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The use of the electroencephalography (EEG) technique in Alzheimer's disease (AD) diagnosis is scarce due to a lack of validation of its neurophysiological information with current biomarkers. Therefore, our goal was to assess correlations between brain spectral power signatures and cerebrospinal fluid markers (CSF) such as amyloid-β 42 load (Aβ-42), total tau (t-tau), and phosphorylated tau (p-tau) in a mild cognitive impairment (MCI) population. Furthermore, given the AD sex-dependent vulnerability related to CSF biomarkers, we went a little forward looking for different electrophysiological correlations for males and females independently.A data-driven approach was employed to determine bidimensional spectral power signatures (space-frequency) that correlated (Spearman) significantly with any of the three CSF markers in 27 patients with MCI in any of the two sex-dependent subsamples (i.e., 12 females and 15 males).Our main significant outcomes evidenced 1) a negative correlation of Aβ-42 load with central-posterior theta power and a negative correlation of t-tau with widespread alpha power within the male subsample, and 2) a significant negative correlation between t-tau and widespread beta power in the female subgroup.There is a distinctive profile of correlations between resting-state electrophysiological signatures and CSF markers in male and female individuals.The combination of these two measures would be pointing out the need of a more personalized approach to promote early AD diagnosis.

Background A close relationship between obstructive sleep apnoea (OSA) and Alzheimer's disease (AD) has been described in recent years. OSA is a risk factor for AD, but the diagnosis and clinical characteristics of OSA in patients with AD is not well understood. This study evaluated the clinical utility of two screening questionnaires, the STOP-Bang questionnaire (SBQ) and the Berlin questionnaire (BQ), to identify which patients with mild AD are at higher risk of having OSA and to determine the clinical predictors of OSA in this population. Methods In this study, 91 consecutive outpatients with mild AD were prospectively evaluated with the SBQ and the BQ. All patients underwent level 1 in-laboratory polysomnography. The predictive performance of the questionnaires were calculated for different apnoea-hypopnoea index (AHI) cut-offs. Results The median age of the patients was 76.0 (73.0; 80.0) years, and 58 (63.7%) were female. Of those, 81 patients (89.02%) were found to have OSA defined by an AHI > 5 events/h. Comparing the predictive performances of the SBQ and the BQ, the SBQ was found to have a higher diagnostic sensitivity (85% vs 4%), a lower specificity (35% vs. 96%), a higher positive predictive value (PPV) (44% vs 33%) and negative predictive value (NPV) (80% vs 65%) for detecting severe OSA at an AHI cut-off of 30 events/h. None of the items alone in the two questionnaires predicted the risk of OSA. A modified version of the SBQ, with new cut-off points for several variables according to the characteristics of AD patients, showed a slightly greater AUC than the standard SBQ (AUC 0.61 vs 0.72). Conclusion There is a high prevalence of OSA among patients with mild AD. The SBQ and the BQ are not good screening tools for detecting OSA in patients with AD. A modified version of SBQ could increase the detection of these patients.

Study Objectives To investigate the association between sleep and cognitive decline of patients with mild-moderate Alzheimer’s disease. Methods Observational, prospective study, including consecutive patients diagnosed with mild-moderate Alzheimer’s disease. Cerebrospinal fluid was collected for amyloid-beta, total-tau, and phospho-tau levels determination. Also, overnight polysomnography was performed, followed by neuropsychological evaluations at baseline and after 12 months of follow-up. Principal component analysis revealed two profiles of patients in terms of sleep: one with a propensity to deepen the sleep (deep sleepers) and the other with a propensity to spend most of the time in the lighter sleep stage (light sleepers). Results The cohort included 125 patients with a median [IQR] of 75.0 [72.0;80.0] years. Deep and light sleepers did not present differences in relation to the cerebrospinal fluid pathological markers and to the cognitive function at the baseline. However, there was a significant difference of −1.51 (95% CI: −2.43 to −0.59) in the Mini-mental state examination after 12 months of follow-up. Accordingly, sleep depth and cognitive decline presented a dose–response relationship (p-for-trend = 0.02). Similar outcomes were observed in relation to the processing speed (Stroop words test, p-value = 0.016) and to the executive function (Verbal fluency test, p-value = 0.023). Conclusions Considering the increased cognitive decline presented by light sleepers, the sleep profile may have a predictive role in relation to the cognitive function of patients with mild-moderate Alzheimer’s disease. The modifiable nature of sleep sets this behavior as a possible useful intervention to prevent a marked cognitive decline. Clinical Trial Information Role of Hypoxia Ans Sleep Fragmentation in Alzheimer’s Disease. and Sleep Fragmentation. Completed. NCT02814045

