pk 11195 has been researched along with Acute Confusional Senile Dementia in 32 studies
PK-11195 : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 1-(2-chlorophenyl)isoquinoline-3-carboxylic acid with the amino group of sec-butylmethylamine
Excerpt | Relevance | Reference |
---|---|---|
"Twenty-six (62%) of 42 mild cognitive impairment cases showed a raised cortical amyloid load compared to healthy controls." | 1.46 | Brain inflammation accompanies amyloid in the majority of mild cognitive impairment cases due to Alzheimer's disease. ( Aanerud, J; Amidi, A; Borghammer, P; Brooks, DJ; Brændgaard, H; Edison, P; Eriksson, BO; Eskildsen, SF; Gottrup, H; Hansen, KV; Hinz, R; Ismail, R; Lund, TE; Mårup, FH; Parbo, P; Pavese, N; Stokholm, MG; Tietze, A, 2017) |
"Longitudinally, Alzheimer's disease subjects showed an increase in microglial activation." | 1.46 | An early and late peak in microglial activation in Alzheimer's disease trajectory. ( Brooks, DJ; Edison, P; Fan, Z; Okello, A, 2017) |
"10 AD, 10 mild cognitive impairment (MCI), 11 PD dementia (PDD), and 16 controls underwent magnetic resonance imaging, [11C](R)PK11195 (1-[2-chlorophenyl]-N-methyl-N-[1-methyl-propyl]-3-isoquinoline carboxamide), [11C]PIB (11C-Pittsburgh compound B), [18F]FDG-PET (18F-2-fluoro-2-deoxyglucose positron emission tomography) scans." | 1.42 | Influence of microglial activation on neuronal function in Alzheimer's and Parkinson's disease dementia. ( Ahmed, I; Aman, Y; Brooks, DJ; Chetelat, G; Edison, P; Fan, Z; Landeau, B; Ray Chaudhuri, K, 2015) |
"At baseline, patients with Alzheimer's disease showed significantly increased microglial activation compared to the control subjects." | 1.42 | Longitudinal influence of microglial activation and amyloid on neuronal function in Alzheimer's disease. ( Brooks, DJ; Edison, P; Fan, Z; Okello, AA, 2015) |
"The pathological features in Alzheimer's disease (AD) brain include the accumulation and deposition of β-amyloid (Aβ), activation of astrocytes and microglia and disruption of cholinergic neurotransmission." | 1.39 | ³H-deprenyl and ³H-PIB autoradiography show different laminar distributions of astroglia and fibrillar β-amyloid in Alzheimer brain. ( Bergfors, A; Gillberg, PG; Marutle, A; Nennesmo, I; Ni, R; Nordberg, A; Voytenko, L; Yu, W, 2013) |
"Data from controls, mild cognitive impairment patients, and patients with Alzheimer's disease were analyzed using various kinetic models including plasma input, the simplified reference tissue model (RPM) and RPM with vascular correction (RPMV(b))." | 1.38 | Optimization of supervised cluster analysis for extracting reference tissue input curves in (R)-[(11)C]PK11195 brain PET studies. ( Boellaard, R; Hinz, R; Lammertsma, AA; Schuitemaker, A; Tomasi, G; Turkheimer, FE; van Berckel, BN; Yaqub, M, 2012) |
"Inflammation in Alzheimer's disease (AD) may be assessed using (R)-[(11)C]PK11195 and positron emission tomography." | 1.34 | Evaluation of reference regions for (R)-[(11)C]PK11195 studies in Alzheimer's disease and mild cognitive impairment. ( Boellaard, R; Jonker, C; Kloet, RW; Kropholler, MA; Lammertsma, AA; Lubberink, MJ; Scheltens, P; Schuitemaker, A; van Berckel, BN, 2007) |
"Ferulic acid is a natural compound that expresses antioxidant and anti-inflammatory activities." | 1.32 | Attenuation of chronic neuroinflammation by a nitric oxide-releasing derivative of the antioxidant ferulic acid. ( Gasparini, L; Hauss-Wegrzyniak, B; Maucci, R; McGann-Gramling, K; Ongini, E; Ronchetti, D; Rosi, S; Wenk, GL, 2004) |
