The 18-kDa translocator protein (TSPO) is gaining recognition as a relevant target in glioblastoma imaging. However, data on the potential prognostic value of TSPO PET imaging in glioblastoma are lacking. Therefore, we investigated the association of TSPO PET imaging results with survival outcome in a homogeneous cohort of glioblastoma patients. Patients were included who had newly diagnosed, histologically confirmed isocitrate dehydrogenase (IDH)-wild-type glioblastoma with available TSPO PET before either normofractionated radiotherapy combined with temozolomide or hypofractionated radiotherapy. SUV on TSPO PET, TSPO binding affinity status, tumor volumes on MRI, and further clinical data, such as -alkylguanine DNA methyltransferase () and telomerase reverse transcriptase () gene promoter mutation status, were correlated with patient survival. Forty-five patients (median age, 63.3 y) were included. Median SUV was 2.2 (range, 1.0-4.7). A TSPO PET signal was associated with survival: High uptake intensity (SUV > 2.2) was related to significantly shorter overall survival (OS; 8.3 vs. 17.8 mo, = 0.037). Besides SUV, prognostic factors for OS were age ( = 0.046), promoter methylation status ( = 0.032), and T2-weighted MRI volume ( = 0.031). In the multivariate survival analysis, SUV in TSPO PET remained an independent prognostic factor for OS ( = 0.023), with a hazard ratio of 2.212 (95% CI, 1.115-4.386) for death in cases with a high TSPO PET signal (SUV > 2.2). A high TSPO PET signal before radiotherapy is associated with significantly shorter survival in patients with newly diagnosed IDH-wild-type glioblastoma. TSPO PET seems to add prognostic insights beyond established clinical parameters and might serve as an informative tool as clinicians make survival predictions for patients with glioblastoma.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10586482 | PMC |
http://dx.doi.org/10.2967/jnumed.122.265247 | DOI Listing |
Alzheimers Dement
December 2024
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Mölndal, Gothenburg, Sweden.
Background: Emerging evidence underscores the importance of neuroinflammation in the progression of Alzheimer's disease (AD) pathophysiology. Recent studies indicate the involvement of the inflammatory mechanisms both in amyloid- β (Aβ) and tau deposition in the brain. Nevertheless, due to the complexity of the immune responses and the intricate interplay between the peripheral and the central nervous systems, identifying biomarkers that reflect the brain´s inflammatory state in AD has been a challenge.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
LC Campbell Cognitive Neurology Research Unit, Sunnybrook Research Institute, University of Toronto, Toronto, ON, Canada.
Background: In-vivo PET imaging studies have demonstrated neuroinflammation (microglia reactivity) in the neocortex of Alzheimer's disease (AD) patients. However, the extent and implication of microglia reactivity in white matter regions remains unclear. Here, we explored microglia reactivity in white matter using PET imaging of the translocator protein (TSPO) in relation to core AD biomarkers (amyloid, tau, and astrogliosis), microstructural damage, and cognitive decline.
View Article and Find Full Text PDFBrain
January 2025
Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh EH16 4SB, UK.
Alzheimers Dement
December 2024
University of São Paulo Medical School, São Paulo, São Paulo, Brazil.
Background: Down syndrome (DS) is associated with mitochondrial dysfunction leading to higher levels of oxidative stress and cell degeneration. This fact, together with the overexpression of AD-related genes in trisomy 21, increases the risk of developing Alzheimer's disease (AD). Thus, it is important to look for interventions that could prevent mitochondrial damage before symptoms occur.
View Article and Find Full Text PDFBackground: Early neuroinflammation is involved in pathophysiology of Alzheimer's Disease (AD) and contributes to faster clinical decline. Thus, neuroinflammation has emerged as a promising therapeutic target for dementia. However, a better understanding of the interaction between central and peripheral inflammation in human disease and in vivo biomarkers are required for successful clinical trials.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!