The effects of total sleep deprivation, selective sleep interruption and sleep recovery on pain tolerance thresholds in healthy subjects

The aim of this study was to compare the effects of total sleep deprivation (TSD), rapid eye movement (REM) sleep and slow wave sleep (SWS) interruption and sleep recovery on mechanical and thermal pain sensitivity in healthy adults. Nine healthy male volunteers (age 26--43 years) were randomly assigned in this double blind and crossover study to undergo either REM sleep or SWS interruption. Periods of 6 consecutive laboratory nights separated by at least 2 weeks were designed as follows: N1 Adaptation night; N2 Baseline night; N3 Total sleep deprivation (40 h); N4 and N5 SWS or REM sleep interruption; N6 Recovery. Sleep was recorded and scored using standard methods. Tolerance thresholds to mechanical and thermal pain were assessed using an electronic pressure dolorimeter and a thermode operating on a Peltier principle. Relative to baseline levels, TSD decreased significantly mechanical pain thresholds (-8%). Both REM sleep and SWS interruption tended to decrease mechanical pain thresholds. Recovery sleep, after SWS interruption produced a significant increase in mechanical pain thresholds (+ 15%). Recovery sleep after REM sleep interruption did not significantly increase mechanical pain thresholds. No significant differences in thermal pain thresholds were detected between and within periods. In conclusion this experimental study in healthy adult volunteers has demonstrated an hyperalgesic effect related to 40 h TSD and an analgesic effect related to SWS recovery. The analgesic effect of SWS recovery is apparently greater than the analgesia induced by level I (World Health Organization) analgesic compounds in mechanical pain experiments in healthy volunteers.     

Symposium: Normal and abnormal rem sleep regulation: Episodic hormone release in relation to REM sleep

Similar periodicities of about 90-100 min characterize both hormone pulsatility and NREM-REM sleep cycles suggesting that both processes could be temporally linked. From the current knowledge of the literature, it appears that, in spite of the diversity of the relationship between hormones and the sleep/wake cycle, systematic relationships exist between hormone pulses and the NREM-REM sleep cycles. Early studies have demonstrated the temporal association between GH and SWS episodes occurring soon after sleep onset. Renin, a key enzyme of the renin-angiotensin system, displays nocturnal oscillations that are associated strongly with the NREM-REM sleep cycles, and represents the first identified biological marker of sleep stage alternation. SWS invariably occurs in the descending phases of TSH and cortisol pulses which suggests that some specific mechanisms of this sleep stage could modulate their levels or, conversely, that increased TSH and cortisol secretion prevents the occurrence of deep sleep. Apart from the period of sleep onset associated with reduced prolactin secretion, no systematic relationship has been found between REM sleep and hormone release. These results highlight the complexity of hormone and sleep interactions and provide a basis for further research into their functional significance.     

Ovarian testosterone secretion during perimenopause

Objective: The aim of the study was to investigate ovarian testosterone secretion during the last few years of reproductive life and after menopause. Materials and methods: Ovarian and peripheral venous levels of total testosterone were analyzed in 52 women aged 42–69 years (mean 51) undergoing hysterectomy with adnexal removal for benign indications at the Department of Obstetrics and Gynecology at Tampere University Hospital, Finland. The study population was divided into pre- (n=19), peri- (n=18) and postmenopausal (n=15) women in addition to the classical division according to menstrual cycle. Corresponding serum estradiol, progesterone and gonadotropin levels were measured, and the degree of ovarian stromal hyperplasia was analyzed. Results: The levels of all steroid hormones were higher in the ovarian vein than in the periphery. A significant positive correlation was found between age and ovarian vein testosterone levels (r=0.3, P=0.01). In premenopausal women, it was 1.5 nmol/l (median; range 0.78–6.0), in perimenopausal women 2.2 nmol/l (range 0.9–13.6), and 2.5 nmol/l (range 0.6–26.6) in postmenopause, respectively. Peripheral testosterone level did not increase with age. Ovarian stromal hyperplasia was significantly associated with increased testosterone secretion (P=0.009). Conclusion: The ovary seems to increase the secretion of testosterone into circulation during the menopausal transition period, as the highest levels were measured in postmenopausal women. High testosterone levels in the ovarian vein, however, were not reflected in the peripheral venous blood.     

