2001
DOI: 10.1016/s0140-6736(01)05625-2
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In-vivo measurement of activated microglia in dementia

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Cited by 976 publications
(749 citation statements)
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“…Yet, NSAIDs were not found to ameliorate Alzheimer neuropathology [37]. Therefore, it is possible, if not likely in our view that activated microglia, identified in the brains of Alzheimer disease patients both histopathologically and in neuroimaging studies [39], and now commonly referred to as ''neuroinflammatory'', may have a completely different function to activated macrophages in the periphery. For instance, we now know that microglia themselves are affected by the disease process in AD [40].…”
Section: Alzheimer's Diseasementioning
confidence: 77%
See 1 more Smart Citation
“…Yet, NSAIDs were not found to ameliorate Alzheimer neuropathology [37]. Therefore, it is possible, if not likely in our view that activated microglia, identified in the brains of Alzheimer disease patients both histopathologically and in neuroimaging studies [39], and now commonly referred to as ''neuroinflammatory'', may have a completely different function to activated macrophages in the periphery. For instance, we now know that microglia themselves are affected by the disease process in AD [40].…”
Section: Alzheimer's Diseasementioning
confidence: 77%
“…Results obtained from imaging activated microglia in vivo [39] have fostered an interest in the role of microglia in psychiatric diseases. Microglial activation, which many authors effectively equate with neuroinflammation, is now considered to be central to the pathogenesis of several psychiatric disorders.…”
Section: Neuroimmunology Of Psychiatric Disordersmentioning
confidence: 99%
“…[ 11 C]PK11195 has been used for the in vivo imaging of PBR in the brain by positron emission tomography (PET), especially for the evaluation of lesions, and [ 11 C]PK11195 binding was reported to have increased in the stroke region (Pappata et al, 2000), plaque of multiple sclerosis (Banati et al, 2000;Debruyne et al, 2002), the cortex of Alzheimer's disease (Cagnin et al, 2001), and epileptic foci (Goerres et al, 2001). Since PBR localizes in glial cells in the brain, definition of the reference region without specific binding is difficult, especially in diseases with a widespread distribution of pathologic changes, such as Alzheimer's disease.…”
Section: Introductionmentioning
confidence: 99%
“…Semiquantification of specific binding was performed using late images, in which the activity of the region of interest was normalized to that of the cerebellum (Groom et al, 1995), cortical gray matter (Debruyne et al, 2003), or the whole brain (Debruyne et al, 2002). However, evaluation of specific binding potential (BP) with a compartment model without arterial blood sampling was performed using cluster analysis for the extraction of voxels with normal ligand kinetics to serve as the reference input function (Banati et al, 2000;Cagnin et al, 2001). Recently, Kropholler et al (2005) analyzed [ 11 C]PK11195 kinetics by a one-tissue or two-tissue compartment model with metabolite-corrected plasma input function, and concluded that a two-tissue reversible compartment model with K 1 /k 2 fixed to the whole cortex value was optimal.…”
Section: Introductionmentioning
confidence: 99%
“…Increased expression has been observed using the specific ligand 11 C-PK11195, which has been shown to reflect the distribution of activated microglia and used as a marker transition from a resting to an activated state in experimental studies and human brain disease [8]. Increased brain binding of 11 C-PK11195 was observed in several acute neurological and neurodegenerative disorders such as strokeinduced brain injury, multiple sclerosis, glioma, refractory epilepsy, AD and HD [8][9][10][11][12][13]. Increased uptake of 11 C-PK11195 was also reported in frontotemporal lobar degeneration [14] and HD [15].…”
Section: Translocator Protein Systemmentioning
confidence: 99%