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Introduction: Although the link between sleep and memory function is well established, associations between sleep macrostructure and memory function in normal cognition and Mild Cognitive Impairment remain unclear. We aimed to investigate the longitudinal associations of baseline objectively assessed sleep quality and duration, as well as time in bed, with verbal memory capacity over a 7-9 year period. Participants are a well-characterized subsample of 148 persons (mean age at baseline: 72.8 ± 6.7 years) from the Cretan Aging Cohort. Based on comprehensive neuropsychiatric and neuropsychological evaluation at baseline, participants were diagnosed with Mild Cognitive Impairment (MCI; n = 79) or found to be cognitively unimpaired (CNI; n = 69). Sleep quality/quantity was estimated from a 3-day consecutive actigraphy recording, whereas verbal memory capacity was examined using the Rey Auditory Verbal Learning Test (RAVLT) and the Greek Passage Memory Test at baseline and follow-up. Panel models were applied to the data using AMOS including several sociodemographic and clinical covariates. Results: Sleep efficiency at baseline directly predicted subsequent memory performance in the total group (immediate passage recall: ß = 0.266, p = 0.001; immediate word list recall: ß = 0.172, p = 0.01; delayed passage retrieval: ß = 0.214, p = 0.002) with the effects in Passage Memory reaching significance in both clinical groups. Wake after sleep onset time directly predicted follow-up immediate passage recall in the total sample (ß = -0.211, p = 0.001) and in the MCI group (ß = -0.235, p = 0.02). In the total sample, longer 24-h sleep duration was associated with reduced memory performance indirectly through increased sleep duration at follow-up (immediate passage recall: ß = -0.045, p = 0.01; passage retention index: ß = -0.051, p = 0.01; RAVLT-delayed recall: ß = -0.048, p = 0.009; RAVLT-retention index:ß = -0.066, p = 0.004). Similar indirect effects were found for baseline 24-h time in bed. Indirect effects of sleep duration/time in bed were found predominantly in the MCI group. Discussion: Findings corroborate and expand previous work suggesting that poor sleep quality and long sleep duration predict worse memory function in elderly. Timely interventions to improve sleep could help prevent or delay age-related memory decline among non-demented elderly.
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Identifying modifiable factors that may predict long-term cognitive decline in the elderly with adequate daily functionality is critical. Such factors may include poor sleep quality and quantity, sleep-related breathing disorders, inflammatory cytokines and stress hormones, as well as mental health problems. This work reports the methodology and descriptive characteristics of a long-term, multidisciplinary study on modifiable risk factors for cognitive status progression, focusing on the 7-year follow-up. Participants were recruited from a large community-dwelling cohort residing in Crete, Greece (CAC; Cretan Aging Cohort). Baseline assessments were conducted in 2013-2014 (Phase I and II, circa 6-month time interval) and follow-up in 2020-2022 (Phase III). In total, 151 individuals completed the Phase III evaluation. Of those, 71 were cognitively non-impaired (CNI group) in Phase II and 80 had been diagnosed with mild cognitive impairment (MCI). In addition to sociodemographic, lifestyle, medical, neuropsychological, and neuropsychiatric data, objective sleep was assessed based on actigraphy (Phase II and III) and home polysomnography (Phase III), while inflammation markers and stress hormones were measured in both phases. Despite the homogeneity of the sample in most sociodemographic indices, MCI persons were significantly older (mean age = 75.03 years, SD = 6.34) and genetically predisposed for cognitive deterioration (APOE ε4 allele carriership). Also, at follow-up, we detected a significant increase in self-reported anxiety symptoms along with a substantial rise in psychotropic medication use and incidence of major medical morbidities. The longitudinal design of the CAC study may provide significant data on possible modifiable factors in the course of cognitive progression in the community-dwelling elderly.
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The study explored associations between hemodynamic changes and psychoemotional status in 32 patients with chronic mild traumatic brain injury (mTBI) and 31 age-matched healthy volunteers. Cerebral blood flow (CBF) and cerebral blood volume (CBV) values were obtained using Dynamic Susceptibility Contrast Magnetic Resonance Imaging in brain regions suspected to play a role in anxiety and depression. Patients were administered self-report measures of anxiety and depression symptoms and underwent neuropsychological assessment. As a group mTBI patients scored significantly below age- and education-adjusted population norms on multiple cognitive domains and reported high rates of anxiety and depression symptomatology. Significantly reduced CBF values were detected in the mTBI group compared to controls in dorsolateral prefrontal areas, putamen, and hippocampus, bilaterally. Within the mTBI group, depressive symptomatology was significantly associated with lower perfusion in the left anterior cingulate gyrus and higher perfusion in the putamen, bilaterally. The latter association was independent from verbal working memory capacity. Moreover, anxiety symptomatology was associated with lower perfusion in the hippocampus (after controlling for verbal episodic memory difficulties). Associations between regional perfusion and psychoemotional scores were specific to depression or anxiety, respectively, and independent of the presence of visible lesions on conventional MRI. Results are discussed in relation to the role of specific limbic and paralimbic regions in the pathogenesis of symptoms of depression and anxiety.