Pituitary hormonal profile in menopause

The hormonal profile of pituitary hormones was studied by measuring serum FSH, LH, TSH, prolactin (PRL) and growth hormone (GH) in a series of postmenopausal women 50–85 yr old who were at least 1 yr postmenopausal.

In 116 women mean (±SD) plasma FSH and LH were 55.8 ± 22 mU/ml and 25.6 ± 13.62. In 27 women, 1–5 yr after the menopause (M), mean FSH was 56 ± 23.8 and LH 24.7 ± 11 mU/ml and in 22 women, 6–9 yr after M, FSH was 60.3 ± 24.6 mU/ml and LH 27.9 ± 17.2 mU/ml. There was then a gradual, but not statistically significant (n.s.) fall of FSH and LH to 51.6 ± 22.6 and 23.9 ± 9 in 23 women, 20 or more years after M.

TSH was measured in 75 women and its mean value was 4.3 ± 2.4 μU/ml. Three hypothyroid values (70, 20 and 13.5 μU/ml) were also found. Mean TSH value in 20 women aged 50–54 yr (4 ± 2.7 μU/ml) was not significant compared to other age-groups or to 8 women aged 70–85 yr (4.57 ± 2.5 μU/ml).

Mean PRL in 62 cases was 0.54 ± 0.20 mU/ml. In 17 other women unexplained increased values (>1 mU/ml) of PRL were found. No significant change of PRL was found with advancing age.

Mean GH in 32 women was 3.7 ± 2.6 ng/ml. Eight other values were found <1 ng/ml and 3 above 10 ng/ml. The distribution of values in the age-group 50–59 yr (n = 22) did not differ from the age-group 60–85 yr (n = 21).

It is concluded that the basal concentration of gonadotrophins, after an initial rise, as well as that of the other pituitary hormones remains practically unaltered with advancing age in postmenopausal women.     

Diurnal preference, sleep habits, circadian sleep propensity and melatonin rhythm in healthy human subjects

After 24-h sleep deprivation, 33 healthy young subjects entered the 10/20 min ultra-short sleep–wake schedule for 26 h. Melatonin rhythm was hourly assessed simultaneously. Results indicated that morning preference was significantly correlated with habitual sleep onset (r=−0.41, P=0.04), habitual sleep offset (r=−0.52, P=0.002), melatonin peak time (r=−0.36, P=0.04), and sleep propensity onset time (r=−0.36, P=0.04). The intervals between habitual sleep mid-point and melatonin peak time and between habitual sleep mid-point and sleep propensity onset time were significantly longer in morning-preference subjects than in evening-preference subjects (P<0.05). These findings suggest that the variance of diurnal preference may be related to differences in phase relations between habitual sleep timing and the circadian pacemaker.     

Delayed Acquisition of Behavioral and Hippocampal Responses During Jaw Movement Conditioning in Aging Rabbits

Young (3–7 months; n = 7) and aging (40–49 months; n = 7) rabbits (Oryctolagus cuniculus) were classically conditioned in a trace jaw movement paradigm (300 ms tone, 450 ms trace, 200 ms intraoral water) after implantation of electrodes into area CA1 of dorsal hippocampus. Aging rabbits took significantly more trials to reach a behavioral criterion of 8 conditioned responses in any 9 consecutive trials than young rabbits (p = 0.04), and their conditioned, but not unconditioned, jaw movement responses were of a lower frequency than those of young rabbits (p = 0.02). Early in training, aging rabbits’ hippocampal responses were significantly smaller just before water onset than corresponding responses of young rabbits (p = .03). The magnitude of this response was negatively correlated with trials to criterion (r = −0.60, p = 0.03). These results are interpreted in terms of age-related differences in the hippocampal contribution to jaw movement learning.     