BACKGROUND AND PURPOSE: The COVID-19 epidemic is affecting almost all individuals worldwide, and patients with Alzheimer's disease (AD) and amnesic mild cognitive impairment (MCI) are particularly at risk due to their characteristics and age. We analysed the impact of the pandemic on these patients' neuropsychiatric symptoms and their quality of life after 5 weeks of lockdown in Spain. METHODS: A total of 40 patients with a diagnosis of MCI (n = 20) or mild AD (n = 20) from the Cognitive Stimulation Program of the Cognitive Disorders Unit were evaluated. All patients had undergone a previous evaluation during the month before the lockdown, and were re-evaluated after 5 weeks of lockdown. The Neuropsychiatric Inventory (NPI) and EuroQol-5D questionnaire (EQ-5D) were used to assess neuropsychiatric symptoms in patients and the quality of life in patients as well in caregivers. RESULTS: The mean (SD) total baseline NPI score was 33.75 (22.28), compared with 39.05 (27.96) after confinement (P = 0.028). The most frequently affected neuropsychiatric symptoms were apathy [4.15 (3.78) vs. 5.75 (4.02); P = 0.002] and anxiety [3.95 (3.73) vs. 5.30 (4.01); P = 0.006] in patients with MCI, and apathy [2.35 (2.70) vs. 3.75 (3.78); P = 0.036], agitation [0.45 (1.14) vs. 1.50 (2.66); P = 0.029] and aberrant motor behaviour [1.25 (2.86) vs. 2.00 (2.93); P = 0.044] in patients with AD. We did not observe differences in EQ-5D scores during the re-evaluation. The 30% of patients and 40% of caregivers reported a worsening of the patients' health status during confinement. CONCLUSIONS: The results of this study show the worsening of neuropsychiatric symptoms in patients with AD and MCI during 5 weeks of lockdown, with agitation, apathy and aberrant motor activity being the most affected symptoms.

We evaluated the influence of untreated obstructive sleep apnoea (OSA) on the magnitude of cognitive decline and on several cognitive subdomains in patients with mild-to-moderate Alzheimer's disease.In this single-centre study, 144 patients were recruited prospectively from a cognitive impairment unit and underwent overnight polysomnography.The mean±sd change in the Alzheimer's Disease Assessment Scale cognitive subscale (ADAS-cog) score at 12 months was 3.19±5.61 in the non-OSA group and 0.08±5.62 in the OSA group, with an intergroup difference of −3.36 (95% CI 0.19–0.16; p=0.002). We did not observe a significant difference in any cognitive subdomains at 12 months. Regarding Mini-Mental State Examination scores at 36 months, the mean change was 1.69 (95% CI −1.26–4.64; p=0.445). No significant differences were found among different OSA severity groups.We observed that ADAS-cog scores were better in the OSA group than in the non-OSA group by a statistically but not clinically significant margin. We did not find differences in the different cognitive subdomains after 1 year or in global cognition after 3 years of follow-up.

Background: Sleep-disordered breathing encompasses a group of diseases, of which obstructive sleep apnea (OSA) is most frequent. Alzheimer's disease (AD) is the most prevalent neurodegenerative disease; it is manifested as an initial deficit of episodic memory that evolves into global cognitive and psychosocial dysfunction, and its prevalence is increasing around the world. OSA has been described as a risk factor for AD, and its prevalence is higher in AD patients. However, little is known about the influence of OSA on cognition in the AD population.The aim of this study was to evaluate the impact of nontreated OSA on the cognitive evolution of patients with mild-moderate AD, to investigate whether the magnitude of the cognitive decline is associated with the severity of OSA and to evaluate the influence of OSA on several cognitive subdomains in AD patients. Methods: In this single-center study, patients with mild-moderate AD were recruited prospectively from a cognitive impairment unit and underwent overnight polysomnography. OSA was defined as an apnea-hypopnea index (AHI) >15/h. AD severity was assessed using the Mini-Mental State Examination (MMSE). The primary outcome was to measure the change in cognitive score on the Alzheimer’s Disease Assessment Scale-cognitive scale (ADAS-cog) from baseline to 12 months in patients with mild AD with and without OSA. An extensive battery of neuropsychological tests, including the Epworth Sleepiness Scale (ESS), were performed and APOE status was measured. Findings: The cohort included 144 patients with a mean (SD) age of 75.19 (5.30) years; 72 (57.6%) were women, and the mean MMSE score was 23.5 (2.24) points at baseline. The mean (SD) change in the ADAS-cog score at 12 months was 3.19 (5.61) in the non-OSA group and 0.08 (5.62) in the OSA group, with a difference between the groups of -3.36 (95%CI 0.19 to 0.16; p=0.002). Regarding the changes in the ADAS-cog subitems at 12 months, ideational praxis, remembering test instructions and commands showed a significant difference between the groups (p

