To investigate whether an intravenously administered compound of the IgG class is able to penetrate the CSF barrier despite its high molecular weight, 12 hepatitis B surface antibody (anti-HBs)-negative patients received 20 ml each of a beta-propiolactone-treated IgG compound with a high anti-HBs titer (1:115,000) as a marker. 8 had an inflammatory CSF syndrome. In cases of inflammatory CSF syndromes, significantly more marked IgG crossed the blood-brain barrier, this could be of considerable clinical importance.
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http://dx.doi.org/10.1159/000115691 | DOI Listing |
Brain
January 2025
Department of Neurology, National Taiwan University Hospital, Taipei, 100225, Taiwan.
Hereditary transthyretin amyloidosis with polyneuropathy (ATTRv-PN) is a neurodegenerative disease caused by mutations in the gene encoding transthyretin (TTR). Despite amyloid deposition being pathognomonic for diagnosis, this pathology in nervous tissues cannot fully account for nerve degeneration, implying additional pathophysiology for neurodegeneration, which, however, has not yet been fully elucidated. In this study, neuroinflammation in ATTRv-PN was investigated by examining nerve morphometry, the blood-nerve barrier, and macrophage infiltration in the sural nerves of ATTRv-PN patients and the sciatic nerves of a complementary mouse system, i.
View Article and Find Full Text PDFMol Divers
January 2025
Department of Biophysics, Panjab University, Chandigarh, 160014, India.
Alzheimer's disease (AD) is a degenerative neurological disorder defined by the formation of β-amyloid (Aβ) plaques and neurofibrillary tangles within the brain. Current pharmacological treatments for AD only provide symptomatic relief, and there is a lack of definitive disease-modifying therapies. Chemical chaperones, such as 4-Phenylbutyric acid (4PBA) and Tauroursodeoxycholic acid, have shown neuroprotective effects in animal and cell culture models.
View Article and Find Full Text PDFJ Alzheimers Dis
January 2025
Department of General Internal Medicine, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Background: Alzheimer's disease (AD) is an irreversible age-related neurodegenerative condition characterized by the deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles. Di Huang Yi Zhi (DHYZ) formula, a traditional Chinese herbal compound comprising several prescriptions, demonstrates properties that improve cognitive abilities in clinical. Nonetheless, its molecular mechanisms on treating AD through improving neuron cells mitochondria function have not been deeply investigated.
View Article and Find Full Text PDFAnal Chem
January 2025
State Key Laboratory of Chemical Resource Engineering, College of Chemistry, Beijing University of Chemical Technology, Beijing 100029, China.
The spontaneous aggregation of amyloid-β (Aβ) leads to neuronal cell death in the brain and causes the development of Alzheimer's disease (AD). The efficient detection of the aggregation state of Aβ holds significant promise for the early diagnosis and subsequent treatment of this neurodegenerative disorder. Currently, most of the fluorescent probes used for the detection of Aβ fibrils share similar recognition moieties, such as the ,-dimethylamino group, ,-diethylamino group, and piperidyl group.
View Article and Find Full Text PDFJ Ginseng Res
January 2025
Department of Convergence Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.
Background: The non-saponin (NS) fraction is an important active component of with multifunctional pharmacological activities including neuroprotective, immune regulatory, anti-inflammatory, and antioxidant effects. However, the effects of NSs on multiple sclerosis (MS), a chronic and autoimmune demyelinating disorder, have not yet been demonstrated.
Purpose: and Methods: The goal of the present study was to demonstrate the pharmacological actions of NSs on movement dysfunctions and the related mechanisms of action using an experimental autoimmune encephalomyelitis (EAE) mouse model of MS.
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