


VL - 8 IS - 1 U1 - http://www.ncbi.nlm.nih.gov/pubmed/30111810?dopt=Abstract ER - TY - JOUR T1 - Brain perfusion during rapid-eye-movement sleep successfully identifies amnestic mild cognitive impairment. JF - Sleep Med Y1 - 2017 A1 - Brayet, Pauline A1 - Petit, Dominique A1 - Baril, Andrée-Ann A1 - Gosselin, Nadia A1 - Gagnon, Jean-François A1 - Soucy, Jean-Paul A1 - Serge Gauthier A1 - Kergoat, Marie-Jeanne A1 - Carrier, Julie A1 - Rouleau, Isabelle A1 - Montplaisir, Jacques AB -

INTRODUCTION: Prodromal markers of Alzheimer's disease (AD) have been derived from wakefulness. However, brain perfusion during rapid-eye movement (REM) sleep could be a sensitive marker of amnestic mild cognitive impairment (aMCI), as activation of REM sleep relies more on the cholinergic system.

METHODS: Eight subjects with aMCI, and 16 controls, underwent two single-photon emission computed tomography (SPECT) scans with tracer injected during REM sleep then wakefulness.

RESULTS: Perfusion in the anterior cingulate cortex was significantly decreased in aMCI cases compared to controls for both conditions. That defect was much larger and more severe in REM sleep (1795 voxels) compared to wakefulness (398 voxels), and extended to the middle cingulate cortex and the olfactory cortex. Hypoperfusion in the anterior cingulate cortex during REM sleep allowed better classification than hypoperfusion found in wakefulness (93.8 vs 81.3%).

CONCLUSION: REM sleep imaging is a valuable tool with which to identify individuals at risk of developing AD.

VL - 34 U1 - http://www.ncbi.nlm.nih.gov/pubmed/28522082?dopt=Abstract ER - TY - JOUR T1 - BDNF Val66Met Polymorphism Interacts with Sleep Consolidation to Predict Ability to Create New Declarative Memories. JF - J Neurosci Y1 - 2016 A1 - Gosselin, Nadia A1 - De Beaumont, Louis A1 - Gagnon, Katia A1 - Baril, Andrée-Ann A1 - Mongrain, Valérie A1 - Blais, Hélène A1 - Montplaisir, Jacques A1 - Gagnon, Jean-François A1 - Pelleieux, Sandra A1 - Judes Poirier A1 - Carrier, Julie AB -

UNLABELLED: It is hypothesized that a fundamental function of sleep is to restore an individual's day-to-day ability to learn and to constantly adapt to a changing environment through brain plasticity. Brain-derived neurotrophic factor (BDNF) is among the key regulators that shape brain plasticity. However, advancing age and carrying the BDNF Met allele were both identified as factors that potentially reduce BDNF secretion, brain plasticity, and memory. Here, we investigated the moderating role of BDNF polymorphism on sleep and next-morning learning ability in 107 nondemented individuals who were between 55 and 84 years of age. All subjects were tested with 1 night of in-laboratory polysomnography followed by a cognitive evaluation the next morning. We found that in subjects carrying the BDNF Val66Val polymorphism, consolidated sleep was associated with significantly better performance on hippocampus-dependent episodic memory tasks the next morning (β-values from 0.290 to 0.434, p ≤ 0.01). In subjects carrying at least one copy of the BDNF Met allele, a more consolidated sleep was not associated with better memory performance in most memory tests (β-values from -0.309 to -0.392, p values from 0.06 to 0.15). Strikingly, increased sleep consolidation was associated with poorer performance in learning a short story presented verbally in Met allele carriers (β = -0.585, p = 0.005). This study provides new evidence regarding the interacting roles of consolidated sleep and BDNF polymorphism in the ability to learn and stresses the importance of considering BDNF polymorphism when studying how sleep affects cognition.

SIGNIFICANCE STATEMENT: Individuals with the BDNF Val/Val (valine allele) polymorphism showed better memory performance after a night of consolidated sleep. However, we observed that middle-aged and older individuals who are carriers of the BDNF Met allele displayed no positive association between sleep quality and their ability to learn the next morning. This interaction between sleep and BDNF polymorphism was more salient for hippocampus-dependent tasks than for other cognitive tasks. Our results support the hypothesis that reduced activity-dependent secretion of BDNF impairs the benefits of sleep on synaptic plasticity and next-day memory. Our work advances the field by revealing new evidence of a clear genetic heterogeneity in how sleep consolidation contributes to the ability to learn.

VL - 36 IS - 32 U1 - http://www.ncbi.nlm.nih.gov/pubmed/27511011?dopt=Abstract ER -