Alzheimer’s disease (AD) is one of the commonest causes of dementia. Normally beginning with affecting one’s ability to think and remember and eventually resulting in a total dependence with limited to no mobility. The pathology of AD is partly understood and beta-amyloid plaques and neurofibrillary tangles caused by hyperphosphorylation of tau protein are its two distinct features. No specific treatment exists to reverse this pathology they mainly attempt to inhibit its propagation. Similarly, the exact causes of AD are not yet established, however, many risk factors have been pointed out. These include aging, diabetes, and genetic basis amongst others. A recent study published in the journal Neurology, now suggests that sleep deprivation can be directly linked to the propagation of AD pathological features.
Sleep deprivation is much more common than what one imagines it to be. According to a report, one in every three American and roughly about 45% of the global population is deprived of sleep. The cerebrospinal fluid (CSF) found in the brain and the spinal cord contains multiple biomarkers which can be used to assess the presence and degree of AD pathology. This particular study comprised of using 101 participants who were cognitively normal but had a greater risk of AD mainly due to family history. The study included both male and female participants and most participants were over 60 years of age. It was found that worse sleep qualities are associated with greater AD pathology as indicated by biomarkers of amyloidal metabolism (Aβ42) and phosphorylated tau (P-tau) and neuronal/axonal degeneration (T-tau).
Biomarkers of AD pathology
Now to the list all those horrible outcomes which come from sleep deprivation one can perhaps add dementia. But there is a slight catch here. While one may say that poor sleep directly relates to detrimental pathology it is also true that the brain itself directly affects the quality and quantity of sleep. It is a bit like the classic chicken and egg problem in a way. The other major caveat of any such a study is the subjectivity of measuring sleep. Given that there is no robust and universal way of classifying sleep deprivation the data cannot be approved with absolute certainty. Nonetheless, it does contribute to some level of understanding of the subject.
Kate E. Sprecher et al. Poor sleep is associated with CSF biomarkers of amyloid pathology in cognitively normal adults, Neurology 2017.