Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Background: Memory consolidation in sleep-dependent individuals involves the circuitry connections of cortex, thalamus and hippocampus, regulating via neural metabolites. However, the disruption of metabolic pattern in thalamus and hippocampus remains unclear.
Objective: We aim to explore the disruptive effects of insomnia on the metabolites during memory consolidation, particularly the underlying neurometabolic mechanisms in comorbidity of failed memory consolidation.
Methods: This study integrates clinical research with animal experiment. In clinical research, 49 participants were divided into four groups: healthy controls (HC, n = 11), insomnia with normal cognition (IS, n = 14), mild cognitive impairment without insomnia (MCI, n = 10), and insomnia with mild cognitive impairment (IS-MCI, n = 14). Magnetic resonance spectroscopy (MRS) was used to evaluate the neural γ-aminobutyric acid (GABA) and glutamate-glutamine (Glx) in bilateral thalamus. In experimental studies, the rat model of sleep deprivation combined with amyloid-β (Aβ) injection was established, after behavior testing, the levels of Glx, choline (Cho) and N-acetyl aspartate (NAA) in the bilateral hippocampus were evaluated with MRS.
Results: The patients in the IS-MCI group exhibited significantly lower GABA level than IS, MCI and HC groups. Results from rat studies showed that sleep deprivation exacerbated asymmetric alterations in Aβ-induced bilateral hippocampal metabolite abnormalities, which correlated with cognition. These neuro-metabolite disruption accompanied with synaptic loss and activation of astrocytes.
Conclusions: The lateralized decrease in GABA levels of thalamus and NAA, Cho, and Glx levels of hippocampus under conditions of sleep disturbance with cognitive decline may provide evidence for the neural metabolic mechanisms underlying the disruption of memory consolidation.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1177/13872877241295401 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Association between Sleep Quality and Cognitive Function in Patients with Non-Functioning Pituitary Adenoma.
Endocr Connect
September 2025
Centre for Higher Education Development, University of Cape Town.
Background: Cortisol and growth hormone are important for sleep regulation and cognition. Sleep is critical for cognitive functioning, and memory consolidation. Patients with pituitary disease experience hormonal dysregulation, impaired sleep quality, and cognitive dysfunction.
View Article and Find Full Text PDFRapid eye movement sleep: Who needs it? Creativity mechanisms and psychiatric applications of REM sleep enhancement.
J Psychopharmacol
September 2025
Florey Institute of Neuroscience and Mental Health, Parkville, VIC, Australia.
Rapid eye movement sleep (REMS) has historically been associated with anecdotal 'creative insights', possibly due to the fantastical and ostensibly illuminating nature of its associated phenomena (dreams). REMS, characterised by rapid eye movements, muscle atonia, and high-energy neuronal activity, has been linked to memory consolidation and information processing, particularly regarding the formation of novel associations or reintegration of consolidated memories into new cognitive networks. However, studies in these domains have largely used methodology which deprived subjects (animal or human) of REMS, rather than enhanced it.
View Article and Find Full Text PDFSocial Buffering of Acute Early Life Stress Sex-Dependently Ameliorates Fear Incubation in Adulthood.
Dev Psychobiol
September 2025
Department of Psychology and Center for Neuroscience and Behavior, Miami University, Oxford, Ohio, USA.
Social buffering may reduce the persistent impacts of acute early life stress (aELS) and, thus, has important implications for anxiety- and trauma-related disorders. First, we assessed whether aELS would induce maladaptive fear incubation in adult mice, a PTSD-like phenotype. Overall, animals showed incubation of fear memory in adulthood, independent of aELS condition.
View Article and Find Full Text PDFRole of CPEBs in Learning and Memory.
J Neurochem
September 2025
Astbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
Memory formation involves a complex interplay of molecular and cellular processes, including synaptic plasticity mechanisms such as long-term potentiation (LTP) and long-term depression (LTD). These processes rely on activity-dependent gene expression and local protein synthesis at synapses. A central unresolved question in neuroscience is how memories can be stably maintained over time, despite the transient nature of the proteins involved in their initial encoding.
View Article and Find Full Text PDFSlow wave sleep is associated with a reorganisation of episodic memory networks.
Neuropsychologia
September 2025
Department of Experimental Psychology and Oxford Centre for Human Brain Activity, Wellcome Centre for Integrative Neuroimaging, Department of Psychiatry, University of Oxford, Oxford, United-Kingdom. Electronic address:
Models of memory consolidation propose that newly acquired memory traces undergo reorganisation during sleep. To test this idea, we recorded high-density electroencephalography (EEG) during an evening session of word-image learning followed by immediate (pre-sleep) and delayed (post-sleep) recall. Polysomnography was employed throughout the intervening night, capturing time spent in different sleep stages.
View Article and Find Full Text PDF