Seminars in Nuclear Medicine, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Molecular Neurodegeneration, Journal Year: 2025, Volume and Issue: 20(1)
Published: March 14, 2025
Abstract Alzheimer’s disease (AD) is neuropathologically characterized by the extracellular deposition of amyloid-β peptide (Aβ) and intraneuronal accumulation abnormal phosphorylated tau (τ)-protein (p-τ). Most frequently, these hallmark lesions are accompanied other co-pathologies in brain that may contribute to cognitive impairment, such as vascular lesions, transactive-response DNA-binding protein 43 (TDP-43), and/or α-synuclein (αSyn) aggregates. To estimate extent AD patients, several biomarkers have been developed. Specific tracers target visualize Aβ plaques, p-τ αSyn pathology or inflammation positron emission tomography. In addition imaging biomarkers, cerebrospinal fluid, blood-based biomarker assays reflecting AD-specific non-specific processes either already clinical use development. this review, we will introduce pathological brain, related discuss what respective determined at post-mortem histopathological analysis. It became evident initial stages plaque not detected with currently available biomarkers. Interestingly, precedes deposition, especially beginning when unable detect it. Later, takes lead accelerates pathology, fitting well known evolution measures over time. Some still lack clinically established today, TDP-43 cortical microinfarcts. summary, specific for AD-related pathologies allow accurate diagnosis based on pathobiological parameters. Although current excellent pathologies, they fail which analysis required. Accordingly, neuropathological studies remain essential understand development early stages. Moreover, there an urgent need co-pathologies, limbic predominant, age-related encephalopathy-related modify interacting p-τ. Novel approaches vesicle-based cryptic RNA/peptides help better future.
Language: Английский
Citations
1
European Journal of Nuclear Medicine and Molecular Imaging, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 21, 2025
Language: Английский
Citations
0
EJNMMI Research, Journal Year: 2025, Volume and Issue: 15(1)
Published: April 1, 2025
Abstract Background Amyloid-β imaging through positron emission tomography (PET) has significantly transformed Alzheimer’s disease (AD) research. [ 11 C]PiB been widely used for β-amyloid plaques due to its high affinity and selectivity amyloid deposits. 18 F]AZD4694 is a more recently developed amyloid-PET agent, which structurally resembles PiB less non-specific binding in the white matter than other F-labeled compounds. The purpose of this study compare vitro properties radiotracers post-mortem human brain tissue. Total was assessed by autoradiography prefrontal, inferior parietal, posterior cingulate cortices hippocampal sections healthy control (HC) AD autopsy-confirmed tissues. Furthermore, displacement unlabeled evaluated above-mentioned Results For both radiotracers, we found significant differences (p < 0.0001) between HC tissues prefrontal cortex ([ Cohen’s d = 3.424, 5.070), parietal 3.156, 3.959), 1.781, 3.434), hippocampus 1.320, 3.696). Higher detected compared cortices, while comparable radioligands. Strong correlations ]AZD4694 were (R 0.959, p 0.0001), 0.893, 0.838, 0.0006) 0.750, 0.0001). Bland–Altman analyses revealed strong agreement but lower hippocampus. Displacement studies confirmed all tissues, indicating that agents compete same sites. Conclusions This head-to-head provides evidence bindings are highly correlated with tracers competing sites, slightly higher effect size when comparing neuropathologically-confirmed
Language: Английский
Citations
0
Seminars in Nuclear Medicine, Journal Year: 2025, Volume and Issue: unknown
Published: April 1, 2025
Language: Английский
Citations
0