Nocturnal cortisol release in relation to sleep structure.

The relationship between the temporal organization of cortisol secretion and sleep structure is controversial. To determine whether the cortisol profile is modified by 4 hours of sleep deprivation, which shifts slow-wave sleep (SWS) episodes, 12 normal men were studied during a reference night, a sleep deprivation night and a recovery night. Plasma cortisol was measured in 10-minute blood samples. Analysis of the nocturnal cortisol profiles and the concomitant patterns of sleep stage distribution indicates that the cortisol profile is not influenced by sleep deprivation. Neither the starting time of the cortisol increase nor the mean number and amplitude of pulses was significantly different between the three nights. SWS episodes were significantly associated with declining plasma cortisol levels (p less than 0.01). This was especially revealed after sleep deprivation, as SWS episodes were particularly present during the second half of the night, a period of enhanced cortisol secretion. In 73% of cases, rapid eye movement sleep phases started when cortisol was reflecting diminished adrenocortical activity. Cortisol increases were not concomitant with a specific sleep stage but generally accompanied prolonged waking periods. These findings tend to imply that cortisol-releasing mechanisms may be involved in the regulation of sleep.     

REM sleep control during aging in SAM mice: a role for inducible nitric oxide synthase

Evidence that nitric oxide (NO) is involved in the regulation of rapid-eye-movement sleep (REMS) is supported by recent studies. During aging, NO generation encounters marked changes mainly related to the activation of the inducible NO-synthase (iNOS). To investigate links existing between iNOS and REMS impairments related to aging, we examine the age-related variations occurring in: mRNA and activity of iNOS in brainstem and frontal cortex; sleep parameters under baseline and after treatment by a selective iNOS inhibitor (AMT) in Senescence Accelerated Mice (SAM). SAMR1 (control) mice are a model of aging while SAMP8 are adequate to study neurodegenerative processes. RT-PCR analysis does not reveal significant variation in iNOS mRNA expression in both strains. However, significant age-related increases in iNOS activity occur in SAMR1 but such variation is not observed in SAMP8. In baseline conditions, aging induces a slight increase in slow-wave sleep (SWS) amounts in both groups and deteriorates greatly REMS architecture in SAMP8 compared to SAMR1. AMT reduces REMS amounts for 4–6 h after treatment in a dose and age-dependent manner in SAMR1. Almost no changes occur in SAMP8. Data reported suggest that NO derived from iNOS contributes to trigger and maintain REMS during aging.     

Significance of slow wave sleep: considerations from a clinical viewpoint

Previous experimental observations, almost exclusively carried out with young healthy subjects, have been interpreted as showing a particular restorative role for human slow wave sleep (SWS). This article considers whether findings from polygraphic sleep studies in patients and elderly subjects lead to similar inferences about the meaning or "function" of SWS. The question was approached in three different ways: (a) by presenting results from a long-term study in elderly subjects whose SWS data were correlated with baseline medical and psychometric findings and with 5-year follow-up results; (b) by correlating nonmanipulated wake-time during days with parameters of SWS on subsequent nights in a group of 30 demented inpatients undergoing 72-h continuous sleep-wake recording; (c) by reviewing and comparing published polygraphic sleep studies for a number of psychiatric conditions. None of these three approaches provided unequivocal evidence for a clinically significant role for SWS. Reasons for the different outcome of SWS studies in young experimental subjects and clinical populations are discussed.     

