The COVID-19 poses an ongoing threat to lives around the world and challenges the existing public health and medical service delivery. The lockdown or quarantine measures adopted to prevent the spread of COVID-19 has caused the interruption in ongoing care and access to medical care including to patients with existing neurological conditions. Besides the passivity, isolation, and withdrawal, patients with neurodegenerative diseases experience difficulties in communication due to a limited access to leisure opportunities and interaction with friends and relatives. The communication difficulties may exacerbate the burden on the caregivers. Therefore, assistive-technologies may be a useful strategy in mitigating challenges associated with remote communication. The current paper presents an overview of the use of assistive technologies using virtual reality and virtual body ownership in providing communication opportunities to isolated patients, during COVID-19, with neurological diseases and moderate-to-severe communication difficulties. We postulate that the assistive technologies-based intervention may improve social interactions in patients with neurodegenerative diseases and acquired brain injury-thereby reducing isolation and improving their quality of life and mental well-being.
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http://dx.doi.org/10.3389/fpubh.2020.635426 | DOI Listing |
Front Biosci (Schol Ed)
December 2024
Biochemical Genetics Department, Human Genetics and Genome Research Institute, National Research Centre, 12622 Cairo, Egypt.
Background: Metachromatic leukodystrophy (MLD) is an autosomal recessive hereditary neurodegenerative disease caused by a deficiency in arylsulfatase A (ARSA) activity and belongs to the group of lysosomal storage diseases. A biochemical diagnosis of MLD is based on determining the residual ARSA activity in leukocytes, skin fibroblasts, and urine. This study documents our biochemical experience and estimates the relative frequency of MLD over 21 years (2001-2022).
View Article and Find Full Text PDFJ Integr Neurosci
December 2024
Department of Human Anatomy, School of Basic Medical Sciences, Wannan Medical College, 241002 Wuhu, Anhui, China.
Background: K48-linked ubiquitin chain (Ub-K48) is a crucial ubiquitin chain implicated in protein degradation within the ubiquitin-proteasome system. However, the precise function and molecular mechanism underlying the role of Ub-K48 in the pathogenesis of Alzheimer's disease (AD) and neuronal cell abnormalities remain unclear. The objective of this study was to examine the function of K48 ubiquitination in the etiology of AD, and its associated mechanism of neuronal apoptosis.
View Article and Find Full Text PDFJ Integr Neurosci
December 2024
Department of Radiology, Affiliated Hospital of North Sichuan Medical College, 637000 Nanchong, Sichuan, China.
Background: The relationship between subregion atrophy in the entire temporal lobe and subcortical nuclei and cognitive decline at various stages of Alzheimer's disease (AD) is unclear.
Methods: We selected 711 participants from the AD Neuroimaging Initiative (ADNI) database, which included 195 cases of cognitively normal (CN), 271 cases of early Mild cognitive impairment (MCI) (EMCI), 132 cases of late MCI (LMCI), and 113 cases of AD. we looked at how subregion atrophy in the temporal lobe and subcortical nuclei correlated with cognition at different stages of AD.
Front Immunol
December 2024
Department of Neurology, University Hospital Ulm, Ulm, Germany.
Introduction: Very rarely, adult NMDAR antibody-associated encephalitis (NMDAR-E) leads to persistent cerebellar atrophy and ataxia. Transient cerebellar ataxia is common in pediatric NMDAR-E. Immune-mediated cerebellar ataxia may be associated with myelin oligodendrocyte glycoprotein (MOG), aquaporin-4 (AQP-4), kelch-like family member 11 (KLHL11), and glutamate kainate receptor subunit 2 (GluK2) antibodies, all of which may co-occur in NMDAR-E.
View Article and Find Full Text PDFNetw Neurosci
December 2024
Institute of Neurosciences and Medicine - Brain and Behaviour (INM-7), Research Centre Jülich, 52425 Jülich, Germany.
The neurodegenerative progression of Parkinson's disease affects brain structure and function and, concomitantly, alters the topological properties of brain networks. The network alteration accompanied by motor impairment and the duration of the disease has not yet been clearly demonstrated in the disease progression. In this study, we aim to resolve this problem with a modeling approach using the reduced Jansen-Rit model applied to large-scale brain networks derived from cross-sectional MRI data.
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