Suboptimal Sleep Linked to Amyloid-Beta Accumulation

 What is your doctor's sleep protocols to ensure this doesn't happen post stroke?

Mine seemed to be, hand out sleeping pills like candy at 10pm, then have the vampire squad come in at 7am to steal blood from at least one person in the quad. Turning on the lights in the process, clinical staff efficiency, not for patient wellbeing.  Do sleeping pills provide decent sleep? Why doesn't your doctor know that answer?

Like maybe this from May 2022?

First-of-its-Kind Study Demonstrates Digital Therapeutic Significantly Improves Sleep and Mental Health for Stroke Patients

Don't expect a damn thing from your doctor, I'm sure s/he does not follow stroke research and certainly doesn't implement it.

Do you prefer your  doctor incompetence NOT KNOWING? OR NOT DOING? Because your doctor is incompetent if nothing is being done to create a sleep protocol, in my opinion.

Suboptimal Sleep Linked to Amyloid-Beta Accumulation

By Nancy Melville

VIRTUAL -- August 5, 2022 -- Deficits in sleep duration and efficiency are significantly associated with increases in the accumulation of amyloid in the brain over time, and the effect is strongest in carriers of the apolipoprotein E (APOE) ε4 allele genetic status, according to a study presented at the 2022 Alzheimer’s Association International Conference (AAIC).

“Our study is the first to report that self-reported sleep quality factors representing markers of poor sleep could be used to predict accumulation of brain amyloid-beta,” said Louise N. Pivac, Murdoch University, Perth, Western Australia, Australia.

“These findings indicate a role for self-reported suboptimal sleep efficiency and duration in the accumulation of Alzheimer's disease neuropathology in cognitively normal individuals,” she said. 

Previous research has linked sleep deficits with an increased risk of Alzheimer’s disease, with 1 study showing that people who are not cognitively impaired but have poor sleep have as much as a 3.78-times-higher risk of having preclinical Alzheimer’s disease.

Conversely, additional studies show that “good quality sleep enhances the clearance of brain amyloid-beta via the glymphatic system,” she said.

To evaluate the relationship between self-reported sleep quality and longitudinal accumulation of amyloid in the brain, considered a hallmark of the development of Alzheimer’s disease, in cognitively normal older adults, Pivac and colleagues analysed data from the Australian Imaging, Biomarkers and Lifestyle Study of Ageing (AIBL).

They identified 158 adults aged >60 years (mean age, 73.8 years; 51.6% women) who had no cognitive deficits and a minimum of 3 amyloid-beta positron emission tomography (PET) scans available. All were classified as amyloid “accumulators,” defined as individuals with a higher amyloid burden, with a centiloid level of ≥20 at baseline or any level of accumulation over 36 months.

Patients’ self-reported sleep characteristics were assessed at baseline based on the Pittsburgh Sleep Quality Index and other factors. PET was used to assess longitudinal levels of amyloid over a minimum of 3 timepoints, ranging from 33.3 to 73.9 months. 

With a follow-up of 6 years, cross-sectional analysis showed that a longer total sleep time of >8 hours significantly predicted lower accumulation of amyloid in the overall cohort (P = .042), and among those who were not carriers of APOE ε4 (P = .043).

In individuals who were carriers of APOE ε4, however, the association was stronger, with sleep duration of <6 hours per night significantly predicting a faster accumulation of brain amyloid over time, after correction (P = .006). Carriers of APOE ε4 who reported an average of <6 hours of sleep had an ~27% greater brain amyloid accumulation than those with sleep duration of 6 to 8 hours.

The results were similar in terms of sleep efficiency (the percentage of time spent in bed asleep), with better sleep efficiency on the scale associated with slower amyloid accumulation in the cohort overall (P = .012) and among APOE ε4 noncarriers (P = .011). 

Meanwhile, sleep efficiency of <65% predicted faster accumulation of amyloid in the whole cohort over time and in APOE ε4 noncarriers (both P = .003). In APOE ε4 noncarriers over a 6-year period, participants with sleep efficiency of <65% accumulated ~32% more amyloid than those with sleep efficiency of >85%,placing them on what seems to be a trajectory similar to that of APOE ε4 carriers who are good sleepers.

“Overall, we found that short sleep duration of <6 hours per night predicted faster brain amyloid-beta accumulation over time in APOE ε4 carriers,” she said. “Poor sleep efficiency of <65% predicted faster brain amyloid-beta accumulation over time in the whole cohort and in APOE ε4 noncarriers.”

“Poor sleep efficiency of <65% suggests a potential mechanism via which APOE ε4 noncarriers progress to brain amyloid-beta positivity and a subsequent increased risk of Alzheimer's disease,” concluded Pivac.

“These thresholds of poor self-reported sleep quality may be of greater clinical utility in determining who may best benefit from sleep interventions and indicate that poor sleep represents a biomarker for subsequent amyloid accumulation,” Pivac added.

Pivac noted that future research is needed to explore whether improvements in sleep quality could slow the accumulation of amyloid-beta.

[Presentation title: Suboptimal Sleep Efficiency and Duration Predicts Rate of Accumulation of Aβ- Amyloid in Cognitively Normal Older Adults]