To assess the prevalence of obstructive sleep apnea (OSA) in patients with mild-moderate Alzheimer’s Disease (AD) and to evaluate cognitive characteristics according to the severity of OSA. Patients with mild-moderate AD, recruited prospectively from a cognitive impairment unit, underwent overnight polysomnography. OSA was defined as an apnea–hypopnea index > 5/h. AD severity was assessed using the Mini-Mental State Examination and extensive neuropsychological battery. Epworth Sleepiness Scale and APOE status were analyzed. The cohort included 128 patients with a median [IQR] age of 75.0 [72.0;79.2] years and 57.8% were women. OSA was diagnosed in 116 subjects (90.6%). The distribution of mild, moderate and severe severity of OSA was 29 (22.7%), 37 (28.9%) and 50 (39.1%), respectively. Regarding sleep symptoms, the cohort showed normal values of daytime sleepiness (median EES score 5 [3, 8]), while nycturia (89.1%) and snoring (71.1%) were the most common symptoms. Participants with severe OSA included a higher proportion of older men, were associated with snoring and sedentariness. No significant differences in cognitive assessment were found between patients with and without severe OSA in any of the domains. The prevalence of APOE e4 was not significantly different between patients with and without severe OSA. There was a high prevalence of OSA in patients with mild-moderate AD. OSA was not associated with sleepiness or worse cognitive function. APOE e4 was not related to the presence or severity of OSA. Further longitudinal studies will be required to evaluate whether OSA impairs cognitive evolution in AD patients.

Stroke is a leading cause of disability in adults. The development of depressive symptoms is the most common emotional complication. To date, most studies of post-stroke depression have excluded patients who have suffered a minor stroke or transient ischaemic attack (TIA), although they are equally vulnerable subgroups of this sickness.We present a review of published studies of post-stroke depression to elucidate aspects that have already been widely demonstrated and those who need more evidence.The post-stroke depression is both frequent in patients with established stroke and minor stroke or TIA. Although there are discrepancies in the definition used, in up to one out of three patients will develop this complication. We have identified risk factors of post-stroke depression with a broad scientific background (female, history of depression or other psychiatric disorders, stroke severity, functional impairment) and other without it (quality of life, cognitive impairment and neuroimaging biomarkers). The main methodological limitations found are: confusion between post-stroke depression and depressive symptoms; variability in rating scales used; and temporal variability in the time of the evaluation of mood. To date very few studies focused on minor stroke or TIA.Further studies are required with improved design in order to help establish the risk of post-stroke depression at different times after the stroke, minor stroke or TIA and the importance of all the factors described above.Actualizacion de la depresion postictus: nuevos retos en pacientes con ictus minor o ataque isquemico transitorio.Introduccion. El ictus es una de las principales causas de discapacidad en la poblacion adulta. El desarrollo de sintomas depresivos es la complicacion afectiva mas frecuente. Hasta ahora, en la mayoria de los estudios sobre depresion postictus se ha excluido a los pacientes que han sufrido un ictus minor o un ataque isquemico transitorio (AIT), si bien es un subgrupo igualmente vulnerable a esta enfermedad. Objetivo. Revisar los estudios publicados de depresion postictus para dilucidar los aspectos que ya se han demostrado ampliamente y los que necesitan mayor evidencia. Desarrollo. La depresion postictus es frecuente tanto en los pacientes con ictus establecido como en los pacientes con ictus minor o AIT. Aunque existen discrepancias en la definicion utilizada, aproximadamente uno de cada tres pacientes desarrollara esta complicacion. Se han identificado factores de riesgo de depresion postictus con un amplio respaldo cientifico (sexo femenino, antecedentes de depresion u otros trastornos psiquiatricos, gravedad del ictus y afectacion funcional) y otros sin el (calidad de vida, deterioro cognitivo y biomarcadores de neuroimagen). Las principales limitaciones metodologicas halladas son la confusion entre depresion postictus y sintomatologia depresiva, la variabilidad en las escalas de evaluacion usadas y la variabilidad en el momento temporal de la evaluacion del estado de animo. Hasta ahora son muy pocos los estudios en el ictus minor o el AIT. Conclusiones. Se necesitan nuevos estudios con mejor diseño que ayuden a establecer el riesgo de depresion postictus a diferentes tiempos tras el ictus, el ictus minor o el AIT, y establecer la importancia de los factores descritos previamente.

Few previous studies have focused on affective impairment after transient ischemic attack (TIA) and/or minor stroke. The aim was to establish the prevalence, evolution and predictors of post-stroke depression (PSD) and post-stroke apathy (PSA) over a 12-month follow-up period. We prospectively included TIA and minor stroke patients (NIHSS ≤4) who had undergone magnetic resonance imaging