Alzheimer’s disease (AD) is a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including sleep disturbances, disorders and circadian rhythm abnormalities. Mounting evidence support the relationship between local sleep processes, circadian rhythm abnormalities and AD pathophysiology. Recent studies show that pathognomonic features of AD including Aβ, tau, and neurodegeneration, all result in specific deficits in local and global sleep and circadian expression that depend on the underlying brain regions affected. More importantly, sleep disturbances and circadian rhythm abnormalities tend to co-occur with other AD modifiable risk factors (e.g. aging, vascular risk factors, mood, physical activity, diet and lifestyle), some of which are associated with established biomarkers for AD progression. What remains unexamined are the combined effects of sleep disturbances/disorders, circadian rhythm abnormalities and other commonly co-occurring modifiable risk factors on biomarkers of AD pathology. Further, methods to examine the confluence of these exposures have been limited, with potential causal mechanisms linking these synergistic exposures to AD progression yet to be fully understood.
Recent evidence show that novel plasma markers of amyloid are associated with established AD markers including cerebral amyloid and tau deposition. Plasma Aβ42/Aβ40 has a high correspondence with amyloid PET and CSF p-tau181/Aβ42. Novel plasma markers of Aβ42, Aβ40, P-tau and T-tau levels have similar trajectories with CSF Aβ42, Aβ40, P-tau and T-tau levels, in terms of biomarker alterations during development of AD. High-precision plasma Aβ42/40 ratio predicts current and future brain amyloidosis. Since novel AD plasma-biomarkers represent a potential minimal-invasive reliable and cost-effective blood test that can potentially power large clinical AD trials, it has become clear that further examination of the impact of risk factors for AD, and their associations with novel AD plasma-biomarkers is critical. Therefore, in this special topic section, we aim to more deeply examine and understand interactions between sleep, circadian rhythm abnormalities and modifiable risk factors on both established and more importantly, novel plasma AD markers by presenting: (1) promising novel research on this topic, (2) systematic reviews and meta-analyses of relevant literature to date, and (3) novel or other closely aligned-field methodological approaches to investigating this research question.
Specific themes we would like contributors to address include novel research examining:
• synergistic or additive impacts of both individual differences of self-reported and/or objective sleep measures and/or circadian rhythm abnormalities with other AD modifiable risk factors (e.g. aging, vascular risk factors, mood, physical activity, diet and lifestyle, genetic and other early life indicators) on established and/or novel plasma AD markers
• synergistic or additive impacts of sleep micro and macro architectural EEG measures and/or circadian rhythm abnormalities with other AD modifiable risk factors within the context of race-specific and/or sex and gender specific susceptibility and/or progression of AD pathology burden
• synergistic or additive impacts of sleep disorders and/or circadian rhythm abnormalities with other AD modifiable risk factors on established and/or novel plasma AD markers
• mechanistic pathways of possible synergistic or additive impacts of sleep, circadian rhythm abnormalities and other physiologic processes on AD progression using AD transgenic mice models
The types of manuscripts we are interested in include:
• Original investigations i.e. cross-sectional, longitudinal and experimental studies
• Systematic reviews and meta-analyses of relevant literature to date
• Perspectives or positional papers are also welcome
• Manuscripts addressing novel or other closely aligned-field methodological
approaches, to examining this research question, are also welcome
Alzheimer’s disease (AD) is a multifactorial and heterogeneous disease with multiple contributors to its pathophysiology, including sleep disturbances, disorders and circadian rhythm abnormalities. Mounting evidence support the relationship between local sleep processes, circadian rhythm abnormalities and AD pathophysiology. Recent studies show that pathognomonic features of AD including Aβ, tau, and neurodegeneration, all result in specific deficits in local and global sleep and circadian expression that depend on the underlying brain regions affected. More importantly, sleep disturbances and circadian rhythm abnormalities tend to co-occur with other AD modifiable risk factors (e.g. aging, vascular risk factors, mood, physical activity, diet and lifestyle), some of which are associated with established biomarkers for AD progression. What remains unexamined are the combined effects of sleep disturbances/disorders, circadian rhythm abnormalities and other commonly co-occurring modifiable risk factors on biomarkers of AD pathology. Further, methods to examine the confluence of these exposures have been limited, with potential causal mechanisms linking these synergistic exposures to AD progression yet to be fully understood.
Recent evidence show that novel plasma markers of amyloid are associated with established AD markers including cerebral amyloid and tau deposition. Plasma Aβ42/Aβ40 has a high correspondence with amyloid PET and CSF p-tau181/Aβ42. Novel plasma markers of Aβ42, Aβ40, P-tau and T-tau levels have similar trajectories with CSF Aβ42, Aβ40, P-tau and T-tau levels, in terms of biomarker alterations during development of AD. High-precision plasma Aβ42/40 ratio predicts current and future brain amyloidosis. Since novel AD plasma-biomarkers represent a potential minimal-invasive reliable and cost-effective blood test that can potentially power large clinical AD trials, it has become clear that further examination of the impact of risk factors for AD, and their associations with novel AD plasma-biomarkers is critical. Therefore, in this special topic section, we aim to more deeply examine and understand interactions between sleep, circadian rhythm abnormalities and modifiable risk factors on both established and more importantly, novel plasma AD markers by presenting: (1) promising novel research on this topic, (2) systematic reviews and meta-analyses of relevant literature to date, and (3) novel or other closely aligned-field methodological approaches to investigating this research question.
Specific themes we would like contributors to address include novel research examining:
• synergistic or additive impacts of both individual differences of self-reported and/or objective sleep measures and/or circadian rhythm abnormalities with other AD modifiable risk factors (e.g. aging, vascular risk factors, mood, physical activity, diet and lifestyle, genetic and other early life indicators) on established and/or novel plasma AD markers
• synergistic or additive impacts of sleep micro and macro architectural EEG measures and/or circadian rhythm abnormalities with other AD modifiable risk factors within the context of race-specific and/or sex and gender specific susceptibility and/or progression of AD pathology burden
• synergistic or additive impacts of sleep disorders and/or circadian rhythm abnormalities with other AD modifiable risk factors on established and/or novel plasma AD markers
• mechanistic pathways of possible synergistic or additive impacts of sleep, circadian rhythm abnormalities and other physiologic processes on AD progression using AD transgenic mice models
The types of manuscripts we are interested in include:
• Original investigations i.e. cross-sectional, longitudinal and experimental studies
• Systematic reviews and meta-analyses of relevant literature to date
• Perspectives or positional papers are also welcome
• Manuscripts addressing novel or other closely aligned-field methodological
approaches, to examining this research question, are also welcome