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| J Korean Med Assoc > Volume 52(2); 2009 > Article |
Abstract
Neurodegenerative diseases are highly morbid and widespread in the nation with aged population. Since these are progressive and irreversible diseases, early detection and differentiation of the disease are important for possible therapeutic intervention. Alzheimer's disease and Parkinson's disease are the most frequent and costly devastating neurodegenerative diseases. Recent advances of molecular imaging, especially positron emission tomography (PET) technique, allows non-invasive evaluation of not only regional cerebral metabolism or perfusion, but also the change of neurotransmission and presence of abnormal protein such as beta amyloid. In Parkinsonism, dopamine transporter and vesicular monoamine transporter imaging are useful in the diagnosis and evaluation of the disease progression since these provide information about the integrity of presynaptic striatal dopaminergic neurons. In Alzheimer's disease, beta-amyloid imaging can assess the amyloid deposition. It improves early diagnosis and possibility of a presymptomatic diagnostic biomarker; improves understanding of the natural history of amyloid deposition; and has the capability to directly measure the effects of newly developed anti-amyloid therapies. Cholinergic and microglial imaging can be also useful in the early diagnosis of dementia and improves understanding of insights into pathophysiology of neurodegenerative diseases. Therefore, the ability of molecular imaging to identify and quantify cerebral pathology has significant implications for early detection, differential diagnosis, and therapeutic monitoring in neurodegenerative diseases.
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Figure 3
[18F]FP-CIT PET images of normal healthy person and patients with early stage (H&Y stage I) and advanced stage (H&Y stage III) of Parkinson's disease. In early Parkinson's disease, bilateral putamina show asymmetrically decreased uptake. Advanced Parkinson's disease show significantly decreased uptake not only in bilateral putamina but also caudate nuclei.
Figure 5
[11C]PIB PET images of normal healthy person and patients with Alzheimer's disease, Mild cognitive impairment, and frontotemporal dementia. In [11C]PIB PET images of normal person and patient with frontotemporal dementia, cerebral cortical uptake is lower than white matter. [11C]PIB PET image of Alzheimer's disease shows increased uptake in bilateral frontal and temporal cortex, and anterior striata. [11C]PIB PET image of mild cognitive impairment also shows increased uptake in bilateral posterior cingulate gyri, suggesting increased beta-amyloid burden.
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