Advances in sleep research in 2024

A study explored the relationship between synaptic strength and electroencephalography delta power in mice.3 The investigators used a multielectrode recording system and a molecular tool for induction of long-term potentiation induction (ie, synapse translocation of the protein kalirin-7) that induces dendritic spine enlargement and synaptic potentiation of excitatory neurons in the prefrontal cortex, they found a longer time of non–rapid eye movement sleep even when the homeostatic sleep drive was minimal. Restless legs syndrome is a common sensorimotor disorder characterised by an urge to move that appears during rest or is exacerbated by rest, occurs in the evening or night, and disappears or is improved in response to movement.4 A meta-analysis of genome-wide association studies in more than 100 000 individuals with restless legs syndrome and 1 500 000 controls of European ancestry confirmed all known loci (such as MEIS1 and BTBD9, two major genes involved) and increased the number of risk loci associated with the disease to 164, including three variants on the X chromosome.5 Although the heritability of restless legs syndrome was significantly higher in women, the genetic correlation between the sexes was close to 1 (revealing largely overlapping genetic predispositions of the sexes). Narcolepsy type 1 is an orphan disease, a central hypersomnolence disorder characterised by daytime sleepiness, cataplexy, and loss of hypocretin or orexin neurons, often triggered by infections such as influenza or by vaccination.6 A large genome-wide association study in people with narcolepsy type 1 confirmed the associations with HLA (eg, HLA-DQB1*06:02) and T-cell receptor α, and found several novel genetic markers, all involved in immune system regulation.7 Previous evidence suggested an autoimmune origin of narcolepsy type 1, with increased T-cell reactivity against hypocretin; however, whether T cells have a primary role in neuronal destruction remains unknown.6 We recently explored whether microglial density was greater in the hypothalamic and thalamic areas in patients with narcolepsy type 1 than in controls (healthy controls and from the general population), and greater in patients with a short rather than a long disease duration.8 Including 41 patients with narcolepsy type 1 (21 adults, 20 children, ten of the cohort of whom had disease onset within the previous year) and 35 controls, we found no evidence of increased microglial density, even when measured cl