"By contrast, patients with Alzheimer's disease showed significantly increased regional [11C](R)-PK11195 binding in the entorhinal, temporoparietal, and cingulate cortex." | 1.31 | In-vivo measurement of activated microglia in dementia. ( Banati, RB; Brooks, DJ; Cagnin, A; Gunn, RN; Jones, T; Kennedy, AM; Myers, R; Turkheimer, FE, 2001) |
"The aetiology and pathogenesis of Alzheimer's disease are currently poorly understood, but symptomatic disease is associated with amyloid plaques, neurofibrillary tangles, neuronal loss and numerous alterations of neurotransmitter systems in the CNS." | 1.29 | Increased monoamine oxidase B activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography. ( Cesura, AM; Chan-Palay, V; Da Prada, M; Huber, G; Löffler, J; Luque, JM; Richards, JG; Saura, J, 1994) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 3 (9.38) | 18.2507 |
2000's | 12 (37.50) | 29.6817 |
2010's | 15 (46.88) | 24.3611 |
2020's | 2 (6.25) | 2.80 |
Authors | Studies |
---|---|
Kim, T | 2 |
Yang, HY | 1 |
Park, BG | 1 |
Jung, SY | 2 |
Park, JH | 2 |
Park, KD | 2 |
Min, SJ | 1 |
Tae, J | 1 |
Yang, H | 1 |
Cho, S | 1 |
Cho, SJ | 2 |
Song, H | 1 |
Mook-Jung, I | 1 |
Lee, J | 2 |
Pae, AN | 2 |
Son, WS | 1 |
Morshed, MN | 1 |
Londhe, AM | 1 |
Park, WK | 1 |
Lim, SM | 1 |
Jeong, KS | 1 |
Parbo, P | 2 |
Madsen, LS | 1 |
Ismail, R | 2 |
Zetterberg, H | 1 |
Blennow, K | 1 |
Eskildsen, SF | 2 |
Vorup-Jensen, T | 1 |
Brooks, DJ | 11 |
Ni, R | 2 |
Röjdner, J | 1 |
Voytenko, L | 2 |
Dyrks, T | 1 |
Thiele, A | 1 |
Marutle, A | 2 |
Nordberg, A | 2 |
Hansen, KV | 1 |
Amidi, A | 1 |
Mårup, FH | 1 |
Gottrup, H | 1 |
Brændgaard, H | 1 |
Eriksson, BO | 1 |
Lund, TE | 1 |
Tietze, A | 1 |
Edison, P | 9 |
Pavese, N | 3 |
Stokholm, MG | 1 |
Borghammer, P | 1 |
Hinz, R | 3 |
Aanerud, J | 1 |
Christensen, A | 1 |
Pike, CJ | 2 |
Barron, AM | 1 |
Garcia-Segura, LM | 1 |
Caruso, D | 1 |
Jayaraman, A | 1 |
Lee, JW | 1 |
Melcangi, RC | 1 |
Gillberg, PG | 1 |
Bergfors, A | 1 |
Yu, W | 1 |
Nennesmo, I | 1 |
Hommet, C | 1 |
Mondon, K | 1 |
Camus, V | 1 |
Ribeiro, MJ | 1 |
Beaufils, E | 1 |
Arlicot, N | 1 |
Corcia, P | 1 |
Paccalin, M | 1 |
Minier, F | 1 |
Gosselin, T | 1 |
Page, G | 1 |
Guilloteau, D | 1 |
Chalon, S | 1 |
Fan, Z | 4 |
Aman, Y | 1 |
Ahmed, I | 1 |
Chetelat, G | 1 |
Landeau, B | 1 |
Ray Chaudhuri, K | 1 |
Okello, AA | 1 |
Femminella, GD | 1 |
Ninan, S | 1 |
Atkinson, R | 1 |
Yokokura, M | 1 |
Terada, T | 1 |
Bunai, T | 1 |
Nakaizumi, K | 1 |
Takebayashi, K | 1 |
Iwata, Y | 1 |
Yoshikawa, E | 1 |
Futatsubashi, M | 1 |
Suzuki, K | 1 |
Mori, N | 1 |
Ouchi, Y | 1 |
Okello, A | 2 |
Tomasi, G | 2 |
Bertoldo, A | 1 |
Roncaroli, F | 1 |
Singh, P | 1 |
Gerhard, A | 3 |
Cobelli, C | 1 |
Turkheimer, FE | 6 |
Archer, HA | 2 |
Hammers, A | 2 |
Tai, YF | 2 |
Fox, N | 2 |
Kennedy, A | 2 |
Rossor, M | 2 |
Kennedy, J | 1 |
Bullock, R | 1 |
Walker, Z | 1 |
Wiley, CA | 2 |
Lopresti, BJ | 2 |
Venneti, S | 2 |
Price, J | 1 |
Klunk, WE | 2 |
DeKosky, ST | 1 |
Mathis, CA | 2 |
Roberts, JC | 1 |
Friel, SL | 1 |
Roman, S | 1 |
Perren, M | 1 |
Harper, A | 1 |
Davis, JB | 1 |
Richardson, JC | 1 |
Virley, D | 1 |
Medhurst, AD | 1 |
Yaqub, M | 1 |
van Berckel, BN | 4 |
Schuitemaker, A | 4 |
Lammertsma, AA | 4 |
Boellaard, R | 4 |
Rapic, S | 1 |
Backes, H | 1 |
Viel, T | 1 |
Kummer, MP | 1 |
Monfared, P | 1 |
Neumaier, B | 1 |
Vollmar, S | 1 |
Hoehn, M | 1 |
Van der Linden, A | 1 |
Heneka, MT | 1 |
Jacobs, AH | 1 |
Kropholler, MA | 3 |
van der Flier, WM | 1 |
