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Blood biomarkers have been considered tools for the diagnosis, prognosis, and monitoring of Alzheimer's disease (AD). Although amyloid-β peptide (Aβ) and tau are primarily blood biomarkers, recent studies have identified other reliable candidates that can serve as measurable indicators of pathological conditions. One such candidate is the glial fibrillary acidic protein (GFAP), an astrocytic cytoskeletal protein that can be detected in blood samples. Increasing evidence suggests that blood GFAP levels can be used to detect early-stage AD. In this systematic review and meta-analysis, we aimed to evaluate GFAP in peripheral blood as a biomarker for AD and provide an overview of the evidence regarding its utility. Our analysis revealed that the GFAP level in the blood was higher in the Aβ-positive group than in the negative groups, and in individuals with AD or mild cognitive impairment (MCI) compared to the healthy controls. Therefore, we believe that the clinical use of blood GFAP measurements has the potential to accelerate the diagnosis and improve the prognosis of AD.
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http://dx.doi.org/10.3390/cells12091309 | DOI Listing |
Elife
September 2025
Human Biology and Primate Evolution, Institute of Biology, Freie Universität Berlin, Berlin, Germany.
Evidence indicates that transposable elements (TEs) can contribute to the evolution of new traits, with some TEs acting as deleterious elements while others are repurposed for beneficial roles in evolution. In mammals, some KRAB-ZNF proteins can serve as a key defense mechanism to repress TEs, offering genomic protection. Notably, the family of KRAB-ZNF genes evolves rapidly and exhibits diverse expression patterns in primate brains, where some TEs, including autonomous LINE-1 and non-autonomous Alu and SVA elements, remain mobile.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2025
Department of Medicine and Surgery, Unit of Neurology, Neurophysiology, Neurobiology and Psychiatry, Università Campus Bio-Medico di Roma, Roma, Italy.
BackgroundAlzheimer's disease (AD) is the most common neurodegenerative disorder. While AD diagnosis traditionally relies on clinical criteria, recent trends favor a precise biological definition. Existing biomarkers efficiently detect AD pathology but inadequately reflect the extent of cognitive impairment or disease heterogeneity.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2025
Paula Costa-Urrutia Medical Affairs, Terumo BCT, Edificio Think MVD, Montevideo, Uruguay.
BackgroundTherapeutic plasma exchange (TPE) with albumin replacement has emerged as a potential treatment for Alzheimer's disease (AD). The AMBAR trial showed that TPE could slow cognitive and functional decline, along with changes in core and inflammatory biomarkers in cerebrospinal fluid.ObjectiveTo evaluate the safety and effectiveness of TPE in a real-world setting in Argentina.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2025
Department of Community Health and Health Behavior, University at Buffalo, Buffalo, NY, USA.
BackgroundFear of developing Alzheimer's disease and other dementias could motivate defensive responses to dementia information, including public health messaging, and reduce willingness to undergo screening or diagnostic testing for the disease.ObjectiveWe sought to assess the pervasiveness of dementia information avoidance and test whether it is associated with lower willingness to be screened for dementia. We also tested whether lower generalized self-efficacy is associated with higher dementia information avoidance, as the former might be a point of intervention for decreasing defensive information avoidance.
View Article and Find Full Text PDFInflammopharmacology
September 2025
Centre for Research Impact & Outcome, Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, 140401, India.
The NOD‑like receptor family pyrin domain containing 3 (NLRP3) inflammasome is a key molecular complex that amplifies inflammatory cascades by maturing interleukin‑1 beta (IL-1β) and interleukin‑18 (IL-18) and inducing pyroptosis. It serves as a major driver and co-driver of numerous diseases associated with chronic inflammation. Dysregulated NLRP3 activation contributes to the progression of disorders such as rheumatoid arthritis, inflammatory bowel disease, neurodegenerative diseases and atherosclerosis.
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