Beneficial effects of regular exercise on sleep in old F344 rats

With aging there is a significant decline in the normal architecture of sleep and a reduction in the diurnal amplitude of core body temperature. Regular moderate exercise has been shown to have a positive impact in the elderly and here we investigate whether sleep–wake patterning can also be improved. Young (3 months) and old (22 months) F344 rats were exercised once a day for 50 min at night onset over an 8-week period. Thereafter, polysomnographic recordings were obtained immediately after exercise. To determine the lasting consequences of exercise, sleep was also recorded 2 days and 2 weeks after exercise had ended. Old rats that were exercised had a significant weight loss, were awake more during the last third of their active period, had less sleep fragmentation and the amplitude of the diurnal rhythm of core body temperature was significantly increased. Old exercised rats also had an overall increase in the amplitude of EEG power (0.5–16 Hz) during wake and theta EEG power during REM sleep. In young rats regular exercise increased EEG delta power (0.5–4 Hz) during NREM sleep. Our data indicate regular exercise in old rats improves sleep architecture, EEG power and diurnal rhythm of temperature.     

Self-reported sleep, demographics, health, and daytime functioning in young old and old old community-dwelling seniors

Sleep, demographics, health, and daytime functioning were examined in young old (60-74 years; n = 175) and old old (75-98 years; n = 147) community-dwelling seniors. Sleep diaries (2 weeks), 6 daytime functioning measures, and a demographics-health questionnaire were collected. The old old reported worse sleep than the young old. Women reported worse sleep than men. Hierarchical regressions revealed demographic information alone was not sufficient for understanding sleep. Specifically, demographic information predicted sleep onset latency and sleep efficiency for both groups, but not number of awakenings or total nap time. Health and daytime functioning accounted for significant increases in the variance in sleep “over and above” that accounted for by demographics alone or demographics and health combined, respectively. All variables combined accounted for 15% to 30% of the variance in sleep. Because the importance of specific measures varied by group and sleep variable, research exploring the differential utility of specific measures for young old versus old old appears warranted.     

Effect of gaboxadol on sleep in adult and elderly patients with primary insomnia: results from two randomized, placebo-controlled, 30-night polysomnography studies

STUDY OBJECTIVES: To evaluate the efficacy and tolerability of gaboxadol in the treatment of adult and elderly patients with primary insomnia. DESIGN: Randomized, double-blind, placebo-controlled, multicenter, 30-night, polysomnography studies. SETTING: Sleep laboratory. PATIENTS: Primary insomnia, 18-64 y (adult study), or > or =65 y (elderly study). INTERVENTIONS: Adult study: gaboxadol 15 mg (GBX15; N = 148), 10 mg (GBX10; N = 154), or placebo (N = 156); elderly study: GBX10 (N = 157), gaboxadol 5 mg (GBX5; N = 153), or placebo (N=176). MEASUREMENTS AND RESULTS: Primary endpoints were wake after sleep onset (WASO) and latency to persistent sleep (LPS). Slow wave sleep (SWS) was a secondary endpoint. Analyses were based on the change from baseline for the average of nights 1/2, and nights 29/30, and compared gaboxadol versus placebo. Exploratory endpoints included patient's subjective assessment of total sleep time (sTST), WASO (sWASO), time to sleep onset (sTSO), and number of awakenings (sNAW); these analyses were based on weekly means. 1) Adult study. GBX15 significantly (P < or = 0.05) improved WASO through nights 29/30 but had no significant effects on LPS. No significant differences were seen for GBX10 versus placebo on WASO or LPS. GBX15 and GBX10 enhanced SWS. GBX15 significantly improved sTST, sWASO, sTSO, and sNAW at weeks 1 and 4. 2) Elderly study. GBX10 significantly improved WASO through nights 29/30; a significant improvement was also seen for GBX5 at nights 1/2 but this was not maintained through nights 29/30. GBX10 significantly improved LPS at nights 1/2 but the improvement was not maintained through nights 29/30; no significant differences were seen for GBX5 versus placebo on LPS. GBX10 and GBX5 enhanced SWS. GBX10 significantly improved sTST at week 1, and sTST, sWASO, and sNAW at week 4. Gaboxadol was generally well tolerated in both studies. CONCLUSIONS: The maximum studied doses of gaboxadol (GBX15 in adult patients and GBX10 in elderly patients) were effective at enhancing objective polysomnography measures of sleep maintenance and SWS, and also some subjective sleep measures, over 30 nights but had little or no effects on sleep onset. The clinical relevance of the enhancement of SWS by gaboxadol is unclear.     