Kloet, RW | 3 |
van der Doef, TF | 1 |
Knol, DL | 1 |
Windhorst, AD | 1 |
Luurtsema, G | 1 |
Barkhof, F | 1 |
Jonker, C | 3 |
Scheltens, P | 3 |
Versijpt, JJ | 1 |
Dumont, F | 1 |
Van Laere, KJ | 1 |
Decoo, D | 1 |
Santens, P | 1 |
Audenaert, K | 1 |
Achten, E | 1 |
Slegers, G | 1 |
Dierckx, RA | 1 |
Korf, J | 1 |
Wenk, GL | 1 |
McGann-Gramling, K | 1 |
Hauss-Wegrzyniak, B | 1 |
Ronchetti, D | 1 |
Maucci, R | 1 |
Rosi, S | 1 |
Gasparini, L | 1 |
Ongini, E | 1 |
Anderson, AN | 1 |
Lubberink, MJ | 1 |
Wang, G | 1 |
Hamilton, RL | 1 |
Apte, UM | 1 |
Saura, J | 1 |
Luque, JM | 1 |
Cesura, AM | 1 |
Da Prada, M | 1 |
Chan-Palay, V | 1 |
Huber, G | 1 |
Löffler, J | 1 |
Richards, JG | 1 |
Groom, GN | 1 |
Junck, L | 1 |
Foster, NL | 1 |
Frey, KA | 1 |
Kuhl, DE | 1 |
Cagnin, A | 1 |
Kennedy, AM | 1 |
Gunn, RN | 1 |
Myers, R | 1 |
Jones, T | 1 |
Banati, RB | 1 |
Bidder, M | 1 |
Ratzoni, G | 1 |
Weizman, A | 1 |
Blumensohn, R | 1 |
Norymberg, M | 1 |
Tyano, S | 1 |
Gavish, M | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
The Relationship Between Neuropsychological Testing and MRI, PET and Blood Biomarkers in Neurodegenerative Disease (COBRE - Project 1): AIM 2[NCT03702816] | Phase 2 | 24 participants (Actual) | Interventional | 2018-12-13 | Terminated (stopped due to GE180 has limited Blood - brain barrier permeation, reducing its utility in neuroinflammation. COVID19 created supply chain issues, impacting enrollment.) | ||
Brain Inflammation In Major Depressive Disorder[NCT01851356] | 61 participants (Actual) | Observational | 2013-05-08 | Completed | |||
Assessment of [11C]ER-176 to Image Translocator Protein in Brain and Whole-Body of Healthy Subjects[NCT02147392] | Early Phase 1 | 16 participants (Actual) | Interventional | 2014-05-14 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
Cingulate SUVR- GE180 binding potential in the cingulate ROI, as a marker of cingulate neuroinflammation. Cingulate neuroinflammation would be expected to relate to cingulate AD pathology, and given known cingulate lobe role in executive system function, is hypothesized to relate to measures of executive function in particular, with greater cingulate GE180 relating to poorer cognitive function. (NCT03702816)
Timeframe: Baseline (Single scan)
Intervention | SUVR (Mean) |
---|---|
Control | 0.9994 |
Mild Cognitive Impairment | 1.0387 |
Alzheimer's Disease | 1.0554 |
Parkinson's Disease | 0.9893 |
DRS- The Dementia Rating Scale is a comprehensive, but relatively brief assessment of overall cognitive functioning. The measure consists of items testing memory, attention, executive skills, and visuospatial skill, for a total of 144 points. A score of less than 124 is indicative of dementia level cognitive functioning. A higher score indicates a better outcome. (NCT03702816)
Timeframe: Baseline (Pre-scan)
Intervention | score on a scale (Mean) |
---|---|
Control | 139.2 |
Mild Cognitive Impairment | 130.4 |
Alzheimer's Disease | 120.3 |
Parkinson's Disease | 139.3 |
The executive function composite score is comprised from data from two gold-standard clinical measures of set-shifting and inhibition (Trail Making Test, part B; Delis Kaplan Executive Functioning Scale Color Word Inhibition, inhibition score). The raw score for each individual assessment is corrected for age based on published normative data for each test. These adjusted scores (T scores and/or scaled scores) are converted to z-scores, then the two z-scores are averaged together to create the composite score. A higher value is indicative of better executive function, a lower value is indicative of worse executive function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
