scholarly journals Is Sleep Disruption a Cause or Consequence of Alzheimer’s Disease? Reviewing Its Possible Role as a Biomarker

2020 ◽  
Vol 21 (3) ◽  
pp. 1168 ◽  
Author(s):  
Maria-Angeles Lloret ◽  
Ana Cervera-Ferri ◽  
Mariana Nepomuceno ◽  
Paloma Monllor ◽  
Daniel Esteve ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Cognitive Processing ◽  
Memory Consolidation ◽  
Sleep Disturbances ◽  
Sleep Disruption ◽  
High Prevalence ◽  
Sleep Microstructure ◽  
Sleep Alterations

In recent years, the idea that sleep is critical for cognitive processing has gained strength. Alzheimer’s disease (AD) is the most common form of dementia worldwide and presents a high prevalence of sleep disturbances. However, it is difficult to establish causal relations, since a vicious circle emerges between different aspects of the disease. Nowadays, we know that sleep is crucial to consolidate memory and to remove the excess of beta-amyloid and hyperphosphorilated tau accumulated in AD patients’ brains. In this review, we discuss how sleep disturbances often precede in years some pathological traits, as well as cognitive decline, in AD. We describe the relevance of sleep to memory consolidation, focusing on changes in sleep patterns in AD in contrast to normal aging. We also analyze whether sleep alterations could be useful biomarkers to predict the risk of developing AD and we compile some sleep-related proposed biomarkers. The relevance of the analysis of the sleep microstructure is highlighted to detect specific oscillatory patterns that could be useful as AD biomarkers.

scholarly journals A Systematic Review of Cognitive Event-Related Potentials in mild cognitive impairment and Alzheimer’s disease

2020 ◽  
Author(s):  
Elizabeth R. Paitel ◽  
Marielle R. Samii ◽  
Kristy A Nielson
Keyword(s):  
Systematic Review ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Cognitive Processing ◽  
Event Related Potentials ◽  
Complex Tasks ◽  
Related Potentials

This systematic review examined whether event-related potentials (ERPs) during higher cognitive processing can detect subtle, early signs of neurodegenerative disease. Original, empirical studies retrieved from PsycINFO and PubMed were reviewed if they analyzed patterns in cognitive ERPs (150ms post-stimulus) differentiating mild cognitive impairment (MCI), Alzheimer’s disease (AD), or cognitively intact elders who carry AD risk through the Apolipoprotein-E ε4 allele (ε4+) from healthy older adult controls (HC). The 100 studies meeting inclusion criteria (MCI=47; AD=47; ε4+=6) analyzed N200, P300, N400, and occasionally, later components. While there was variability across studies, patterns of reduced amplitude and delayed latency were apparent in pathological aging, consistent with AD-related brain atrophy and cognitive impairment. These effects were particularly evident in advanced disease progression (i.e., AD > MCI) and in later ERP components measured during complex tasks. Although ERP studies in intact ε4+ elders are thus far scarce, a similar pattern of delayed latency was notable, along with a contrasting pattern of increased amplitude, consistent with compensatory neural activation. This limited work suggests ERPs might be able to index early neural changes indicative of future cognitive decline in otherwise healthy elders. As ERPs are also accessible and affordable relative to other neuroimaging methods, their addition to cognitive assessment might substantively enhance early identification and characterization of neural dysfunction, allowing opportunity for earlier differential diagnosis and targeting of intervention. To evaluate this possibility there is urgent need for well-powered studies assessing late cognitive ERPs during complex tasks, particularly in healthy elders at risk for cognitive decline.

scholarly journals Sleep disturbance: an emerging opportunity for Alzheimer's disease prevention?

2016 ◽  
Vol 29 (4) ◽  
pp. 529-531 ◽  
Author(s):  
Adam P. Spira ◽  
Rebecca F. Gottesman
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Sleep Disturbances ◽  
Sleep Disordered Breathing ◽  
Later Life ◽  
Optimal Timing ◽  
Modifiable Risk Factors ◽  
Dementia Prevalence ◽  
Ad Prevention

