Sleep matters: Neurodegeneration spectrum heterogeneity, combustion and friction ultrafine particles, industrial nanoparticle pollution, and sleep disorders-Denial is not an option.

Sustained exposures to ubiquitous outdoor/indoor fine particulate matter (PM2.5), including combustion and friction ultrafine PM (UFPM) and industrial nanoparticles (NPs) starting in utero, are linked to early pediatric and young adulthood aberrant neural protein accumulation, including hyperphosphorylated tau (p-tau), beta-amyloid (Aß1 - 42), α-synuclein (α syn) and TAR DNA-binding protein 43 (TDP-43), hallmarks of Alzheimer's (AD), Parkinson's disease (PD), frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). UFPM from anthropogenic and natural sources and NPs enter the brain through the nasal/olfactory pathway, lung, gastrointestinal (GI) tract, skin, and placental barriers. On a global scale, the most important sources of outdoor UFPM are motor traffic emissions. This study focuses on the neuropathology heterogeneity and overlap of AD, PD, FTLD, and ALS in older adults, their similarities with the neuropathology of young, highly exposed urbanites, and their strong link with sleep disorders. Critical information includes how this UFPM and NPs cross all biological barriers, interact with brain soluble proteins and key organelles, and result in the oxidative, endoplasmic reticulum, and mitochondrial stress, neuroinflammation, DNA damage, protein aggregation and misfolding, and faulty complex protein quality control. The brain toxicity of UFPM and NPs makes them powerful candidates for early development and progression of fatal common neurodegenerative diseases, all having sleep disturbances. A detailed residential history, proximity to high-traffic roads, occupational histories, exposures to high-emission sources (i.e., factories, burning pits, forest fires, and airports), indoor PM sources (tobacco, wood burning in winter, cooking fumes, and microplastics in house dust), and consumption of industrial NPs, along with neurocognitive and neuropsychiatric histories, are critical. Environmental pollution is a ubiquitous, early, and cumulative risk factor for neurodegeneration and sleep disorders. Prevention of deadly neurological diseases associated with air pollution should be a public health priority.

Fall Risk, Sleep Behavior, and Sleep-Related Movement Disorders in Young Urbanites Exposed to Air Pollution.

BACKGROUND: Quadruple aberrant hyperphosphorylated tau, amyloid-ß, α-synuclein, and TDP-43 pathology had been documented in 202/203 forensic autopsies in Metropolitan Mexico City ≤40-year-olds with high exposures to ultrafine particulate matter and engineered nanoparticles. Cognition deficits, gait, equilibrium abnormalities, and MRI frontal, temporal, caudate, and cerebellar atrophy are documented in young adults. OBJECTIVE: This study aimed to identify an association between falls, probable Rapid Eye Movement Sleep Behavior Disorder (pRBD), restless leg syndrome (RLS), and insomnia in 2,466 Mexican, college-educated volunteers (32.5±12.4 years). METHODS: The anonymous, online study applied the pRBD and RLS Single-Questions and self-reported night-time sleep duration, excessive daytime sleepiness, insomnia, and falls. RESULTS: Fall risk was strongly associated with pRBD and RLS. Subjects who fell at least once in the last year have an OR = 1.8137 [1.5352, 2.1426] of answering yes to pRBD and/or RLS questions, documented in 29% and 24% of volunteers, respectively. Subjects fell mostly outdoors (12:01 pm to 6:00 pm), 43% complained of early wake up hours, and 35% complained of sleep onset insomnia (EOI). EOI individuals have an OR of 2.5971 [2.1408, 3.1506] of answering yes to the RLS question. CONCLUSION: There is a robust association between falls, pRBD, and RLS, strongly suggesting misfolded proteinopathies involving critical brainstem arousal and motor hubs might play a crucial role. Nanoparticles are likely a significant risk for falls, sleep disorders, insomnia, and neurodegenerative lethal diseases, thus characterizing air particulate pollutants' chemical composition, emission sources, and cumulative exposure concentrations are strongly recommended.

TXT me I'm only sleeping: adolescents with mobile phones in their bedroom.

The purpose of this study was to determine if mobile phones interfere with adolescent sleep. We conducted a pilot test in a pediatric primary care practice of 454 patients, half female (51.2%), 12 to 20 years old (mean = 15) attending a well-child visit. Adolescents completed paper-and-pencil surveys in the waiting room. More than half took their mobile phone to bed (62.9%) and kept it turned on while sleeping (56.8%). Almost half used their phone as their alarm (45.7%). More than one-third texted after going to bed (36.7%). Two or more times per week, 7.9% were awakened by a text after going to sleep.

Ethical considerations in REM sleep behavior disorder.

A patient diagnosed with REM behavior sleep disorder (RBD) has as much as a 65% risk of developing an α-synucleinopathy. Currently, it is not possible to predict whether an individual will develop a disease, or, if so, which disease.The neurologist treating the patient must consider (1) the difference between disclosing a diagnosis and disclosing the risk of a diagnosis; (2) whether to disclose this risk to patients; and (3) if deciding to disclose the risk, the appropriate timing of such a conversation.

Headache complaints in relation to nocturnal oxygen saturation among patients with sleep apnea syndrome.

BACKGROUND: Morning headaches are often ascribed to patients with sleep apnea syndrome (SAS) but the etiology of headaches in SAS is unclear. Given the relationship between oxygen and other headache syndromes, nocturnal hypoxia might be one factor contributing to headaches in SAS. METHODS: All subjects 18-80 years of age who were determined to have SAS and who underwent a continuous positive airway pressure trial in our sleep laboratory between March 1, 1997 and March 18, 1998 were considered for inclusion. Subjects were grouped according to whether they endorsed that waking with headaches is a problem for them. Polysomnography and standardized questionnaires were used to test the main hypothesis that patients with SAS and headaches would spend more time at lower oxyhemoglobin levels than those SAS patients without headache. RESULTS: Headache and non-headache patients did not differ in the percentage of time spent with an oxygen saturation less than 90%, either in total sleep time or in rapid eye movement sleep (REM). The headache patients were more likely to be female and spend a lower percentage of time in REM sleep. The REM sleep difference was not accounted for by the use of REM suppressing medications or by depression (as measured by the Zung scale). CONCLUSIONS: These data do not support the hypothesis that the duration of nocturnal hypoxemia relates to headache complaints in patients with SAS. The lower REM sleep percentage and higher variability in REM apnea index among the headache patients warrants further investigation.