Intervention | z score (Mean) |
---|---|
Control | 0.572 |
Mild Cognitive Impairment | -0.011 |
Alzheimer's Disease | -1.361 |
Parkinson's Disease | 0.029 |
Frontal SUVR- GE180 binding potential in the frontal cortical ROI, as a marker of frontal neuroinflammation. Frontal neuroinflammation would be expected to relate to frontal lobe AD pathology, and given known frontal lobe role in executive system function, is hypothesized to relate to measures of executive function in particular, and also to memory and language dysfunction, as these have executive components. Greater frontal lobe GE180 is expected to relate to poorer cognitive function. (NCT03702816)
Timeframe: Baseline (Single scan)
Intervention | SUVR (Mean) |
---|---|
Control | 0.8893 |
Mild Cognitive Impairment | 0.9436 |
Alzheimer's Disease | 0.8855 |
Parkinson's Disease | 0.8850 |
The language composite score is comprised from data from two gold-standard clinical measures of confrontation naming and semantic fluency (Boston Naming Test; Animal Naming Test). The raw score for the Animal Naming Test is converted directly to a z-score based on published normative data. The Boston Naming Test is corrected for age based on published normative data, resulting in a scaled score, which is then converted to a z-score. Then the two z-scores are averaged together to create the composite score. A higher value is indicative of better language function, a lower value is indicative of worse language function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
Intervention | z score (Mean) |
---|---|
Control | 0.584 |
Mild Cognitive Impairment | -0.234 |
Alzheimer's Disease | -0.7272 |
Parkinson's Disease | 0.541 |
The memory composite score is comprised from data from two gold-standard clinical measures of verbal and nonverbal memory (Rey Auditory Verbal Learning Test, delayed recall score; Brief Visuospatial Memory Test, Revised, delayed recall score). The raw score for each individual assessment is corrected for age based on published normative data for each test. These adjusted scores (T scores and/or scaled scores) are converted to z-scores, then the two z-scores are averaged together to create the composite score. A higher value is indicative of better memory function, a lower value is indicative of worse memory function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
Intervention | z score (Mean) |
---|---|
Control | 0.367 |
Mild Cognitive Impairment | -0.675 |
Alzheimer's Disease | -2.483 |
Parkinson's Disease | -0.404 |
MoCA -The Montreal Cognitive Assessment is a brief screening tool, originally designed to detect patients with MCI in a memory disorders clinic [10]. Standard administration consists of 12 individual tasks grouped into seven cognitive domains (visuospatial/executive, naming; attention, language, abstraction, memory, and orientation). Task performance is summed generating both domain and a total score. An education correction of one point is added to the total score for individuals with 12 years of education or less. Scores range from 0-30, with a score of 26 or less indicating cognitive impairment. (NCT03702816)
Timeframe: Baseline (Pre-scan)
Intervention | score on a scale (Mean) |
---|---|
Control | 26.0 |
Mild Cognitive Impairment | 23.4 |
Alzheimer's Disease | 18.3 |
Parkinson's Disease | 27.5 |
