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Molecular imaging, central nervous system CNS diseases, positron emission tomography PETsingle photon emission computed tomography SPECT Introduction The human brain is the most complex organ which acts as the center of the nervous system.
- Microglial activation and amyloid deposition in mild cognitive impairment
Although the neural mechanisms behind these brain dysfunctions are being studies in neuroscience field, how these cells interact with one another and the detailed molecular or subcellular processes underlying the neurological disorders are yet not well understood 1.
Traditionally, the mechanism of the CNS disorders can be investigated in the late stage or through postmortem analysis. However, the emerging molecular neuroimaging techniques such as magnetic resonance imaging MRIX-ray computed tomography CTpositron emission tomography PET and single photon emission computed tomography SPECT have made it possible to noninvasively identify the fundamental biological processes of the CNS diseases.
In particular, the advantages of molecular imaging lie in that the sophisticated biological processes and specific pathways in a given disease can be elucidated at the cellular and molecular levels in human and other living systems 2.
In addition, molecular imaging can provide the information of clinical changes before the pathological features occurred, making it possible to diagnose the diseases at early stage and to help in therapeutic trials of many CNS disorders 3. Then the major applications of the two modalities in the field of CNS disorders such as neurodegenerative disorders AD and PD are discussed.
Finally we will talk about the future trends in this specific field. PET and SPECT have many advantages such as high sensitivity, good spatial resolution and limitless penetration depth, leading to their vital role in molecular imaging for both preclinical and clinical studies. In this section, we will first give a brief introduction to the classical molecular neuroimaging modalities.
Classical modalities for molecular neuroimaging Table 1 briefly lists some of the general characteristics of representative molecular imaging techniques include CT, MRI, radionuclide imaging, optical imaging and ultrasound imaging.
We quantified PIB retention in the anterior cingulate, posterior cingulate, frontal, temporal, and parietal cortex. Additionally, whole brain retention was quantified, although not considered as a region when performing statistical analysis. We, therefore, used a supervised clustering technique to derive a nonspecific uptake tissue reference input function in all groups studied. This technique produces BP estimates that are reproducible and comparable to those derived from plasma input.
The supervised clustering algorithm avoids regions with specific binding such as association cortex in AD and large vessels, and the resulting cluster of voxels is clear of unwanted spurious signals arising from areas of the brain known to have a rich density of PBBS receptors such as the meninges.
The minute summation image contains blood flow dependent signal, providing good anatomic detail, enabling accurate coregistration.
Spatial normalization and creation of gray matter object maps were performed by the same methods described for analysis of PIB images, and PK BPs quantified in the same brain regions described earlier. Repeated measures analysis of variance was applied to test for global differences in PIB and PK binding between MCI groups and controls, using the Greenhouse Geisser factor to correct for variance heterogeneity across regions.
Univariate analysis of variance was used to detect significant differences in regional PIB and PK binding between groups, using age as a covariate and the p plot method to control for multiple comparisons.
Microglial activation and amyloid deposition in mild cognitive impairment
Quantitative analysis revealed PIB uptake ratio values comparable to our AD group, with twofold increased uptake in cingulate and frontal regions.
However, after correction for multiple comparisons, only frontal cortex PK uptake remained significantly raised.
Grouped mean PK BPs in the subject groups are shown in table 3.