Treatment of sleep-related eating disorder with suvorexant: A case report on the potential benefits of replacing benzodiazepines with orexin receptor antagonists.

Background: Nocturnal eating behavior in patients with sleep-related eating disorder (SRED) is difficult to control and can become chronic, causing weight gain and psychological distress. Here, we report a case of SRED comorbid with major depressive disorder successfully treated by switching from brotizolam to suvorexant, that is, from a benzodiazepine to an orexin receptor antagonist.

Case Presentation: A 25-year-old woman complained of night snacking with partial/complete amnesia and sleepwalking for 1 year.

The use of a scented face mask in pediatric patients may facilitate mask acceptance before anesthesia induction.

Background: Scented face masks are commonly used during the induction phase of anesthesia. The present study investigated whether the use of a scented mask improved mask acceptance before the slow induction of anesthesia in pediatric patients.

Methods: This prospective, randomized controlled trial enrolled patients aged 2-10 years who were scheduled to undergo surgery under general anesthesia.

A simple method to evaluate the pentagon copy test of the Mini-Mental State Examination for the differentiation of dementia with Lewy bodies.

There are many commonalities between the clinical symptoms of dementia with Lewy bodies (DLB) and those of Alzheimer's disease (AD). The accurate differentiation of these two diseases is an important neuropsychological issue. The Mini-Mental State Examination (MMSE) is often used as a screening test for dementing disorders.

Brain p3-Alcβ peptide restores neuronal viability impaired by Alzheimer's amyloid β-peptide.

We propose a new therapeutic strategy for Alzheimer's disease (AD). Brain peptide p3-Alcβ37 is generated from the neuronal protein alcadein β through cleavage of γ-secretase, similar to the generation of amyloid β (Aβ) derived from Aβ-protein precursor/APP. Neurotoxicity by Aβ oligomers (Aβo) is the prime cause prior to the loss of brain function in AD.

Cats Did Not Change Their Problem-Solving Behaviours after Human Demonstrations.

Humans learn by observing the behaviour of others, which can lead to more efficient problem-solving than by trial-and-error learning. Numerous studies have shown that animals, other than humans, are also capable of social learning. Dogs, as humans' closest companion animals, can learn to obtain rewards following behavioural demonstrations by humans.

Sleep disturbance and health-related quality of life in Parkinson's disease: A clear correlation between health-related quality of life and subjective sleep quality.

Introduction: Comorbid insomnia and poor sleep quality in Parkinson's disease (PD) are associated with a poor health-related quality of life (HRQoL). However, the relationship between HRQoL and sleep measures obtained using polysomnography (PSG) remains unclear. We aimed to examine the association between various sleep measures and HRQoL in PD patients.

Assessment of thrombocytopenia, sleep apnea, and cardiac involvement in GNE myopathy patients.

Introduction: We previously identified UDP-N-acetylglucosamine 2-epimerase (GNE) myopathy patients with sleep apnea and a past history of thrombocytopenia, but without disease-specific cardiac involvement. This study aimed to clarify the occurrence, severity, and serial changes of these complications.

Methods: Thirty-three genetically confirmed GNE myopathy patients who participated in a 5-y longitudinal observational history study underwent platelet count and platelet-associated immunoglobulin G (PA-IgG) measurements, a sleep study, and electrocardiography (ECG), Holter ECG, and echocardiogram examinations.

Decrease in p3-Alcβ37 and p3-Alcβ40, products of Alcadein β generated by γ-secretase cleavages, in aged monkeys and patients with Alzheimer's disease.

Introduction: Neuronal p3-Alcβ peptides are generated from the precursor protein Alcadein β (Alcβ) through cleavage by α- and γ-secretases of the amyloid β (Aβ) protein precursor (APP). To reveal whether p3-Alcβ is involved in Alzheimer's disease (AD) contributes for the development of novel therapy and/or drug targets.

Methods: We developed new sandwich enzyme-linked immunosorbent assay (sELISA) systems to quantitate levels of p3-Alcβ in the cerebrospinal fluid (CSF).

Alternative Selection of β-Site APP-Cleaving Enzyme 1 (BACE1) Cleavage Sites in Amyloid β-Protein Precursor (APP) Harboring Protective and Pathogenic Mutations within the Aβ Sequence.

β-Site APP-cleaving enzyme 1 (BACE1) cleaves amyloid β-protein precursor (APP) at the bond between Met and Asp (β-site) to generate the carboxyl-terminal fragment (CTFβ/C99). BACE1 also cleaves APP at another bond between Thr and Gln (β'-site), yielding CTFβ'/C89. Cleavage of CTFβ/C99 by γ-secretase generates Aβ(1-XX), whereas cleavage of CTFβ'/C89 generates Aβ(11-XX).

Facilitation of brain mitochondrial activity by 5-aminolevulinic acid in a mouse model of Alzheimer's disease.

The activities of mitochondrial enzymes, which are essential for neural function, decline with age and in age-related disease. In particular, the activity of cytochrome c oxidase (COX/complex IV) decreases in patients with Alzheimer's disease (AD). COX, a mitochondrial inner membrane protein complex that contains heme, plays an essential role in the electron transport chain that generates ATP.

Stabilization of intracellular trafficking and metabolism of amyloid β-protein precursor and Alcadein β by apolipoprotein E.

Intracellular metabolism of amyloid β-protein precursor (APP) is important for the pathogenesis of Alzheimer's disease (AD). Alcadeins (Alcα, Alcβ, and Alcγ) are neural membrane proteins similar to APP in their localization, metabolism, and cellular function. Isoform ε4 of apolipoprotein E (ApoE) is a major risk factor for AD.

Cytoplasmic fragment of Alcadein α generated by regulated intramembrane proteolysis enhances amyloid β-protein precursor (APP) transport into the late secretory pathway and facilitates APP cleavage.

The neural type I membrane protein Alcadein α (Alcα), is primarily cleaved by amyloid β-protein precursor (APP) α-secretase to generate a membrane-associated carboxyl-terminal fragment (Alcα CTF), which is further cleaved by γ-secretase to secrete p3-Alcα peptides and generate an intracellular cytoplasmic domain fragment (Alcα ICD) in the late secretory pathway. By association with the neural adaptor protein X11L (X11-like), Alcα and APP form a ternary complex that suppresses the cleavage of both Alcα and APP by regulating the transport of these membrane proteins into the late secretory pathway where secretases are active. However, it has not been revealed how Alcα and APP are directed from the ternary complex formed largely in the Golgi into the late secretory pathway to reach a nerve terminus.

Mechanism of intramembrane cleavage of alcadeins by γ-secretase.

Background: Alcadein proteins (Alcs; Alcα, Alcβand Alcγ) are predominantly expressed in neurons, as is Alzheimer's β-amyloid (Aβ) precursor protein (APP). Both Alcs and APP are cleaved by primary α- or β-secretase to generate membrane-associated C-terminal fragments (CTFs). Alc CTFs are further cleaved by γ-secretase to secrete p3-Alc peptide along with the release of intracellular domain fragment (Alc ICD) from the membrane.