Neurodegenerative diseases have been often associated with sleep disorders, mainly when they are characterized by abnormal accumulation of alpha-synuclein, such as multiple system atrophy (MSA), Parkinson's disease (PD) and Lewy body disease (LBD).[21][22][23][24][25][26][27] For instance, people diagnosed with PD have often presented different kinds of sleep concerns, commonly regard to insomnia (around 70% of the PD population), hypersomnia (more than 50% of the PD population), and REM sleep behavior disorder (RBD) - that may affect around 40% of the PD population and it is associated with increased motor symptoms.[21][22][23][24][25][27] Importantly, RBD has been also highlighted as a strong precursor of developing dementia in PD patients over several years in prior, which seems to be a great opportunity for improving the treatments of the disease.[22][24]
Even if you’ve struggled with sleep problems for so long that it seems normal, you can still learn to sleep better. You can start by tracking your symptoms and sleep patterns, and then making healthy changes to your daytime habits and bedtime routine. If self-help doesn’t do the trick, you can turn to sleep specialists who are trained in sleep medicine. Together, you can identify the underlying causes of your sleeping problem and find ways to improve your sleep and quality of life.
Sort of a milder cousin of sleep apnea, UARS occurs when some type of resistance slows or blocks air in the nasal passages. The most common causes are mild nasal congestion or a tongue position during sleep that blocks breathing. Because the resistance makes it harder work simply to breathe, your body is half-waking up over and over again during the night, so you don't feel refreshed in the morning.
In addition, an evidence-based synopses suggests that the sleep disorder, idiopathic REM sleep behavior disorder (iRBD), may have a hereditary component to it. A total of 632 participants, half with iRBD and half without, completed self-report questionnaires. The results of the study suggest that people with iRBD are more likely to report having a first-degree relative with the same sleep disorder than people of the same age and sex that do not have the disorder.[19] More research needs to be conducted to gain further information about the hereditary nature of sleep disorders.

One factors that could explain this change in sleep architecture is a change in circadian rhythm, which regulates sleep.[29] A disruption of the circadian rhythm would therefore generate sleep disturbances.[29] Some studies show that people with AD have a delayed circadian rhythm, whereas in normal aging we will find an advanced circadian rhythm.[29][31]

Although the exact mechanisms and the causal relationship between sleep disturbances and AD are not yet clear, these findings already provide a better understanding. In addition, they open up ideas for the implementation of treatments to curb the cognitive decline of patients suffering from this disease. In the same way, it also makes it possible to better target at risk population.
Some of the biggest differences between the 2nd and 3rd editions are how the various sleep disorders were divided into categories. The 2005 edition used 3 broad categories to organize all of the sleep disorders under either dysommnias (disorders making getting to sleep or staying asleep difficult), parasomnias (disorders that intrude into the sleep process), and sleep disorders associated with a mental, neurologic, or other medical disorders (disorders whose symptoms are not primary unto themselves but caused by other conditions).
Sleep disturbances have been also observed in Alzheimer's disease (AD), affecting about 45% of its population.[22][24][26] Moreover, when it is based on caregiver reports this percentage is even higher, about 70%.[28] As well as in PD population, insomnia and hypersomnia are frequently recognized in AD patients, which have been associated with accumulation of Beta-amyloid, circadian rhythm sleep disorders (CRSD) and melatonin alteration.[22][24][28] Additionally, changes in sleep architecture are observed in AD too.[22][24][26] Even though with ageing the sleep architecture seems to change naturally, in AD patients it is aggravated. SWS is potentially decreased (sometimes totally absent), spindles and the time spent in REM sleep are also reduced, while its latency is increased.[28] The poorly sleep onset in AD has been also associated with dream-related hallucination, increased restlessness, wandering and agitation, that seem to be related with sundowning - a typical chronological phenomenon presented in the disease.[24][28]

If sleeping with a mask on doesn't work for you, other options are surgery; oral appliances; and newer, minimally invasive outpatient surgical treatments. These include the Pillar procedure, which involves using permanent stitches to firm up the soft palate; coblation, which uses radiofrequency to shrink nasal tissues; and even use of a carbon dioxide laser to shrink the tonsils.