Slow wave sleep enhancement with gaboxadol reduces daytime sleepiness during sleep restriction

STUDY OBJECTIVES: To evaluate the impact of enhanced slow wave sleep (SWS) on behavioral, psychological, and physiological changes resulting from sleep restriction. DESIGN: A double-blind, parallel group, placebo-controlled design was used to compare gaboxadol (GBX) 15 mg, a SWS-enhancing drug, to placebo during 4 nights of sleep restriction (5 h/night). Behavioral, psychological, and physiological measures of the impact of sleep restriction were assessed in both groups at baseline, during sleep restriction and following recovery sleep. SETTING: Sleep research laboratory. PARTICIPANTS: Forty-one healthy adults; 9 males and 12 females (mean age: 32.0 +/- 9.9 y) in the placebo group and 10 males and 10 females (mean age: 31.9 +/- 10.2 y) in the GBX group. INTERVENTIONS: Both experimental groups underwent 4 nights of sleep restriction. Each group received either GBX 15 mg or placebo on all sleep restriction nights, and both groups received placebo on baseline and recovery nights. MEASUREMENTS AND RESULTS: Polysomnography documented a SWS-enhancing effect of GBX with no group difference in total sleep time during sleep restriction. The placebo group displayed the predicted deficits due to sleep restriction on the multiple sleep latency test (MSLT) and on introspective measures of sleepiness and fatigue. Compared to placebo, the GBX group showed significantly less physiological sleepiness on the MSLT and lower levels of introspective sleepiness and fatigue during sleep restriction. There were no differences between groups on the psychomotor vigilance task (PVT) and a cognitive test battery, but these measures were minimally affected by sleep restriction in this study. The correlation between change from baseline in MSLT on Day 6 and change from baseline in SWS on Night 6 was significant in the GBX group and in both group combined. CONCLUSIONS: The results of this study are consistent with the hypothesis that enhanced SWS, in this study produced by GBX, reduces physiological sleep tendency and introspective sleepiness and fatigue which typically result from sleep restriction.     

Performance and sleepiness following moderate sleep disruption and slow wave sleep deprivation

Recent studies have shown that periodically disrupted sleep resulted in significant daytime sleepiness and performance loss in normal young adults. One study suggested that the periodicity of disturbance rather than the total number of sleep disturbances was the primary factor in causing degraded function. However, in that study, increased performance levels could have been associated with increased levels of slow wave sleep. The present study was designed to determine whether the amount of SWS rather than the periodic disruption of sleep accounts for decreased performance of Ss with disrupted sleep. Twelve normal young adults spent two 4-night periods in the laboratory. During one 4-night series, Ss were briefly aroused either following each 10 min of sleep or whenever they entered stage 3 sleep (No SWS condition). During the second series of nights, Ss were briefly aroused after each 10 min of sleep (SWS condition). In the second series, additional arousals were performed after 5-min periods (but not when Ss were in SWS) to equalize the total number of arousals in the SWS conditions with those in the No SWS condition. Total experimental arousals were equal in the disruption conditions, and the experimental manipulation was successful in reducing total SWS to infrequent epochs of stage 3 in the No SWS condition while allowing significantly more SWS in the SWS condition. In terms of sleep stages, this difference was balanced by increased stage 2 in the No SWS condition. Despite the differential occurrence of SWS, no performance, mood, or nap latency measure was different in the SWS vs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hormonal replacement therapy reduces forearm fracture incidence in recent postmenopausal women - results of the Danish Osteoporosis Prevention Study

