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A major cause of death in the elderly worldwide is attributed to neurodegenerative diseases, such as AD (Alzheimer's disease), PD (Parkinson's disease), ALS (Amyotrophic lateral sclerosis), FRDA (Friedreich's ataxia), VaD (Vascular dementia) etc. These can be caused due to multiple factors such as genetic, physiological problems like stroke or tumor, or even external causes like viruses, toxins, or chemicals. T3s (tocotrienols) exhibit various bioactive properties where it acts as an antioxidant, anti-inflammatory, anti-tumorigenic, and cholesterol lowering agent. Since T3 interferes with and influences several anti-inflammatory mechanisms, it aids in combating inflammatory responses that lead to disease progression. T3s are found to have a profound neuroprotective ability, however, due to their poor oral bioavailability, their full potential could not be exploited. Hence there is a need to explore other drug delivery techniques, especially focusing on aspects of nanotechnology. In this review paper we explore the anti-inflammatory mechanisms of T3 to apply it in the treatment of neurodegenerative diseases and also discusses the possibilities of nano methods of administering tocotrienols to target neurodegenerative diseases.
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http://dx.doi.org/10.12688/f1000research.131863.1 | DOI Listing |
Acta Neuropathol Commun
December 2024
Brain Science Institute, Johns Hopkins University School of Medicine, Johns Hopkins University, 855 N. Wolfe St., Rangos 275, Baltimore, MD, 21205, USA.
The GC hexanucleotide repeat expansion in C9ORF72 is the major genetic cause of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) (C9-ALS/FTD). Despite considerable efforts, the development of mouse models of C9-ALS/FTD useful for therapeutic development has proven challenging due to the intricate interplay of genetic and molecular factors underlying this neurodegenerative disorder, in addition to species differences. This study presents a robust investigation of the cellular pathophysiology and behavioral outcomes in a previously described AAV mouse model of C9-ALS expressing 66 GC hexanucleotide repeats.
View Article and Find Full Text PDFMol Genet Genomics
December 2024
Department of Medical Genetics, Faculty of Medicine, Karadeniz Technical University, Trabzon, Turkey.
Tuberous sclerosis complex (TSC) is a rare genetic disorder characterized by the formation of benign tumors in various organs, particularly in the central nervous system. We aimed to delineate the molecular profile of Turkish individuals diagnosed with TSC by analyzing the TSC1 and TSC2 genes using next-generation sequencing (NGS). Sophia Genetics' Sophia Inherited Disease Panel was used to perform NGS on 22 individuals diagnosed with TSC and to identify pathogenic variants in the TSC1 and TSC2 genes.
View Article and Find Full Text PDFOrphanet J Rare Dis
December 2024
Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, Hubei province, China.
Objective: Spinal muscular atrophy (SMA) is an autosomal recessive neuromuscular disease characterized by proximal muscle weakness and atrophy. The increasing availability of disease-modifying therapies has prompted the development of biomarkers to facilitate clinical assessments. We explored the association between disease severity and serum creatinine (Crn) levels in SMA patients undergoing up to two years of treatment with nusinersen.
View Article and Find Full Text PDFParkinsonism Relat Disord
December 2024
Centre for Movement Disorders, Stavanger University Hospital, Stavanger, Norway; Department of Chemistry, Bioscience and Environmental Engineering, University of Stavanger, Stavanger, Norway. Electronic address:
Introduction: Parkinson's disease (PD) is a progressive neurodegenerative disease, and biomarkers are needed to enhance earlier detection and monitoring. Alpha-synuclein, phosphorylated at serine 129 (pS129-α-syn), is the predominant form of α-syn found in Lewy bodies implicating an involvement in disease pathology. This review aims to systematically evaluate the evidence for pS129-α-syn detection in human biofluid samples of PD utilizing ELISA-based protein detection methods.
View Article and Find Full Text PDFRedox Biol
December 2024
Baruch College and CUNY Graduate Center, 1 Baruch Way, New York, NY, 10010, USA. Electronic address:
The elevated emission of reactive oxygen species (ROS) from presynaptic mitochondria is well-documented in several inflammatory and neurodegenerative diseases. However, the potential role of mitochondrial ROS in presynaptic function and plasticity remains largely understudied beyond the context of disease. Here, we investigated this potential ROS role in presynaptic function and short-term plasticity by combining optogenetics, whole cell electrophysiological recordings, and live confocal imaging using a well-established protocol for induction and measurement of synaptic potentiation in Drosophila melanogaster neuromuscular junctions (NMJ).
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