Age-related cognitive impairment and dementia are an increasing societal burden. Epidemiological studies indicate that lifestyle factors, e.g. physical, cognitive and social activities, correlate with reduced dementia risk; moreover, positive effects on cognition of physical/cognitive training have been found in cognitively unimpaired elders. Less is known about effectiveness and action mechanisms of physical/cognitive training in elders already suffering from Mild Cognitive Impairment (MCI), a population at high risk for dementia. We assessed in 113 MCI subjects aged 65–89 years, the efficacy of combined physical-cognitive training on cognitive decline, Gray Matter (GM) volume loss and Cerebral Blood Flow (CBF) in hippocampus and parahippocampal areas, and on brain-blood-oxygenation-level-dependent (BOLD) activity elicited by a cognitive task, measured by ADAS-Cog scale, Magnetic Resonance Imaging (MRI), Arterial Spin Labeling (ASL) and fMRI, respectively, before and after 7 months of training vs. usual life. Cognitive status significantly decreased in MCI-no training and significantly increased in MCI-training subjects; training increased parahippocampal CBF, but no effect on GM volume loss was evident; BOLD activity increase, indicative of neural efficiency decline, was found only in MCI-no training subjects. These results show that a non pharmacological, multicomponent intervention improves cognitive status and indicators of brain health in MCI subjects.
With respect to AD, FTD patients had several sleep parameters similarly or even more affected by neurodegeneration, but in a much shorter time span. The findings probably indicate a centrally originating sleep deregulation. Since in FTD patients sleep disturbances may be obvious from an early stage of their disease, and possibly earlier than in AD patients, physicians and caregivers should be alert for the early detection and treatment of these symptoms.
The main condition at increased risk of dementia is considered to be mild cognitive impairment. Mild cognitive impairment has been defined as a transitional state between normal aging and dementia, of which it may represent a prodrome. The aim of our study was to evaluate whether sleep variables (both conventional and microstructural ones) in subjects with mild cognitive impairment correlate with conversion to dementia. Nineteen subjects with amnestic mild cognitive impairment (mean age 68.5 ± 7.0 years) and 11 cognitively intact healthy elderly individuals (mean age 69.2 ± 12.6 years) underwent ambulatory polysomnography for the evaluation of nocturnal sleep architecture and cyclic alternating pattern parameters. Amnestic mild cognitive impairment subjects were clinically and cognitively re‐evaluated after 2 years, during routine follow‐up, and further classified as amnestic mild cognitive impairment converters (that is, patients developing Alzheimer's disease, N = 11) and amnestic mild cognitive impairment non‐converters. Compared with healthy elderly individuals, amnestic mild cognitive impairment showed disrupted sleep with decreased rapid eye movement sleep, cyclic alternating pattern rate and cyclic alternating pattern slow‐wave‐related phases (A1 index). Standard sleep architecture analysis did not show significant differences between the two subgroups of amnestic mild cognitive impairment, whereas cyclic alternating pattern analysis showed that cyclic alternating pattern rate, A1 index and A3 index are significantly reduced in converters compared with non‐converters. Our data confirm that in amnestic mild cognitive impairment subjects there is a sleep impairment, particularly when considering more refined sleep parameters and that sleep variables at baseline are different among converters versus non‐converters at the 2‐year follow‐up. Specific sleep alterations might represent potential further biomarkers for the diagnosis and prognosis of early‐phase cognitive impairment.
Objective: Patients with obstructive sleep apnea syndrome exhibit accelerated vascular aging and renal damage. Aim of the study was to investigate whether vascular dysfunction is a feature of obstructive sleep apnea syndrome per se or instead related to the presence of traditional cardiovascular risk factors.Methods: Forty patients with moderate-severe obstructive sleep apnea syndrome (20 with, 20 without traditional risk factors) and 20 matched healthy controls were enrolled. Renal vasodilating capacity, endothelium-dependent vasodilation in the brachial artery, carotid-femoral pulse wave velocity and carotid stiffness were measured. Oxidative stress, endothelial biomarkers and leukocyte adhesion molecule levels were also evaluated.Results: Apneic patients without traditional cardiovascular risk factors presented reduced endothelium-dependent vasodilation (3.7 AE 2.1 versus 6.1 AE 3.0%, P < 0.05), increased serum E-selectin (49.8 AE 11.5 versus 38.9 AE 17.9 ng/ml, P < 0.05), and impaired renal vasodilating capacity (6.0 AE 4.3 versus 10.4 AE 6.1%, P < 0.05), as compared to healthy controls. Endothelial NO synthase expression was reduced (0.0133 versus 0.0221 Â 10 6 copies/mg RNA, P < 0.05), whereas oxidative stress parameters and leukocyte adhesion molecules were similar to controls. Patients with obstructive sleep apnea syndrome and traditional risk factors also exhibit increased aortic and carotid stiffness, increased renal resistive index and intima-media thickness, and reduced expression of the endothelial progenitor cell marker CD34: however, these parameters were similar to those of healthy controls in patients with isolated obstructive sleep apnea syndrome.Conclusion: Obstructive sleep apnea syndrome is characterized by endothelial dysfunction and activation and impaired renal vasodilating capacity even in the absence of traditional cardiovascular risk factors, possibly due to reduced endothelial NO synthase expression.
Our aim was to evaluate the EEG and clinical modifications induced by the new antiepileptic drug lacosamide (LCM) in patients with epilepsy. We evaluated 10 patients affected by focal pharmacoresistant epilepsy in which LCM (mean 250 mg/day) was added to the preexisting antiepileptic therapy, which was left unmodified. Morning waking EEG recording was performed before (t0) and at 6 months (t1) after starting LCM. At t0 and t1, patients were also administered questionnaires evaluating mood, anxiety, sleep, sleepiness, and fatigue (Beck Depression Inventory; State-Trait Anxiety Inventory Y1 and Y2; Pittsburgh Sleep Quality Index; Epworth Sleepiness Scale; Fatigue Severity Scale). We performed a quantitative analysis of EEG interictal abnormalities and background EEG power spectrum analysis. LCM as an add-on did not significantly affect anxiety, depression, sleepiness, sleep quality, and fatigue scales. Similarly, adding LCM to preexisting therapy did not modify significantly patient EEGs in terms of absolute power, relative power, mean frequency, and interictal abnormalities occurrence. In conclusion, in this small cohort of patients, we confirmed that LCM as an add-on does not affect subjective parameters which play a role, among others, in therapy tolerability, and our clinical impression was further supported by evaluation of EEG spectral analysis.
Our study showed (1) a loss of the dynamics of delta band power across the night sleep, in dementia, and (2) a different distribution of delta waves during slow-wave sleep in dementia compared with control subjects. This kind of computer-based analysis can highlight the presence of a pathologic delta activity during slow-wave sleep in dementia and may support the hypothesis of a dynamic interaction between sleep alteration and cognitive decline.
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