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Huntington’s Disease and Stem Cells
Published in Deepak A. Lamba, Patient-Specific Stem Cells, 2017
Karen Ring, Robert O’Brien, Ningzhe Zhang, Lisa M. Ellerby
Neuroimaging techniques have been utilized to monitor changes in the brain in both asymptomatic and symptomatic HD patients (10). The most commonly utilized techniques are positron emission tomography (PET) and magnetic resonance imaging (MRI). The atrophy in the striatum and the cortex and the enlargement of the anterior horns of the lateral ventricles can be severe and easily visualized by MRI (Figure 6.2). MRI detects a progressive loss of volume in the striatum even 15–20 years before the onset of the disease symptoms in HD patients. MRI also detects cortical thinning in HD patients along with changes in white matter and whole brain. Most importantly, gray matter and striatal atrophy are predictors of clinical diagnosis of HD. PET studies in HD patients reveal disruption of the postsynaptic dopaminergic system. Dopamine D1 receptor density is reduced in HD patients when compared to controls using radioligand SCH23390 (10).
Imaging of Beta-Receptors in the Heart
Published in Robert J. Gropler, David K. Glover, Albert J. Sinusas, Heinrich Taegtmeyer, Cardiovascular Molecular Imaging, 2007
Jeanne M. Link, John R. Stratton, Wayne C. Levy, Jeanne Poole, James H. Caldwell
The rate of binding of an agonist or antagonist (ligand binding) to the receptor follows a second order rate equation (15). Agonists tend to bind quickly (large association constant kon) but to not remain bound for very long (large dissociation constant koff). The ratio of koff/kon is termed the equilibrium dissociation constant, KD. The KD is a measure of the stability of the ligand bound to the receptor and has a significant impact on the potential of a radioligand to be a useful imaging agent. Antagonists have a range of kinetic constants, and thus a range of KDs. In general, an agonist is not used for β-AR imaging because it will also be taken up in the pre-synaptic system by the norepinephrine transporter (NETl, also known as uptake-1). Consequently, an agonist becomes a marker of both pre- and postsynaptic binding, primarily presynaptic, so the image cannot be uniquely interpreted for β-AR.
Radionuclide-based Diagnosis and Therapy of Prostate Cancer
Published in Michael Ljungberg, Handbook of Nuclear Medicine and Molecular Imaging for Physicists, 2022
Sven-Erik Strand, Mohamed Altai, Joanna Strand, David Ulmert
PSMA-617, a ligand with optimized tumour cell internalization and low kidney retention with DOTA chelator, was developed for PSMA-targeted radioligand therapy. 177Lu-PSMA-617 has been increasingly used for therapy of metastatic PCa patients (see next section). These prompted research to clinically investigate the potential of using a 68Ga-labeled PSMA-617 as a companion diagnostic agent for PET imaging [89]. This study clearly demonstrated that 68Ga-PSMA-617 is capable of detecting lesions of PCa with high contrast, especially in late time images.
The New Zealand Parkinson’s progression programme
Published in Journal of the Royal Society of New Zealand, 2023
Michael R. MacAskill, Toni L. Pitcher, Tracy R. Melzer, Daniel J. Myall, Kyla-Louise Horne, Reza Shoorangiz, Mustafa M. Almuqbel, Leslie Livingston, Sophie Grenfell, Maddie J. Pascoe, Ethan T. Marshall, Steven Marsh, Sarah E. Perry, Wassilios G. Meissner, Catherine Theys, Campbell J. Le Heron, Ross J. Keenan, John C. Dalrymple-Alford, Tim J. Anderson
We have applied more established imaging sequences such as T1-weighted structural imaging with a focus on cognitive status in Parkinson’s. Both cortical grey matter atrophy (Melzer et al. 2012) and striatal volume loss (Pitcher et al. 2012) were shown to be related to the degree of cognitive impairment. Diffusion tensor imaging (DTI) also showed that white matter tracts were extensively disrupted even in the mild stage of cognitive impairment (Melzer et al. 2013): with rapidly improving technical advances, this imaging modality is becoming increasingly useful (Melzer 2013). We also applied the non-image-forming technique of MR spectroscopy to measure ratios of metabolites (N-acetylaspartate, choline, creatine, and myo-inositol) that are sensitive to neuronal loss, axonal damage, and impaired metabolism. In a longitudinal study we found that this did not appear to be useful in our Parkinson’s sample (Almuqbel et al. 2016), and subsequently dropped spectroscopy from the protocol, in favour of adding resting-state BOLD (to assess functional connectivity) and quantitative susceptibility mapping (to measure iron deposition). Another approach to molecular imaging is via PET, using a radioligand to target a particular substance. In 118 Parkinson’s participants (Figure 4), we used 18F-Florbetaben (FBB) to measure the distribution of amyloid accumulation throughout the brain. Abnormal deposits of misfolded amyloid protein are characteristic of Alzheimer’s, and a natural question was whether they are also associated with the dementia due to Parkinson’s. We found that FBB binding was indeed higher on average in the PDD group compared to PDN and PD-MCI, but this was accounted for by the older age of that group. There were no associations between amyloid levels and other cognitive or disease severity measures. On this basis, we posit that amyloid does not play a major role in advanced idiopathic Parkinson’s. Developing a PET tracer for alpha-synuclein has not yet been possible (Korat et al. 2021), but is keenly awaited to allow in vivo rather than post mortem characterisation of the pathological process specific to Parkinson’s.