Parietal SUVR - GE180 binding potential in the parietal cortical ROI, as a marker of parietal neuroinflammation. Parietal neuroinflammation would be expected to relate to parietal lobe AD pathology, and given known parietal lobe role in visual and executive system function, is hypothesized to relate to measures of visuospatial and executive skills in particular, with greater parietal lobe GE180 relating to poorer cognitive function. (NCT03702816)
Timeframe: Baseline (Single scan)
Intervention | SUVR (Mean) |
---|---|
Control | 0.8701 |
Mild Cognitive Impairment | 0.9241 |
Alzheimer's Disease | 0.8847 |
Parkinson's Disease | 0.8562 |
The speed composite score is comprised from data from two gold-standard clinical measures of speeded attention and psychomotor speed (Trail Making Test, part A; Symbol Digit Modalities Test, oral version). The raw score for the Symbol Digit Modalities Test, oral version is converted directly to a z-score based on published normative data. The Trail making Test, part A is corrected for age based on published normative data, resulting in a T-score, which is then converted to a z-score. Then the two z-scores are averaged together to create the composite score. A higher value is indicative of better speed function, a lower value is indicative of worse speed function. A z-score of 0 represents the sample mean. Composite Z-scores do not have direct clinical relevance. (NCT03702816)
Timeframe: Baseline (Pre-scan)
Intervention | z score (Mean) |
---|---|
Control | 0.285 |
Mild Cognitive Impairment | -0.013 |
Alzheimer's Disease | -1.585 |
Parkinson's Disease | -0.731 |
Temporal SUVR-- GE180 binding potential in the temporal cortical ROI, as a marker of temporal neuroinflammation. Temporal neuroinflammation would be expected to relate to temporal lobe AD pathology, and given known temporal lobe role in memory and language system function, is hypothesized to relate to measures of memory in particular, with greater temporal lobe GE180 relating to poorer memory and language function. (NCT03702816)
Timeframe: Baseline (Single scan)
Intervention | SUVR (Mean) |
---|---|
Control | 0.9127 |
Mild Cognitive Impairment | 0.9779 |
Alzheimer's Disease | 0.9146 |
Parkinson's Disease | 0.8899 |
Whole Brain GE180- GE180 binding potential in the whole brain, as a marker of global neuroinflammation. Global neuroinflammation would be expected to relate to more widespread pathology on average, and is hypothesized to relate to global measures of cognition, including the MoCA and DRS, with greater whole brain GE180 relating to poorer cognitive function overall. (NCT03702816)
Timeframe: Baseline (Single scan)
Intervention | SUVR (Mean) |
---|---|
Control | 0.9179 |
Mild Cognitive Impairment | 0.9711 |
Alzheimer's Disease | 0.9351 |
Parkinson's Disease | 0.9051 |
1 review available for pk 11195 and Acute Confusional Senile Dementia
Article | Year |
---|---|
Neuroinflammation and β amyloid deposition in Alzheimer's disease: in vivo quantification with molecular imaging.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Benzothiazoles | 2014 |
31 other studies available for pk 11195 and Acute Confusional Senile Dementia
Article | Year |
---|---|
Discovery of benzimidazole derivatives as modulators of mitochondrial function: A potential treatment for Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Animals; Benzimidazoles; Cognition; Humans; Ligands; Male; | 2017 |
Discovery of thienopyrrolotriazine derivatives to protect mitochondrial function against Aβ-induced neurotoxicity.
