Amyloid-β (Aβ) positron emission tomography (PET) imaging and cerebrospinal fluid (CSF) biomarkers are now established tools in the diagnostic workup of patients with Alzheimer's disease (AD), and their use is anticipated to increase with the introduction of new disease-modifying therapies. Although these biomarkers are comparable alternatives in research settings to determine Aβ status, biomarker testing in clinical practice requires careful consideration of the strengths and limitations of each modality, as well as the specific clinical context, to identify which test is best suited for each patient. This article provides a comprehensive review of the pathologic processes reflected by Aβ-PET and CSF biomarkers, their performance, and their current and future applications and contexts of use. The primary aim is to assist clinicians in making better-informed decisions about the suitability of each biomarker in different clinical situations, thereby reducing the risk of misdiagnosis or incorrect interpretation of biomarker results. HIGHLIGHTS: Recent advances have positioned Aβ PET and CSF biomarkers as pivotal in AD diagnosis. It is crucial to understand the differences in the clinical use of these biomarkers. A team of experts reviewed the state of Aβ PET and CSF markers in clinical settings. Differential features in the clinical application of these biomarkers were reviewed. We discussed the role of Aβ PET and CSF in the context of novel plasma biomarkers.
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http://dx.doi.org/10.1002/alz.14528 | DOI Listing |
BMC Rheumatol
March 2025
Department of Medicine, Albury-Wodonga Health, Albury, NSW, Australia.
Background: Giant cell arteritis (GCA) is a vasculitis primarily affecting medium- and large-sized arteries. The diagnosis may be challenging and lead to delays in treatment. Cerebrospinal fluid (CSF) pleocytosis is an uncommon association but may occur due to central nervous system (CNS) vasculitis or pachymeningitis.
View Article and Find Full Text PDFEur J Med Res
March 2025
Department of Neurology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, 450003, Henan, China.
Background/purpose: GRN mutations act as causative factors in patients with FTD clinical phenotype or FTD pathology and exhibit high clinical heterogeneity. The discovery of these mutations and the analysis of their associations with resembling Alzheimer's disease should be critical to understand the pathogenesis of FTD.
Methods: Clinical analysis, neuroimaging, target region capture and high-throughput sequencing were performed in a family of 3 generations.
Value Health
March 2025
Fortrea, Leeds, United Kingdom.
Objectives: Amyloid-targeting therapies (ATTs) for Alzheimer's disease (AD), such as lecanemab, target and reduce brain β-amyloid plaques. To initiate therapy accurately, confirming the presence of brain β-amyloid plaques is necessary. This research investigated the added value and cost-effectiveness of F-flutemetamol positron emission tomography (PET) in the United States (US).
View Article and Find Full Text PDFEur J Neurol
March 2025
Department of Neurology and Institute of Neurology, Huashan Hospital, Fudan University, Shanghai, China.
Background And Purpose: Whether microglial activation plays an important role in the pathogenesis of autoimmune encephalitis (AE), such as anti-leucine-rich, glioma-inactivated-1 (LGI1) encephalitis, remains unknown. [F]-DPA714 PET targeting the translocator protein (TSPO) is a novel method to detect neuroinflammation via visualizing activated microglia. In this study, we aimed to investigate the application of [F]-DPA714 PET in anti-LGI1 encephalitis.
View Article and Find Full Text PDFAlzheimers Res Ther
March 2025
Genomics of Neurodegenerative Diseases and Aging, Department of Human Genetics, Amsterdam UMC Location VUmc, Amsterdam, The Netherlands.
Background: Rare variants of the triggering receptor expressed on myeloid cell 2 (TREM2) gene are strong risk factors for Alzheimer's disease (AD), and drugs targeting the TREM2 protein are being developed. However, it is unknown what the effect of TREM2 variants is on the AD phenotype.
Methods: Here we studied a full range of clinical and biomarker measures in a large cohort of TREM2 variant carriers (n = 123, 7.
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