J Korean Med Assoc.  2009 Feb;52(2):151-167. 10.5124/jkma.2009.52.2.151.

Molecular Imaging in Neurodegenerative Diseases

Affiliations
  • 1Department of Nuclear Medicine, University of Ulsan College of Medicine, Korea. jaeskim@amc.seoul.kr, sjoh@amc.seoul.kr, dhmoon@amc.seoul.kr

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.

Keyword

Molecular imaging; Alzheimer's disease; Parkinson's disease; Neurodegenerative disease; Radiopharmaceuticals; PET

MeSH Terms

Aged
Alzheimer Disease
Amyloid
Dementia
Diagnosis, Differential
Disease Progression
Dopamine Plasma Membrane Transport Proteins
Dopaminergic Neurons
Early Diagnosis
Humans
Molecular Imaging
Natural History
Neurodegenerative Diseases
Parkinson Disease
Parkinsonian Disorders
Perfusion
Plaque, Amyloid
Positron-Emission Tomography
Radiopharmaceuticals
Synaptic Transmission
Vesicular Monoamine Transport Proteins
Amyloid
Dopamine Plasma Membrane Transport Proteins
Radiopharmaceuticals
Vesicular Monoamine Transport Proteins

Figure

  • Figure 1 Modification of cocaine chemical structure.

  • Figure 2 [18F]Fluoride labeling procedure for [18F]FP-CIT.

  • 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 4 Chemical structure of [11C]PIB and it's derivatives.

  • 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.

  • Figure 6 Chemical structure of [123I]IBVM and [18F]FEOBV.

  • Figure 7 Four stereochemical structure of [123I]IQNB derivatives.

  • Figure 8 Radiopharmaceuticals for microglia activation imaging.


Cited by  1 articles

Beta-amyloid imaging in dementia
Kyung Ah Chun
Yeungnam Univ J Med. 2018;35(1):1-6.    doi: 10.12701/yujm.2018.35.1.1.


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