From Fox News: A new study has found a link between rapid eye movement (REM) sleep and Alzheimer’s disease.
The research from China, published in the journal Alzheimer’s & Dementia by the Alzheimer’s Association, analyzed the sleep cycles of 128 adults in varying states of cognition.
The study found that the highest occurrence of REM latency — which is when it takes longer for someone to reach the first REM period after drifting off to sleep — was associated with the highest risk of Alzheimer’s.
The researchers concluded that prolonged REM latency may serve as a “novel marker of risk factor” for Alzheimer’s disease and related dementias.
CLICK HERE to read an article by the Alzheimer’s Research Association about the study. Below is an important excerpt from the report:
Sleep is vital for physical and mental health. Researchers are trying to figure out how sleep could influence or be impacted by illnesses like dementia.
A recent study investigated the connection between Alzheimer’s disease and the amount of time it takes to reach the rapid eye movement (REM) stage of sleep. The study published in Alzheimer’s & Dementia discovered that taking longer to enter REM sleep was connected with major plasma biomarkers linked to Alzheimer’s disease [1].
Taking longer to enter the dreaming phase, often known as rapid eye movement (REM) sleep, can be an early symptom of Alzheimer’s, offering up new avenues for diagnosing and treating the debilitating disorder before it progresses.
Additionally, below is an important excerpt from an article published June 22 by the Alzheimer’s Association:
An estimated 6.7 million Americans over the age of 65 are living with Alzheimer’s disease (AD), and this number is expected to double by 2060.1 Though AD is primarily driven by heritable-contributing genetic risk factors, ~ 35% of AD risk may be influenced by modifiable risk factors.2
Poor sleep may be an emerging modifiable risk factor for AD,3 and this relationship is thought to be bidirectional.4 Impaired sleep in patients with AD likely results from disruptions in sleep–wake signaling due to the progression of AD pathology in brain regions that regulate sleep.5 Conversely, disturbances in key neurobiological processes that occur during sleep (e.g., anti-inflammatory processes, memory consolidation, and the clearance of adverse toxins including amyloid beta [Aβ] plaques) may contribute to the cascade of events leading to AD pathogenesis, including neurodegeneration and brain atrophy.6
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