Background: Multiple sclerosis (MS) is the most common chronic inflammatory, demyelinating disorder. Given its variable prognosis, the identification of new prognostic biomarkers is needed.
Objectives: The aims of our study were to assess the prognostic values of CSF β-amyloid-42 (Aβ42) and β-amyloid-40 (Aβ40) levels in MS patients.
Methods: Eighty-nine (55 RRMS, 34 PPMS) patients with a recent diagnosis and 27 controls were included in this single-centre retrospective study. Clinical, MRI and CSF data have been collected and were analysed to evaluate the potential value of CSF Aβ42 and Aβ40 levels as MS biomarkers.
Results: CSF Aβ levels as well as Aβ42/Aβ40 ratio were identical in MS patients and controls. Although CSF Aβ42 and Aβ40 levels were higher in PPMS than in RRMS and in patients with higher EDSS, a multivariate analysis including age and EDSS demonstrated that only age of patients was associated with CSF amyloid levels. Additionally, 55 RRMS patients were followed for 3 years. We found no association between baseline amyloid levels and 3-year disability.
Conclusion: Our data do not support an association between CSF amyloid levels and MS status and disease severity. We suggest that CSF amyloid levels are not a prognostic biomarker in recently diagnosed RRMS.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.msard.2022.104096 | 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 PDFAging Cell
January 2025
Department of Rehabilitation Medicine, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong, China.
Physical exercise is known to slow synaptic neurodegeneration and cognitive aging in Alzheimer's disease (AD). The benefits of physical exercise are related to reduced amyloid beta (Aβ) deposition and increased synaptic plasticity. Yet little is known about the mechanisms that mediate these effects.
View Article and Find Full Text PDFAlzheimers Res Ther
January 2025
Translational Neurodegeneration Research and Neuropathology Lab, Department of Clinical Medicine (KlinMed), Medical Faculty, University of Oslo (UiO) and Section of Neuropathology Research, Department of Pathology (PAT), Clinics for Laboratory Medicine (KLM), Oslo University Hospital (OUS), Sognsvannsveien 20, Oslo, NO-0372, Norway.
Background: Specific genetic variants in the ATP-binding cassette transporter A7 locus (ABCA7) are associated with an increased risk of Alzheimer's disease (AD). ABCA7 transports lipids from/across cell membranes, regulates Aβ peptide processing and clearance, and modulates microglial and T-cell functions to maintain immune homeostasis in the brain. During AD pathogenesis, neuroinflammation is one of the key mechanisms involved.
View Article and Find Full Text PDFMol Neurodegener
January 2025
Sam and Ann Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX, 78229, USA.
Alzheimer's disease (AD) is among the most devastating neurodegenerative disorders with limited treatment options. Emerging evidence points to the involvement of lipid dysregulation in the development of AD. Nevertheless, the precise lipidomic landscape and the mechanistic roles of lipids in disease pathology remain poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Xicheng District, Beijing, China.
Alzheimer's disease (AD) is a degenerative disease characterized by progressive cognitive dysfunction. The strong link between nutrition and the occurrence and progression of AD pathology has been well documented. Poor nutritional status accelerates AD progress by potentially aggravating amyloid beta (Aβ) and tau deposition, exacerbating oxidative stress response, modulating the microbiota-gut-brain axis, and disrupting blood-brain barrier function.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!