Objectives: To study the fracture reducing potential of hormonal replacement therapy (HRT) in recent postmenopausal women in a primary preventive scenario. Methods: Prospective controlled comprehensive cohort trial: 2016 healthy women aged 45–58 years, from three to 24 months past last menstrual bleeding were recruited from a random sample of the background population. Mean age was 50.8±2.8 years, and the number of person years followed was 9335.3. There were two main study arms: a randomised arm (randomised to HRT; n=502, or not; n=504) and a non-randomised arm (on HRT; n=221, or not; n=789 by own choice). First line HRT was oral sequential oestradiol/norethisterone in women with intact uterus and oral continuous oestradiol in hysterectomised women. Results: After five years, a total of 156 fractures were sustained by 140 women. There were 51 forearm fractures in 51 women. By intention-to-treat analysis (n=2016), overall fracture risk was borderline statistically significantly reduced (RR=0.73, 95% CI: 0.50–1.05), and forearm fracture risk was significantly reduced (RR=0.45, 95% CI: 0.22–0.90) with HRT. Restricting the analysis to women who had adhered to their initial allocation of either HRT (n=395) or no HRT (n=977) showed a significant reduction in both the overall fracture risk (RR=0.61, 95% CI: 0.39–0.97) and the risk of forearm fractures (RR=0.24, 95% CI: 0.09–0.69). Compliance with HRT was 65% after five years. Conclusions: It is possible to reduce the number of forearm fractures and possibly the total number of fractures in recent postmenopausal women by use of HRT as primary prevention.     

Neuroendocrine effect of a short-term treatment with DHEA in postmenopausal women

Objectives: A progressive decline of plasma dehydroepiandrosterone (DHEA) levels occurs in women during aging related to the reduction of adrenocortical secretion. A specific action of DHEA on the central nervous system (CNS) is suggested by the improvement of psychological and physical well-being in postmenopausal women after DHEA supplementation. The aim of the present study was to investigate the neuroendocrine effects of short-term DHEA supplementation in postmenopausal women, evaluating changes of plasma β-endorphin (β-EP) and growth hormone (GH) before and after oral DHEA (100 mg/day) for 7 days in postmenopausal women (n=6). Methods: Before and after 7 days of DHEA supplementation, postmenopausal women underwent a neuroendocrine test with clonidine, an 2 presinaptic agonist for adrenergic system, (1.25 mg i.v.). Basal plasma DHEA, androstenedione (A), testosterone (T), estrone (E₁) and estradiol (E₂) levels were evaluated before and after treatment, while plasma β-EP and GH levels were measured before and 15, 30, 45, 60 and 90 min after clonidine injection. Results: Basal plasma β-EP and GH levels did not show a significant difference before and after short-term DHEA administration, while circulating A, T, E₁ and E₂ significantly increased after treatment. The clonidine test induced a significant increase of plasma β-EP levels in women after receiving DHEA supplementation but not before; conversely, plasma GH levels increased both before and after treatment. Conclusions: The present study indicates that short-term DHEA supplementation in postmenopausal women is able to restore the impaired response of pituitary β-EP to clonidine, an 2 presinaptic agonist. According to these data it is possible to hypothesize that DHEA could play a role in the psychological and physical well-being of postmenopausal women acting via a restoration of neuroendocrine control of antero-pituitary β-EP secretion.     

