β-Endorphins are peptides that exert a wide variety of effects throughout the body. Produced through the cleavage pro-opiomelanocortin (POMC), β-endorphins are the primarily agonist of mu opioid receptors, which can be found throughout the body, brain, and cells of the immune system that regulate a diverse set of systems. As an agonist of the body’s opioid receptors, β-endorphins are most noted for their potent analgesic effects, but they also have their involvement in reward-centric and homeostasis-restoring behaviors, among other effects. These effects have implicated the peptide in psychiatric and neurodegenerative disorders, making it a research target of interest. This review briefly summarizes the basics of endorphin function, goes over the behaviors and regulatory pathways it governs, and examines the variability of β-endorphin levels observed between normal and disease/disorder affected individuals.

Over the past few years there has been a large rise in the field of robotics. Robots are being in used in many industries, but there has not been a large surge of robots in the medical field, especially the robots for healthcare use. However, as the aging population keeps growing, current medical staff and healthcare providers are increasingly burdened by caring for the ever-growing number of senior patients, especially those with cognitive impairment of Alzheimer’s disease (AD) and Alzheimer’s disease-related dementia (ADRD) patients. As a result, we can expect to see a large increase in the field of medical robotics, especially in forms of socially assistive robots (SARs) for senior patients and healthcare providers. In fact, SARs can alleviate AD and ADRD patients and their caregivers’ unmet medical needs. Herein, we propose a design outline for such a SAR, based on a review of the current literature. We believe the next generation of SARs will enhance health and well-being, reduce illness and disability, and improve quality of life for AD and ADRD patients and their caregivers.

As the global population ages, the incidence of major neurocognitive disorders (major NCDs), such as the most common geriatric major NCD, Alzheimer’s disease (AD), has grown. Thus, the need for more definitive cognitive assessment or even effective non-pharmacological intervention for age-related NCDs is becoming more and more pressing given that no definitive diagnostics or efficacious therapeutics are currently unavailable for them. We evaluate the current state of the art of cognitive assessment for major NCDs, and then briefly glance ahead at potential application of virtual reality (VR) technologies in major NCD assessment and in cognition training of visuospatial reasoning in a 3D environment, as well as in the alleviation of depression and other symptoms of cognitive disorders. We believe that VR-based technologies have tremendous potentials in cognitive assessment and non-pharmacological therapy for major NCDs.

Alzheimer’s disease (AD) imposes a considerable burden on those diagnosed. Faced with a neurodegenerative decline for which there is no effective cure or prevention method, sufferers of the disease are subject to judgement, both self-imposed and otherwise, that can have a great deal of effect on their lives. The burden of this stigma is more than just psychological, as reluctance to face an AD diagnosis can lead people to avoid early diagnosis, treatment, and research opportunities that may be beneficial to them, and that may help progress towards fighting AD and its progression. In this review, we discuss how recent advents in information technology may be employed to help fight this stigma. Using artificial intelligence (AI) technologies, specifically natural language processing (NLP), to classify the sentiment and tone of texts, such as those of online posts on various social media sites, has proven to be an effective tool for assessing the opinions of the general public on certain topics. These tools can be used to analyze the public stigma surrounding AD. Additionally, there is much concern among individuals that an AD diagnosis, or evidence of pre-clinical AD such as a biomarker or imaging test results, may wind up unintentionally disclosed to an entity that may discriminate against them. The lackluster security record of many medical institutions justifies this fear to an extent. Adopting more secure and decentralized methods of data transfer and storage, and giving patients enhanced ability to control their own data, such as a blockchain-based method, may help to alleviate some of these fears.

Fe₂O₃, CuO and ZnO nanoparticles (NP) have found various industrial and biomedical applications. However, there are growing concerns among the general public and regulators about their potential environmental and health impacts as their physio-chemical interaction with biological systems and toxic responses of the latter are complex and not well understood. Herein we first reported that human SH-SY5Y and H4 cells and rat PC12 cell lines displayed concentration-dependent neurotoxic responses to insults of CuO nanoparticles (CuONP), but not to Fe₂O₃ nanoparticles (Fe₂O₃NP) or ZnO nanoparticles (ZnONP). This study provides evidence that CuONP induces neuronal cell apoptosis, discerns a likely p53-dependent apoptosis pathway and builds out the relationship between nanoparticles and Alzheimer’s disease (AD) through the involvement of reactive oxygen species (ROS) and increased Aβ levels in SH-SY5Y and H4 cells. Our results implicate that exposure to CuONP may be an environmental risk factor for AD. For public health concerns, regulation for environmental or occupational exposure of CuONP are thus warranted given AD has already become a pandemic.

Amyloid precursor protein (APP) is directly related to Aβ amyloidosis—a hallmark of Alzheimer’s disease (AD). However, the impact of environmental factors upon APP biology and Aβ amyloid pathology have not been well studied. The increased use of nanoparticles (NPs) or engineered nanomaterials (ENMs) has led to a growing body of evidence suggesting that exposure to metal/metal oxide NPs, such as Fe₂O₃, CuO, and ZnO, may contribute to the pathophysiology of neurodegenerative diseases such as AD through neuroinflammation. Our previous studies indicated that exposure to CuO nanoparticles (CuONPs) induce potent in vitro neurotoxicity. Herein, we investigated the effects on APP expression in neuronal cells exposed to different metal oxide NPs. We found a low dose of CuONPs effectively activated the NFκB signaling pathway and increased APP expression. Moreover, the inhibition of p65 expression using siRNA abolished CuONP-mediated APP expression, suggesting that NFκB-regulated APP expression in response to CuONP exposure may be associated with AD pathology.