Topics: Adenosine Triphosphate; Alzheimer Disease; Amyloid beta-Peptides; Animals; Dogs; Dose-Response Relat | 2017 |
Low plasma neurofilament light levels associated with raised cortical microglial activation suggest inflammation acts to protect prodromal Alzheimer's disease.
Topics: Aged; Alzheimer Disease; Biomarkers; Carbon Radioisotopes; Cognitive Dysfunction; Female; Humans; In | 2020 |
In vitro Characterization of the Regional Binding Distribution of Amyloid PET Tracer Florbetaben and the Glia Tracers Deprenyl and PK11195 in Autopsy Alzheimer's Brain Tissue.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Autopsy; Brain | 2021 |
Brain inflammation accompanies amyloid in the majority of mild cognitive impairment cases due to Alzheimer's disease.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Amyloid; Aniline Compounds; Case-Control Studies; Cerebr | 2017 |
TSPO ligand PK11195 improves Alzheimer-related outcomes in aged female 3xTg-AD mice.
Topics: Aging; Alzheimer Disease; Amyloid beta-Peptides; Animals; Brain; Female; Isoquinolines; Ligands; Maz | 2018 |
Ligand for translocator protein reverses pathology in a mouse model of Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Benzodiazepinones | 2013 |
³H-deprenyl and ³H-PIB autoradiography show different laminar distributions of astroglia and fibrillar β-amyloid in Alzheimer brain.
Topics: Aged; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Astrocytes; Autoradiography; Benz | 2013 |
Influence of microglial activation on neuronal function in Alzheimer's and Parkinson's disease dementia.
Topics: Alzheimer Disease; Amyloid; Brain; Brain Mapping; Carbon Radioisotopes; Cognitive Dysfunction; Fluor | 2015 |
Longitudinal influence of microglial activation and amyloid on neuronal function in Alzheimer's disease.
Topics: Aged; Alzheimer Disease; Amyloid; Aniline Compounds; Brain; Case-Control Studies; Disease Progressio | 2015 |
Does Microglial Activation Influence Hippocampal Volume and Neuronal Function in Alzheimer's Disease and Parkinson's Disease Dementia?
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Antineoplastic Agents; Brain Mapping; Cognition; Female; | 2016 |
Depiction of microglial activation in aging and dementia: Positron emission tomography with [
Topics: Acetamides; Aged; Aging; Alzheimer Disease; Brain; Carbon Radioisotopes; Dementia; Humans; Isoquinol | 2017 |
An early and late peak in microglial activation in Alzheimer's disease trajectory.
Topics: Aged; Alzheimer Disease; Aniline Compounds; Antineoplastic Agents; Brain Mapping; Carbon Radioisotop | 2017 |
Novel reference region model reveals increased microglial and reduced vascular binding of 11C-(R)-PK11195 in patients with Alzheimer's disease.
Topics: Alzheimer Disease; Binding Sites; Brain; Carbon Radioisotopes; Humans; Isoquinolines; Microglia; Mod | 2008 |
Microglia, amyloid, and cognition in Alzheimer's disease: An [11C](R)PK11195-PET and [11C]PIB-PET study.
Topics: Aged; Alzheimer Disease; Amyloid; Aniline Compounds; Carbon Radioisotopes; Cerebral Cortex; Cluster | 2008 |
Microglial activation and amyloid deposition in mild cognitive impairment: a PET study.