The effects of alcoholism on auditory evoked potentials during sleep

Normal aging is associated with a reduction in the probability that an auditory stimulus will evoke a K-complex during sleep. Additional concomitants of aging are a reduction in the amplitude of the K-complex-related N550, an augmentation of the P2 component and the appearance of a long-lasting positivity (LLP) in the auditory evoked potential. Normal aging is also associated with a dramatic reduction in slow wave sleep (SWS) and a reduction in the volume of cortical gray matter, particularly in the frontal and prefrontal regions of the brain. As in aging, alcoholism is associated with reductions in both cortical gray matter and SWS. It can, therefore, be hypothesized that alcoholics would show similar evoked potential changes to those seen in aging. To test this hypothesis, we studied seven middle-aged abstinent long-term alcoholics and eight age-matched normal controls. Each subject spent one night in the laboratory. Electroencephalogram (EEG) was recorded from six midline scalp sites and auditory stimuli were presented during stage 2 non-rapid eye movement sleep. N550 amplitude in the K-complex average was lower in the alcoholics as compared with controls as was the likelihood of K-complex production. No differences were noted in either amplitude or latency of the P2 or N350 components, and both groups displayed a prominent LLP potential. The pattern of reduced K-complex production and N550 amplitude in alcoholics as compared with age-matched controls is consistent with an hypothesized association between atrophy of the frontal lobes and reductions in SWS and K-complexes. The finding also suggests that the evoked K-complex may be a relatively simple measure of the effect of alcoholism on EEG during sleep.     

The GABA uptake inhibitor tiagabine promotes slow wave sleep in normal elderly subjects

Aging is associated with a dramatic decrease in slow wave sleep (SWS) and sleep consolidation. Previous studies revealed that various GABA(A) agonists and the GABA uptake inhibitor tiagabine augment slow frequency components in the EEG within non-REM sleep, and thus promote deep sleep in young individuals and/or rats. In the present double-blind, placebo-controlled study, we assessed the effect of a single oral dose of 5 mg tiagabine on nocturnal sleep in ten healthy elderly volunteers (6 females). During the placebo night the subjects displayed a low sleep efficiency, due to high amounts of intermittent wakefulness, and little SWS. Tiagabine significantly increased sleep efficiency, tendentially decreased wakefulness and prominently increased both SWS and low-frequency activity in the EEG within non-REM sleep. The present findings demonstrate that tiagabine increases sleep quality in aged subjects. Moreover, the effects of tiagabine closely match those evoked by the GABA(A) agonist gaboxadol in young subjects and indicate that such compounds may have prospects in the treatment of sleep disturbances, particularly of those commonly occurring in the elderly.     

Age-related progression of tau pathology in brains of baboons

Recently, cytoskeletal changes associated with abnormally phosphorylated tau protein were demonstrated in neurons and glial cells of two aged baboons (Papio). The present study examines the effects of age on the development of tau pathology in baboons. Brains of 50 baboons ranging in age from 1 to 30 years were categorized into four age groups: Group I: 1–10 years [n = 9], group II: 11–20 years [n = 13], group III: 21–25 years [n = 17], group IV: 26–30 years [n = 11]). Whole hemisphere sections (100 μm) were examined using phosphorylation-dependent anti-tau antibodies. Cytoskeletal changes were completely absent in animals of group I. In group II four animals (31%) exhibited cytoskeletal changes which were rated as mild or moderate. In group III abnormal tau was found in 12 brains (71%) ranging in severity from mild to severe. Finally, in group IV 10 out of 11 animals (91%) exhibited some degree of tau pathology which was rated as severe in 4 animals (36%). A statistically significant relationship was found between advancing age and progression of tau pathology in baboons. In conclusion, the present findings underline the value of the baboon as a potential nonhuman primate model for age-related tau pathology afflicting the human brain.     

A 50-Hz electromagnetic field impairs sleep

In view of reports of health problems induced by low frequency (50-60 Hz) electromagnetic fields (EMF), we carried out a study in 18 healthy subjects, comparing sleep with and without exposure to a 50 Hz/1 mu Tesla electrical field. We found that the EMF condition was associated with reduced: total sleep time (TST), sleep efficiency, stages 3 + 4 slow wave sleep (SWS), and slow wave activity (SWA). Circulating melatonin, growth hormone, prolactin, testosterone or cortisol were not affected. The results suggest that commonly occurring low frequency electromagnetic fields may interfere with sleep.