Brain-specific biomolecules are being increasingly investigated as a viable alternative to the clinical scores and radiological features, on which we still rely upon for stratification, therapy and predicting outcome in traumatic brain injury (TBI). TBI generally leads to release of various chemical compound within the cerebrospinal fluid (CSF) or blood depending on the severity of injury, which were studied variedly in last decades. However, most of these compounds being non-specific to brain, their applicability was challenged further. This review encompasses the novel and promising biomarkers being studied in the present decade, with encouraging results in laboratory and animal or human models.
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http://dx.doi.org/10.1016/j.cca.2018.10.025 | DOI Listing |
EMBO J
January 2025
Division of Neurology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
Polyglucosans are glycogen molecules with overlong chains, which are hyperphosphorylated in the neurodegenerative Lafora disease (LD). Brain polyglucosan bodies (PBs) cause fatal neurodegenerative diseases including Lafora disease and adult polyglucosan body disease (ABPD), for which treatments, biomarkers, and good understanding of their pathogenesis are currently missing. Mutations in the genes for the phosphatase laforin or the E3 ubiquitin ligase malin can cause LD.
View Article and Find Full Text PDFMol Neurobiol
January 2025
Department of Neurology, Huai'an First People's Hospital, The Affiliated Huai'an No.1 People's Hospital of Nanjing Medical University, No.1 Huanghe West Road, Huai'an, 223300, Jiangsu, China.
A comprehensive genome-wide association study (GWAS) has validated the identification of the Plexin-A 4 (PLXNA4) gene as a novel susceptibility factor for Alzheimer's disease (AD). Nonetheless, the precise role of PLXNA4 gene polymorphisms in the pathophysiology of AD remains to be established. Consequently, this study is aimed at exploring the relationship between PLXNA4 gene polymorphisms and neuroimaging phenotypes intimately linked to AD.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Chromosome Biomedical Engineering, School of Life Science, Faculty of Medicine, Tottori University, 86 Nishi-cho, Yonago, Tottori, 683‑8503, Japan.
Duchenne muscular dystrophy (DMD) is an X-linked recessive disorder caused by mutations of the dystrophin gene, which spans 2.4 Mb on the X chromosome. Creatine kinase (CK) activity in blood and titin fragment levels in urine have been identified as biomarkers in DMD to monitor disease progression and evaluate therapeutic intervention.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Gastrointestinal Surgery, Third Xiangya Hospital, Central South University, Changsha, 410006, China.
G-protein gamma subunit 2 (GNG2) plays a vital role in various cellular processes, yet its specific function in colorectal cancer (CRC), particularly in highly invasive cases and brain metastasis, remains unclear. This study identifies GNG2 as a key regulator in metastatic colorectal cancer (mCRC) through bioinformatics analysis and experimental validation. Functional enrichment analyses reveal that GNG2 is related to the PI3K/AKT/mTOR signaling pathway and cell cycle regulation.
View Article and Find Full Text PDFAJNR Am J Neuroradiol
January 2025
From the Department of Department of Radiology, Brain Health Imaging Institute (A.R-F, J.I, S.P, M.d, G.C.C) Weill Cornell Medicine, New York-Presbyterian Hospital, New York, New York, USA; the Department of Neurology (A.R-F), Pontificia Universidad Javeriana, Bogota, Colombia; the Department of Radiology, Division of Molecular Imaging and Therapeutics (A.R-F, J.I) Weill Cornell Medicine, New York-Presbyterian Hospital, New York, New York, USA; the Department of Neurology (D.Z, MM, L.R, A.S.N) Weill Cornell Medicine, New York-Presbyterian Hospital, New York, New York, USA.
Amyloid-targeting therapy has recently become widely available in the U.S. for the treatment of patients with symptomatic mild Alzheimer's disease (AD).
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