Autism spectrum disorder (ASD), commonly referred to as autism, is a neurodevelopmental condition characterized by differences in social interactions, communication, behavior and the processing of sensory stimuli. Notably, the experiences, aptitudes and needs of autistic people can vary significantly.
This 3D camera estimates depth by comparing blur across two differently focused images of the same scene. The prototype generates real-time 3D maps while using less than a watt of power, sidestepping more energy-intensive approaches.
By borrowing a trick from tiny jumping spiders, Northwestern University engineers have developed an extremely energy-efficient 3D camera. Called SpiderCam, the new device senses depth the same way that jumping spiders judge distances before making a high-precision hop. To estimate depth, the system captures two images of the same scene with slightly different focus settings and measures subtle differences in blurriness between the two images.
With this strategy, the camera produces real-time 3D maps while consuming less than a watt of power. That’s less energy than used by a standard nightlight.
The innovation could enable a new generation of battery-powered devices that need to gauge their surroundings, like wearable technologies, assistive devices, robots and drones.
A new nanotechnology treatment reversed Alzheimer’s symptoms in mice by restoring the brain’s natural cleanup system. The specially engineered nanoparticles helped clear toxic amyloid proteins from the brain and repair the blood-brain barrier, which normally protects and regulates the brain’s environment. In one striking experiment, elderly mice treated with the therapy later behaved like healthy younger mice.
One of the major challenges for nanotechnology deals with the diagnosis and treatment of BBB-related dysfunctions involving stroke, brain tumors and cancer. Tight junction (TJ) barriers protect the CNS. These barriers are located in three main locations inside CNS: the brain endothelium, the arachnoid epithelium, and the choroid plexus epithelium (Figure 3, Abbott et al., 2006). BBB consists of endothelial cells connected by close fitting junctions that separate the flowing blood from the brain extracellular fluid. Therefore, BBB controls the entrance of biomolecules into the brain and protects the brain from many common bacterial infections. However, the BBB presents a few limitations for nanomedicine approaches. For instance, due to the presence of BBB, the drug delivery to the brain area for tumor therapy or other neurodegenerative diseases such as Alzheimer’s is a crucial challenge. The majority of diagnosed brain tumors are currently treated with surgery, radiation, and chemotherapy; nanoscience and technology could be a promising solution to this challenge. There are several comprehensive reviews on the interaction of BBB with nanomaterials that focus on various methods to transfer nanomaterials across BBB (Chen and Liu, 2012; Khawli and Prabhu, 2013; Krol et al., 2013).
Figure 4 (Chen and Liu, 2012) presents the main, well-recognized, transport pathways across BBB, which are commonly used for carrying solute molecules. Among all the pathways shown in Figure 4, the “g” route is the most suitable for drug delivery via liposomes or nanoparticles. A summary of the conventional methods used for BBB permeability assessment is given in Stam’s work (Stam, 2010).
Different approaches and routes possible for transport of drugs across the BBB as summarized in Table 1. Biocompatible nanomaterials such as nanoparticles, liposomes, and supramolecular aggregates are promising drug carriers since their size can be tuned to fit the BBB transport. In addition, their surfaces can be functionalized to facilitate their transport through the BBB. It should be mentioned that the cytotoxicity of NPs must be precisely monitored, using various well-recognized methodologies (Mahmoudi et al., 2010, 2011a; Mao et al., 2013), to ensure their biocompatibility. The surface functional groups enhance the BBB permeability by various mechanisms such as adsorptive-mediated transcytosis and receptor-mediated transcytosis. As an example, Lactoferrin is a receptor located on cerebral endothelial cells that facilitates the transport of NPs across BBB by receptor-mediated transcytosis (Qiao et al., 2012).
Gene triplication may compromise different body functions but invariably impairs intellectual abilities starting from infancy. Moreover, after the fourth decade of life people with DS are likely to develop Alzheimer’s disease. Neurogenesis impairment during fetal life stages and dendritic pathology emerging in early infancy are thought to be key determinants of alterations in brain functioning in DS. Although the progressive improvement in medical care has led to a notable increase in life expectancy for people with DS, there are currently no treatments for intellectual disability. Increasing evidence in mouse models of DS reveals that pharmacological interventions in the embryonic and neonatal periods may greatly benefit brain development and cognitive performance. The most striking results have been obtained with pharmacotherapies during embryonic life stages, indicating that it is possible to pharmacologically rescue the severe neurodevelopmental defects linked to the trisomic condition. These findings provide hope that similar benefits may be possible for people with DS. This review summarizes current knowledge regarding (i) the scope and timeline of neurogenesis (and dendritic) alterations in DS, in order to delineate suitable windows for treatment; (ii) the role of triplicated genes that are most likely to be the key determinants of these alterations, in order to highlight possible therapeutic targets; and (iii) prenatal and neonatal treatments that have proved to be effective in mouse models, in order to rationalize the choice of treatment for human application. Based on this body of evidence we will discuss prospects and challenges for fetal therapy in individuals with DS as a potential means of drastically counteracting the deleterious effects of gene triplication.
Down syndrome (DS) is a relatively high-incidence pathology (∼1 in every 800–1,000 live births; see Antonarakis et al., 2020; Hughes-McCormack et al., 2020) caused by triplication of Hsa21. Increased expression of Hsa21 genes (and genes on other chromosomes) impairs development and functions of various organs, including the brain (Bull, 2020). While some disorders may not be present in all individuals with DS, intellectual disability (ID) is the invariable hallmark of DS (Zigman, 2013; Ballard et al., 2016; Lott and Head, 2019). ID scores range from moderately (IQ of 50–70) to severely (IQ of 20–35; Bull, 2020) affected; even in its milder form, intellectual performance may compromise the ability to live independently. ID is already detectable in children with DS, especially regarding language, memory, and adaptive behavior, and is exacerbated with age (Godfrey and Lee, 2020).
Early intervention and environmental optimization have been central to management of Down syndrome (DS) and much of current treatment is still focused in strategies that involve early education plans. This approach has provided significant improvements for Down syndrome but it is not providing a full success. The discovery of an increasing number of genes and molecular pathways linked to intellectual disability and involving a range of synaptic and plasticity-related mechanisms has open new treatment opportunities that focus on targeted treatments boosting neural plasticity. We here discuss some of these approaches, focusing on the effects of environmental enrichment and on the discovery of pharmacological therapies showing beneficial effects even in some clinical trials in adult individuals with Down syndrome. Targeting plasticity impairments in DS is thus a promising strategy to promote cellular mechanisms involved in learning and memory within key cognitive brain region and could lead to improved connectivity.
Keywords: EGCG; Environ-mimetic drugs; Environmental enrichments; Epigenetics; Neuronal plasticity.
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