Topics: Aged; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Benzothiazoles; Brain Mapping; Ca | 2009 |
Carbon 11-labeled Pittsburgh Compound B and carbon 11-labeled (R)-PK11195 positron emission tomographic imaging in Alzheimer disease.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides; Aniline Compounds; Antineoplastic | 2009 |
Autoradiographical imaging of PPARgamma agonist effects on PBR/TSPO binding in TASTPM mice.
Topics: Acetamides; Age Factors; Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides; Amyloid | 2009 |
Optimization of supervised cluster analysis for extracting reference tissue input curves in (R)-[(11)C]PK11195 brain PET studies.
Topics: Adult; Aged; Aged, 80 and over; Algorithms; Alzheimer Disease; Blood Volume; Carbon Radioisotopes; C | 2012 |
Imaging microglial activation and glucose consumption in a mouse model of Alzheimer's disease.
Topics: Alzheimer Disease; Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Analysis of Variance; Anim | 2013 |
Microglial activation in Alzheimer's disease: an (R)-[¹¹C]PK11195 positron emission tomography study.
Topics: Aged; Alzheimer Disease; Analysis of Variance; Brain Mapping; Carbon Radioisotopes; Cluster Analysis | 2013 |
Assessment of neuroinflammation and microglial activation in Alzheimer's disease with radiolabelled PK11195 and single photon emission computed tomography. A pilot study.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Brain Mapping; Dominance, Cerebral; Encephalitis; Female | 2003 |
Attenuation of chronic neuroinflammation by a nitric oxide-releasing derivative of the antioxidant ferulic acid.
Topics: Alzheimer Disease; Animals; Anti-Inflammatory Agents; Antioxidants; Butanes; Chronic Disease; Coumar | 2004 |
Evaluation of methods for generating parametric (R-[11C]PK11195 binding images.
Topics: Adult; Aged; Alzheimer Disease; Brain; Carbon Radioisotopes; Evaluation Studies as Topic; Humans; Im | 2007 |
A systematic comparison of kinetic modelling methods generating parametric maps for [(11)C]-(R)-PK11195.
Topics: Alzheimer Disease; Brain; Brain Mapping; Carbon Radioisotopes; Cluster Analysis; Computer Graphics; | 2007 |
Evaluation of reference regions for (R)-[(11)C]PK11195 studies in Alzheimer's disease and mild cognitive impairment.
Topics: Adult; Aged; Algorithms; Alzheimer Disease; Antineoplastic Agents; Blood Volume; Cluster Analysis; C | 2007 |
PK11195 labels activated microglia in Alzheimer's disease and in vivo in a mouse model using PET.
Topics: Aged; Aged, 80 and over; Aging; Alzheimer Disease; Amyloid beta-Protein Precursor; Animals; Astrocyt | 2009 |
Increased monoamine oxidase B activity in plaque-associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Astrocytes; Autoradiography; Brain; Female; Humans; Imag | 1994 |
PET of peripheral benzodiazepine binding sites in the microgliosis of Alzheimer's disease.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Brain; Carbon Radioisotopes; Case-Control Studies; Deoxy | 1995 |
In-vivo measurement of activated microglia in dementia.
Topics: Adult; Aged; Aged, 80 and over; Alzheimer Disease; Atrophy; Brain; Carbon Radioisotopes; Case-Contro | 2001 |
In-vivo measurement of activated microglia in dementia.
Topics: Adult; Aged; Aged, 80 and over; Alzheimer Disease; Atrophy; Brain; Carbon Radioisotopes; Case-Contro | 2001 |
In-vivo measurement of activated microglia in dementia.
Topics: Adult; Aged; Aged, 80 and over; Alzheimer Disease; Atrophy; Brain; Carbon Radioisotopes; Case-Contro | 2001 |
In-vivo measurement of activated microglia in dementia.
Topics: Adult; Aged; Aged, 80 and over; Alzheimer Disease; Atrophy; Brain; Carbon Radioisotopes; Case-Contro | 2001 |
Platelet benzodiazepine binding in Alzheimer's disease.
Topics: Aged; Aged, 80 and over; Alzheimer Disease; Blood Platelets; Dementia, Multi-Infarct; Diagnosis, Dif | 1990 |