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Background Mild parkinsonian signs (MPS) are common in older people and are associated with an increased risk of different neurodegenerative diseases. This study prospectively evaluates the longitudinal course of cognitive performance in older individuals with MPS. Methods From the TREND study, 480 individuals neurologically healthy at baseline, aged between 50 and 80 years, with complete follow-up data for three assessments within a mean of 43.8 months, were included in this analysis. Participants underwent a detailed cognitive test battery, evaluation of prodromal markers for neurodegenerative diseases and history of vascular diseases at each study visit. In addition, plasma levels of amyloid-beta (Aβ)1–40 and Aβ1–42 were evaluated longitudinally. Results In 52 (11 %) of the 480 participants, MPS could be detected at baseline. These individuals had cognitive deficits significantly more often compared with controls at each time point and their cognitive performance showed a steeper decline during follow-up. In addition, their levels of plasma Aβ1–42 were significantly lower than those of controls, and declined more rapidly over time. Conclusions This longitudinal study shows that MPS are associated with cognitive decline and decrease in plasma Aβ1–42, possibly indicating an ongoing neurodegenerative process. Electronic supplementary material The online version of this article (doi:10.1186/s13195-016-0209-7) contains supplementary material, which is available to authorized users.

STUDY OBJECTIVES Rapid eye movement (REM) sleep is considered critical to the consolidation of procedural memory - the memory of skills and habits. Many antidepressants strongly suppress REM sleep, however, and procedural memory consolidation has been shown to be impaired in depressed patients on antidepressant therapy. As a result, it is important to determine whether antidepressive therapy can lead to amnestic impairment. We thus investigated the effects of the anticholinergic antidepressant amitriptyline on sleep-dependent memory consolidation. DESIGN Double-blind, placebo-controlled, randomized, parallel-group study. SETTING Sleep laboratory. PARTICIPANTS Twenty-five healthy men (mean age: 26.8 ± 5.6 y). INTERVENTIONS 75 mg amitriptyline versus placebo. MEASUREMENTS/RESULTS To test memory consolidation, a visual discrimination task, a finger-tapping task, the Rey-Osterrieth Complex Figure Test, and the Rey Auditory-Verbal Learning Test were performed. Sleep was measured using polysomnography. Our findings show that amitriptyline profoundly suppressed REM sleep and impaired perceptual skill learning, but not motor skill or declarative learning. CONCLUSIONS Our study is the first to demonstrate that an antidepressant can affect procedural memory consolidation in healthy subjects. Moreover, considering the results of a recent study, in which selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors were shown not to impair procedural memory consolidation, our findings suggest that procedural memory consolidation is not facilitated by the characteristics of REM sleep captured by visual sleep scoring, but rather by the high cholinergic tone associated with REM sleep. Our study contributes to the understanding of potentially undesirable behavioral effects of amitriptyline.

Although the analogy between dreams and ancient mnemotechniques is tempting because they share several phenomenological characteristics, this analogy is superficial at a closer look. Unlike mneomotechnically encoded material, rapid eye movement (REM) dreams are inherently difficult to remember, do not usually allow conscious subsequent retrieval of all interconnected elements, and have been found to support subsequent episodic memory in only rare cases.

Summary While the consolidation of declarative memory is supported by slow wave sleep (SWS) in healthy subjects, it has been shown to be associated with rapid eye movement (REM) sleep in patients with insomnia. Sleep during a subject’s first night in an unfamiliar environment is often disturbed, and this so-called first-night effect (FNE) has often been used as a model of transient insomnia. Additionally, sleeping for the first time in an unfamiliar environment can lead to increased cortisol secretion, and declarative memory consolidation likely depends on low cortisol levels, especially during the early part of the night. Accounting for intersubject variability in the FNE, we examined the relationship between sleep stages, cortisol secretion and declarative memory performance in 27 healthy young men. Declarative memory performance improved significantly after sleep. Whereas memory performance during the learning session and retrieval testing was strongly associated with cortisol secretion, the overnight gain was not. Post hoc analyses indicated that the overnight gain appears to be modulated by the extent of the FNE: a significant overnight improvement in memory performance was found only in subjects with a weak FNE (n = 12). In these subjects, no association was found between any sleep stage and the improvement observed in their memory performance. In subjects with a strong FNE (n = 12), however, the overnight change in memory performance was associated with the proportion of REM sleep and the total number of REMs. Disturbed sleep in an unfamiliar environment therefore appears to affect the memory consolidation process.