Longer REM Latency correlates with raised ad -biomarkers, which emphasizes a potential new diagnostic marker.
Study: Association of Sleep Latency of Rapid Eye Movement with multimodal biomarkers of Alzheimer’s disease. Image Credit: Small365/Shutterstock.com
Published in a recent study in Alzheimer and dementiaResearchers assessed the relationship between sleep architecture and biomarkers of Alzheimer’s disease (AD) and related dementies (ADRDS).
Background
Sleep disorders occur in dementia patients and are increasingly associated with AD/ADRD -Biomarkers. There are indications that sleep quality, duration and excessive sleepiness during the day are associated with amyloid -β (AP) deposit in older adults.
One study reported associations between lack of sleep and increased AP values in the brain, especially in the Thalamus and Hippocampus, which are critical regions involved in ad -pathogenesis.
Slowwave Sleep (SWS), the deepest sleeping stage, has received a lot of attention for its role in gymphatic clearance (of metabolic waste) and memory consolidation.
Age-bound SWS reductions are reportedly associated with an increased risk of incident dementia. Nevertheless, it is which aspects of sleep are the most relevant to AD/ADRD pathophysiology, disputable.
About the study
In the current study, researchers investigated associations between sleep architecture and AD/ADRD biomarkers. They recruited persons of ≥ 50 years of the neurology unit of the China-Japan Friendship Hospital in China.
People with sleep -related breathing or movement disorders, use of sedative hypnotica or antipsychotic drugs, other neurodegenerative diseases in addition to AD, or other psychiatric disorders in addition to anxiety and depression were excluded.
Participants underwent an extensive diagnostic process, including symptom evaluation, neurological and physical examinations, imaging of magnetic resonance and cognitive and laboratory tests. Blood samples were collected for measurements of biomarkers.
AD/ADRD-Biomarkers were apolipoprotein e (Apoe) ε4-carrier status, brain derived neurotrophe factor (BDNF), neuro-movie lamp (NFL) and fosphorylored TAU (P-TAU) at Threonine 181 (P-TAU181).
Real-time fluorescence quantitative polymerase chain reaction was carried out to determine the Apoe ε4 status, and the presence of at least one ε4 allel was considered Apoe ε4 positive.
18F-Florpetapir Positron-EmissietoMography (PET) Imaging was carried out to assess AP-Plaque deposition. All subjects underwent an overnight stay Polysomnography (PSG).
PSG parameters include sleep efficiency (SE), Rapid Eye Movement (REM) Latency (REML), Total Sleep Time (TST), Sleep initial impairment (SOL) and percentages of time spent in non-REM stage 1 (N1), N2, N3 or SWS, and brake.
The researchers used Chi squared and Krankal-Wallis tests to compare differences in categorical and continuous variables between participants with normal cognition (NC), mild cognitive disorders (MCI) and AD.
Univariable and multivariable linear regression analyzes rated associations between lettuce makers and biomarkers.
Analyzes were initially adapted for gender and age and then for Apoe ε4 status, smoking, body mass index (BMI), mini-mentally state exam (MMSE) score and diabetes mellitus. Sleeping device tertiles were investigated to further explore non-linear relationships.
Findings
The study recruited an average of 128 people aged 70.8 aged 70.8 years. All participants were Han Chinese, 57% were women, 64 were diagnosed with AD, 41 had mci and 23 had NC. AD patients had a larger proportion of Apoe ε4 carriers and lower MMSE scores.
Persons with AD or MCI had lower SWS percentages and longer Sol and Reml than with NC, albeit statistically insignificant. There was a significant correlation of Reml with AP -deposition and BDNF.
Participants in the highest tertile of Reml had significantly raised levels of P-TAU181, lower BDNF and higher AP deposition than those in the lowest tertile. In addition, individuals in the highest tertile REM percentage showed a significantly reduced P-TAU181.
Gender and age corrected analyzes yielded consistent findings; In analyzes with additional adjustments, Reml was significantly associated with increased P-TAU181 and lower BDNF.
Lower SWS and REM percentages were associated with raised P-TAU181. In sensitivity analyzes, the associations between Reml and BDNF and AP last significance after correction for false discovery speed, while those of lower SWS and REM percentages with higher P-TAU181 levels were no longer maintained.
Furthermore, the associations of Reml with AD/ADRD biomarkers were independent of SOL, SE and TST.
Conclusions
In short, the findings indicate an association of long-term Reml with a higher AP load, lower BDNF and increased P-TAU181 in middle and older adults on AD continums. These associations were considerable, even after adjustments for different confounders.
Since these pathological changes precede clinical symptoms, long -term Reml could be an early neurodegeneration marking. Further studies are needed to assess whether the target of Reml could change the AD/ADRD risk.