BTA-1 is a fluorescent thioflavin-T derivative with 50-fold higher affinity for β-amyloid aggregates.
BTA-1 is a probe for β-amyloid aggregates; fluorescent thioflavin-T derivative; exhibits high affinity for amyloid deposits; displays 50-fold higher affinity than thioflavin-T; selectively stains cerebral plaques and cerebrovascular amyloid deposits in the brains of PS1/APP transgenic mice, as well as Aβ fibrils in postmortem brain tissue obtained from AD patients; crosses the blood brain barrier.
Intrinsic optical emissions, such as autofluorescence and second harmonic generation (SHG), are potentially useful for functional fluorescence imaging and biomedical disease diagnosis for neurodegenerative diseases such as Alzheimer's disease (AD). Here, using multiphoton and SHG microscopy, we identified sources of
Journal of nuclear medicine : official publication, Society of Nuclear Medicine, 59(6), 960-966 (2018-02-09)
Fibrillary tau aggregates in Alzheimer disease and allied neurodegenerative disorders have been visualized in vivo by PET, whereas mechanistic links between PET-detectable tau deposits and neurotoxicity remain elusive. Here, we took advantage of transgenic mouse models of tauopathies to evaluate
The synthesis of a new lipophilic thioflavin-T analogue (2-[4' -(methylamino)phenyl]benzothiazole, 6) with high affinity for amyloid is reported. Intravenous injection of [(11)C]-labeled 6 in control mice resulted in high brain uptake. Amyloid deposits were imaged with multiphoton microscopy in the
European journal of medicinal chemistry, 175, 149-161 (2019-05-13)
Six novel 2-arylimidazo[2,1-b]benzothiazole (IBT) derivatives were synthesized as potential tridentate radiotracers for AD imaging purposes. Two of these ligands (6a,b) were successfully labeled with 99mTc radionuclide at high radiochemical purity using fac-[99mTc(CO)3(H2O)3]+ synthon. [99mTc]7a and [99mTc]7b were evaluated as single
European journal of nuclear medicine and molecular imaging, 42(7), 1119-1132 (2015-04-22)
Pathological studies suggest that neuroinflammation is exacerbated by increased beta-amyloid (Aβ) levels in the brain early in Alzheimer's disease (AD). The time course and relationships between astrocytosis and Aβ deposition were examined using multitracer in vivo positron emission tomography (PET)
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