Subjects with MDD had regional brain metabolic abnormalities at baseline that tended to normalize with treatment. Regional metabolic changes appeared similar with the 2 forms of treatment. These results should be interpreted with caution because of study limitations (small sample size, lack of random assignment to treatment groups, and differential treatment response between treatment subgroups).
[F-18]MPPF ͉ brain 5-HT1A receptors ͉ neuronal loss ͉ positron emission tomography E xtensive brain cell loss in vulnerable cortical neuronal populations is one of the most striking hallmarks of Alzheimer's disease (AD). Neuronal loss appears to be correlated with the presence of abundant intraneuronal neurofibrillary tangles (NFTs) and is also an excellent parameter to correlate with the degree of dementia (1). Among the vulnerable neurons affected in the earliest stages of the disease are large pyramidal neurons in the CA1 and subicular regions of hippocampus, a part of the medial temporal lobe (MTL) system supporting declarative memory (2). The pattern of neuronal loss in AD is distinctively different from the cell loss observed in normal aging and is highest in entorhinal cortex and hippocampus CA1 region (1, 3). Although these large pyramidal neurons are glutamatergic in nature, they receive inhibitory serotonergic input from the dorsal raphe nucleus via the serotonin 1A (5-HT 1A ) receptors located on their axonal hillock (4). The correlation between the loss of glutamatergic pyramidal neurons in CA1 field of hippocampus and the decrease in 5-HT 1A receptor densities in the same areas was demonstrated earlier by using in vitro 4- [F-18] and can be partially attributed to the neuronal loss in epileptic foci (6). Availability of methods for 5-HT 1A receptor density quantification with PET therefore offers an excellent opportunity for in vivo assessment of neuronal damage in 5-HT 1A receptor-rich areas in AD, particularly in hippocampus. In this work, changes in 5-HT 1A receptor densities in the living brain of AD patients (ADs) and mild cognitive impairment patients (MCIs) were also correlated with global and regional measures of glucose metabolic activity, with the extent and spatial distribution of the NFT͞-amyloid senile plaque deposition and with behavioral measures [e.g., Mini Mental State Exam (MMSE) and Buschke scores]. In vitro autoradiography in ADs and normal subject brain specimens was used in support of the observations in living subjects.
In patients with coronary artery disease, non-invasive measurements of myocardial blood flow and flow reserve by PET are inversely and nonlinearly related to stenosis severity as defined by quantitative angiography. Importantly, coronary lesions of intermediate severity have a differential flow reserve that decreases as stenosis increases that can be detected noninvasively by PET, thus allowing better definition of the functional importance of known coronary stenosis.
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