success at 6 months and failure at 10 months, but the SRI-exposed infants failed to discriminate the language differences at either age, and the infants with the untreated mothers succeeded at 10 months instead of 6 months of age.
“Exposure to maternal depressed mood seems to delay stable discrimination, which ultimately extends the period of sensitivity to nonnative distinctions. Thus, exposure to maternal depression and prenatal SRI exposure appear to exhibit opposite effects on the development of infant perception,” wrote the researchers, who noted that whether this reflects the impact of pre- or postnatal maternal mood remains to be determined.
Data from the 2010 National Health Interview Survey show that cancer survivors experience poorer physical and mental health than the general population, and researchers at the Wake Forest School of Medicine say interventions are needed to improve survivor health at a population level. The researchers identified 1,822 cancer survivors and a control group of 24,804 adults with no cancer history from the survey and used the PROMIS Global Health Scale to assess health-related quality of life (HRQOL). Poor physical and mental HRQOL were reported by 24.5 percent and 10.1 percent of survivors, respectively, compared with 10.2 percent and 5.9 percent of adults without a history of cancer. “This represents a population of approximately 3.3 million and 1.4 million U.S. survivors with poor physical and mental HRQOL,” wrote the researchers. They noted that the HRQOL varied according to the type of cancer experienced: Survivors of breast or prostate cancer or melanoma reported scores similar to adults without cancer. Survivors of cervical, colorectal, hematologic, short-survival, and other cancers had worse physical HRQOL. Cervical and short-survival cancer survivors reported worse mental HRQOL. “Not all survivors report they are thriving,” wrote the researchers, who urged that easily implemented interventions be pursued for high-risk groups.
Reduced glucose metabolism in the posterior cingulate cortex may be an early sign of Alzheimer’s disease in middle-aged people with the APOE-e4 variant. The APOE-e4 variant is a well-documented risk factor for the illness.
The study, headed by Hillary Protas, Ph.D., of the Banner Alzheimer’s Institute in Phoenix, appeared this month online in the Archives of Neurology.
The scientists conducted PET scans of the brains of 149 cognitively normal middle-aged subjects with one copy of the variant, two copies of the variant, or no copy of the variant.
The scientists found no significant differences among the three groups as far as hippocampal volume or metabolism was concerned. But they did find a dose-dependent reduction in glucose metabolism in a region of the parietal lobe (the posterior cingulate cortex) in the APOE-e4 subjects compared with the subjects without any copies of the variant.
The results suggest that reduced glucose metabolism in the posterior cingulate cortex may be an early sign of Alzheimer’s in middle-aged people with the APOE-e4 variant. And if that is indeed the case, then middle-aged APOE-e4 carriers who have reduced glucose metabolism in this region might be ideal candidates on which to test potential therapies for Alzheimer’s.
It is also known that cognitively normal APOE-e4 carriers possess more beta amyloid in the brain than noncarriers do. Consequently, the scientists are collecting data to determine the time course of beta-amyloid acquisition in the brains of cognitively normal APOE-e4 carriers so that they can compare it to the trajectory of glucose metabolism reduction in the posterior cingulate cortex.
Still other questions press for answers, William Jagust, M.D., of the University of California, Berkeley, pointed out in an accompanying editorial. For example, hypometabolism in the posterior cingulate cortex is also seen in asymptomatic APOE-e4 carriers in their 20s and 30s, ages at which Alzheimer’s pathology is rare. So when does such hypometabolism actually represent preclinical Alzheimer’s? “The answer is not clear,” Jagust wrote, “because we lack sufficient human data and also because our understanding of Alzheimer’s is incomplete.”
The work was supported by the National Institute of Mental Health, the National Institute on Aging, the state of Arizona, and the Banner Alzheimer’s Foundation and the Mayo Clinic Foundation.
A group of Taiwanese researchers recently sought to examine the risk of dementia in patients with long-term insomnia, and the contribution to that risk of hypnotics. Their data were collected from Taiwan’s Longitudinal Health Insurance Database, and their study cohort comprised all patients aged 50 years or older with a insomnia first diagnosed between 2002 and 2007. The comparison cohort consisted of randomly selected patients matched by age and gender. Each patient was individually tracked for three years from their insomnia index date to identify whether the patient had a first diagnosis of dementia.
The researchers identified 5,693 patients with long-term insomnia and 28,465 individuals without. After adjusting for hypertension, diabetes mellitus, hyperlipidemia, and stroke, those with long-term insomnia had significantly higher risk of dementia. Patients with long-term insomnia and aged 50 to 65 years had a higher increased risk of dementia than those older than 65 years. The use of hypnotics with a longer half-life and at a higher prescribed dose predicted a greater increased risk of dementia.
“We suggest giving careful consideration to prescribing benzodiazepine or non-benzodiazepine hypnotics to patients with long-term insomnia, especially those that are aged between 50 and 65 years,” concluded the authors. “In addition, the lower the dosage and half-life values of the hypnotics used the better, because greater exposure to these medications leads to a higher risk of developing dementia.”
The study was funded by a grant from the National Institutes of Health, and by Eli Lilly and Co. ■