As the older segment of our population grows, cognitive decline and dementia will increase in prevalence, with Alzheimer's disease (AD) as the cause in most cases. Until a cure exists, prevention through the identification and manipulation of modifiable risk factors for dementia, in general, or AD, in particular, will be our only means of reducing dementia prevalence or delaying its onset. Furthermore, it is likely that eventual treatments for AD, when available, will depend on the ability to identify individuals at greatest risk for developing AD. Sleep disturbances are common in later life – roughly half of older adults experience regular insomnia (Ohayon, 2002) and about as many have some degree of sleep-disordered breathing (SDB) (Ancoli-Israel et al., 1991) – and accumulating evidence suggests they may contribute to cognitive decline, at least in part, by promoting the development of AD pathology (Spira et al., 2014). Because they are treatable, sleep disturbances are an important potential target for ongoing study in AD prevention. Moreover, understanding the mechanisms underlying an effect of sleep on subsequent cognitive decline and AD would allow for better identification of opportunities and optimal timing for treatment of sleep disorders, and ultimately perhaps, AD prevention.

scholarly journals Association of Sleep Disturbances and Cognitive Decline among Cognitively Normal Elders Over Time

2021 ◽  
Author(s):  
Wei Feng ◽  
Mandela William Nzoyoum Kuetche ◽  
Meng Zhang ◽  
MengMeng Liu ◽  
Deginet Aklilu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Function ◽  
Cognitive Decline ◽  
Regression Models ◽  
Sleep Disturbances ◽  
Amyloid Pet ◽  
Longitudinal Impact ◽  
Cognitively Normal ◽  
Over Time

Abstract Background: While sleep disturbances (SD) has been shown to be associated with worse cognition, but the causal relationship between the two subjects to debate. Our objective was to investigate the longitudinal impact of SD on cognitive function.Objective: To determine the effect of self-reported clinical diagnosis of SD on longitudinal changes in brain amyloid-PET, CSF-biomarkers (Aβ42, T-tau and P-tau) and cognitive function in cognitively normal.Methods: A total of 463 cognitively normal elders (357 normal and 106 SD) were included. Alzheimer’s Disease Neuroimaging Initiative (ADNI) participants were collected from 2005 to 2020. The generalized linear mixed models adjusting variables which were selected by the Akaike Information Criterion (AIC) and the marginal effect estimation method was used to estimate the risk effect of SD. Cox proportional hazards regression models estimated the relative hazard of Alzheimer’s Disease (AD), among baseline SD patients.Results: The age range of participants was 73.60±5.71 years old, and the female proportion was 43.63%. In adjusted regression models, Participants with baseline SD had higher likelihood of developing worse cognition over subsequent follow-up, PACC (decrease 7.53 points [95%CI, 7.36-7.70]; P<0.001), MMSE (decrease 5.26 points [95%CI, 5.17-5.35]; P<0.001), and CDR–Sum of Boxes (increase 5.61 points [95%CI, 5.67-5.54]; P=0.001). Similarly, Cox regression analysis suggested that sleep disturbances is a risk factor of AD (HR=1.55, 95% CI=1.08 to 2.22).Conclusion: SD probably is a warning sign of AD, because it is associated with greater likelihood of cognitive decline or dementia over time. Associations are likely multifactorial and could be explained by intervening variables in the path from SD to dementia, or by common risk factors for pathological processes in brain. These findings suggest need for more attentions of older adults with sleep compromise.

scholarly journals Plasma Total Tau and Neurobehavioral Symptoms of Cognitive Decline in Cognitively Normal Older Adults

2021 ◽  
Vol 12 ◽  
Author(s):  
James R. Hall ◽  
Melissa Petersen ◽  
Leigh Johnson ◽  
Sid E. O’Bryant
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Significant Relationship ◽  
Sleep Disturbances ◽  
Cognitively Normal ◽  
Total Tau ◽  
Neurobehavioral Symptoms ◽  
The Impact

Depression and related neurobehavioral symptoms are common features of Alzheimer’s disease and other dementias. The presence of these potentially modifiable neurobehavioral symptoms in cognitively intact older adults may represent an early indication of pathophysiological processes in the brain. Tau pathology is a key feature of a number of dementias. A number of studies have found an association between tau and neurobehavioral symptoms. The current study investigated the relationship of a blood-based biomarker of tau and symptoms of depression, anxiety, worry, and sleep disturbances in 538 community based, cognitively normal older adults. Logistic regression revealed no significant relationship between plasma total tau and any measures of neurobehavioral symptoms. To assess the impact of level of tau on these relationships, participants were divided into those in the highest quintile of tau and those in the lower four quintiles. Regression analyses showed a significant relationship between level of plasma total tau and measures of depression, apathy, anxiety, worry and sleep. The presence of higher levels of plasma tau and elevated neurobehavioral symptoms may be an early indicator of cognitive decline and prodromal Alzheimer’s disease. Longitudinal research is needed to evaluate the impact of these factors on the development of dementia and may suggest areas for early intervention.

