The Causes Of Preclinical AD
As previously mentioned, preclinical AD begins approximately 15 years before the cognitive system actually begins to get impacted by the chemical imbalances of the brain. The cause of preclinical AD revolves around the formation of amyloid plaques that begin to slowly deposit in various regions of the brain, particularly forming in the hypothalamus and the cerebral cortex which are areas imperative to regulating one’s circadian clock; the amyloid plaques form gradually over time as the disease progresses due to sleeplessness, the earliest symptoms being sleep-wake disturbances and prolonged wakefulness (Limm et al., 2014). The more plaque there is in these important regions, the more sleep-wake fragmentation occurs in the person, usually stemming
from sleep deprivation. These plaques and chemical imbalances are discovered through a system known as polysomnography which involves an analysis of the brain’s activity during sleep, such as observing one’s leg and eye movements during their rest and monitoring their heart rate. Some of the symptoms involved in AD connected to sleep disorders are decreases in slow-wave sleep, heavy sleep fragmentation and rapid eye movement; records show that approximately 25%-60% of patients suffering AD have common complaints of sleeplessness, with the most common complaints being insomnia, lingering drowsiness throughout the daytime, and waking up frequently through their sleep (Limm et al., 2014). An experiment that establishes the direct connection between amyloid plaque and sleep-wake disturbances involves mice with a Swedish mutation known as Tg2576 line that caused amyloid plaques to form in the brain stem which holds neurons that regulate REM sleep, resulting in heavy abnormalities in their sleep-wake cycle and daily cognitive functions (Limm et al., 2014). There is a certain reciprocality involved in sleep-wake cycles and formation of the amyloid plaques that result in the increased cause of dementia, being that restlessness results in the formation of the plaques, and more plaques equals more fragmentation during sleep and more time awake despite being exhausted, and the cycle continues to worsen with age due to the spreading of the plaques on the imperative regions of the brain for sleep regulation.
from sleep deprivation. These plaques and chemical imbalances are discovered through a system known as polysomnography which involves an analysis of the brain’s activity during sleep, such as observing one’s leg and eye movements during their rest and monitoring their heart rate. Some of the symptoms involved in AD connected to sleep disorders are decreases in slow-wave sleep, heavy sleep fragmentation and rapid eye movement; records show that approximately 25%-60% of patients suffering AD have common complaints of sleeplessness, with the most common complaints being insomnia, lingering drowsiness throughout the daytime, and waking up frequently through their sleep (Limm et al., 2014). An experiment that establishes the direct connection between amyloid plaque and sleep-wake disturbances involves mice with a Swedish mutation known as Tg2576 line that caused amyloid plaques to form in the brain stem which holds neurons that regulate REM sleep, resulting in heavy abnormalities in their sleep-wake cycle and daily cognitive functions (Limm et al., 2014). There is a certain reciprocality involved in sleep-wake cycles and formation of the amyloid plaques that result in the increased cause of dementia, being that restlessness results in the formation of the plaques, and more plaques equals more fragmentation during sleep and more time awake despite being exhausted, and the cycle continues to worsen with age due to the spreading of the plaques on the imperative regions of the brain for sleep regulation.