The intersection of electromagnetic radiation and neuronal communication, focusing on the potential role of biophoton emission in brain function and neurodegenerative diseases is an emerging research area. Traditionally, it is believed that neurons encode and communicate information via electrochemical impulses, generating electromagnetic fields detectable by EEG and MEG. Recent discoveries indicate that neurons may also emit biophotons, suggesting an additional communication channel alongside the regular synaptic interactions. This dual signaling system is analyzed for its potential in synchronizing neuronal activity and improving information transfer, with implications for brain-like computing systems. The clinical relevance is explored through the lens of neurodegenerative diseases and intrinsically disordered proteins, where oxidative stress may alter biophoton emission, offering clues for pathological conditions, such as Alzheimer's and Parkinson's diseases. The potential therapeutic use of Low-Level Laser Therapy (LLLT) is also examined for its ability to modulate biophoton activity and mitigate oxidative stress, presenting new opportunities for treatment. Here, we invite further exploration into the intricate roles the electromagnetic phenomena play in brain function, potentially leading to breakthroughs in computational neuroscience and medical therapies for neurodegenerative diseases.
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http://dx.doi.org/10.1016/j.pbiomolbio.2024.12.004 | 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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