Alzheimer's disease is the most common form of dementia worldwide, accounting for 60-70% of diagnosed cases. According to the current understanding of molecular pathogenesis, the main hallmarks of this disease are the abnormal accumulation of amyloid plaques and neurofibrillary tangles. Therefore, biomarkers reflecting these underlying biological mechanisms are recognized as valid tools for an early diagnosis of Alzheimer's disease. Inflammatory mechanisms, such as microglial activation, are known to be involved in Alzheimer's disease onset and progression. This activated state of the microglia is associated with increased expression of the translocator protein 18 kDa. On that account, PET tracers capable of measuring this signature, such as (R)-[C]PK11195, might be instrumental in assessing the state and evolution of Alzheimer's disease. This study aims to investigate the potential of Gray Level Co-occurrence Matrix-based textural parameters as an alternative to conventional quantification using kinetic models in (R)-[C]PK11195 PET images. To achieve this goal, kinetic and textural parameters were computed on (R)-[C]PK11195 PET images of 19 patients with an early diagnosis of Alzheimer's disease and 21 healthy controls and submitted separately to classification using a linear support vector machine. The classifier built using the textural parameters showed no inferior performance compared to the classical kinetic approach, yielding a slightly larger classification accuracy (accuracy of 0.7000, sensitivity of 0.6957, specificity of 0.7059 and balanced accuracy of 0.6967). In conclusion, our results support the notion that textural parameters may be an alternative to conventional quantification using kinetic models in (R)-[C]PK11195 PET images. The proposed quantification method makes it possible to use simpler scanning procedures, which increase patient comfort and convenience. We further speculate that textural parameters may also provide an alternative to kinetic analysis in (R)-[C]PK11195 PET neuroimaging studies involving other neurodegenerative disorders. Finally, we recognize that the potential role of this tracer is not in diagnosis but rather in the assessment and progression of the diffuse and dynamic distribution of inflammatory cell density in this disorder as a promising therapeutic target.
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http://dx.doi.org/10.1093/braincomms/fcad148 | DOI Listing |
Age Ageing
January 2025
Centre for Psychiatry and Mental Health, Wolfson Institute of Population Health, Queen Mary University of London, London, E13 8SP, United Kingdom of Great Britain and Northern Ireland.
Background: Behavioural and psychological symptoms of dementia (BPSD) can complicate acute hospital care, but evidence on BPSD in this setting is heterogeneous.
Objective: To determine the prevalence of BPSD in acute hospitals and explore related risk factors, treatments, and outcomes (PROSPERO: CRD42023406294).
Methods: We conducted a systematic review and meta-analysis by searching Cochrane Library, MEDLINE, and PsycINFO for studies on BPSD prevalence among older people with dementia during their acute hospital admissions (up to 5 March 2024).
Brain
January 2025
Reina Sofia Alzheimer Centre, CIEN Foundation, ISCIII, Madrid, Spain.
Lewy body (LB) pathology is present as a co-pathology in approximately 50% of Alzheimer's disease (AD) dementia patients and may even represent the main neuropathologic substrate in a subset of patients with amnestic impairments. However, the degree to which LB pathology affects the neurodegenerative course and clinical phenotype in amnestic patients is not well understood. Recently developed α-synuclein seed amplification assays (αSyn-SAAs) provide a unique opportunity for further investigating the complex interplay between AD and LB pathology in shaping heterogeneous regional neurodegeneration patterns and clinical trajectories among amnestic patients.
View Article and Find Full Text PDFGeroscience
January 2025
Institute of Biomedical Engineering, School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Brain network dynamics have been extensively explored in patients with subjective cognitive decline (SCD). However, these studies are susceptible to individual differences, scanning parameters, and other confounding factors. Therefore, how to reveal subtle SCD-related subtle changes remains unclear.
View Article and Find Full Text PDFEur J Nucl Med Mol Imaging
January 2025
Reina Sofia Alzheimer Center, CIEN Foundation, ISCIII, Madrid, Spain.
Purpose: Imaging biomarkers bear great promise for improving the diagnosis and prognosis of cognitive impairment in Parkinson's disease (PD). We compared the ability of three commonly used neuroimaging modalities to detect cortical changes in PD patients with mild cognitive impairment (PD-MCI) and dementia (PDD).
Methods: 53 cognitively normal PD patients (PD-CN), 32 PD-MCI, and 35 PDD underwent concurrent structural MRI (sMRI), diffusion-weighted MRI (dMRI), and [F]FDG PET.
Alzheimers Dement
January 2025
Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, Illinois, USA.
Introduction: This study investigates the inter-related roles of hippocampal neuronal loss (HNL), limbic-predominant age-related TAR-DNA binding protein of 43 kDa (TDP-43) encephalopathy neuropathologic changes (LATE-NC), and Alzheimer's disease neuropathologic changes (ADNC) on cognitive decline.
Methods: Participants underwent annual cognitive testing and autopsy. HNL, ADNC, LATE-NC, and other age-related pathologies were evaluated.
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