Subjective Spatial Navigation Complaints - A Frequent Symptom Reported by Patients with Subjective Cognitive Decline, Mild Cognitive Impairment and Alzheimer's Disease

2018 ◽  
Vol 15 (3) ◽  
pp. 219-228 ◽  
Author(s):  
Jiri Cerman ◽  
Ross Andel ◽  
Jan Laczo ◽  
Martin Vyhnalek ◽  
Zuzana Nedelska ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Spatial Navigation ◽  
Subjective Cognitive Decline ◽  
Great Effort ◽  
Frequent Symptom ◽  
Normal Controls

Background: Great effort has been put into developing simple and feasible tools capable to detect Alzheimer's disease (AD) in its early clinical stage. Spatial navigation impairment occurs very early in AD and is detectable even in the stage of mild cognitive impairment (MCI). Objective: The aim was to describe the frequency of self-reported spatial navigation complaints in patients with subjective cognitive decline (SCD), amnestic and non-amnestic MCI (aMCI, naMCI) and AD dementia and to assess whether a simple questionnaire based on these complaints may be used to detect early AD. Method: In total 184 subjects: patients with aMCI (n=61), naMCI (n=27), SCD (n=63), dementia due to AD (n=20) and normal controls (n=13) were recruited. The subjects underwent neuropsychological examination and were administered a questionnaire addressing spatial navigation complaints. Responses to the 15 items questionnaire were scaled into four categories (no, minor, moderate and major complaints). Results: 55% of patients with aMCI, 64% with naMCI, 68% with SCD and 72% with AD complained about their spatial navigation. 38-61% of these complaints were moderate or major. Only 33% normal controls expressed complaints and none was ranked as moderate or major. The SCD, aMCI and AD dementia patients were more likely to express complaints than normal controls (p's<0.050) after adjusting for age, education, sex, depressive symptoms (OR for SCD=4.00, aMCI=3.90, AD dementia=7.02) or anxiety (OR for SCD=3.59, aMCI=3.64, AD dementia=6.41). Conclusion: Spatial navigation complaints are a frequent symptom not only in AD, but also in SCD and aMCI and can potentially be detected by a simple and inexpensive questionnaire.

Pharmacogenetics of Angiotensin-Converting Enzyme Inhibitors in Patients with Alzheimer's Disease Dementia

2018 ◽  
Vol 15 (4) ◽  
pp. 386-398 ◽  
Author(s):  
Fabricio Ferreira de Oliveira ◽  
Elizabeth Suchi Chen ◽  
Marilia Cardoso Smith ◽  
Paulo Henrique Ferreira Bertolucci
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Converting Enzyme ◽  
Cognitive Decline ◽  
Enzyme Inhibitors ◽  
Late Onset ◽  
Amyloid Β ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Alzheimer’S Disease Dementia

Background: While the angiotensin-converting enzyme degrades amyloid-β, angiotensinconverting enzyme inhibitors (ACEis) may slow cognitive decline by way of cholinergic effects, by increasing brain substance P and boosting the activity of neprilysin, and by modulating glucose homeostasis and augmenting the secretion of adipokines to enhance insulin sensitivity in patients with Alzheimer’s disease dementia (AD). We aimed to investigate whether ACE gene polymorphisms rs1800764 and rs4291 are associated with cognitive and functional change in patients with AD, while also taking APOE haplotypes and anti-hypertensive treatment with ACEis into account for stratification. Methods: Consecutive late-onset AD patients were screened with cognitive tests, while their caregivers were queried for functional and caregiver burden scores. Prospective pharmacogenetic correlations were estimated for one year, considering APOE and ACE genotypes and haplotypes, and treatment with ACEis. Results: For 193 patients, minor allele frequencies were 0.497 for rs1800764 – C (44.6% heterozygotes) and 0.345 for rs4291 – T (38.9% heterozygotes), both in Hardy-Weinberg equilibrium. Almost 94% of all patients used cholinesterase inhibitors, while 155 (80.3%) had arterial hypertension, and 124 used ACEis. No functional impacts were found regarding any genotypes or pharmacological treatment. Either for carriers of ACE haplotypes that included rs1800764 – T and rs4291 – A, or for APOE4- carriers of rs1800764 – T or rs4291 – T, ACEis slowed cognitive decline independently of blood pressure variations. APOE4+ carriers were not responsive to treatment with ACEis. Conclusion: ACEis may slow cognitive decline for patients with AD, more remarkably for APOE4- carriers of specific ACE genotypes.

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