ArticleJournal of nuclear medicine : official publication, Society of Nuclear Medicine2008
Imaging neuroinflammation in Alzheimer's disease with radiolabeled arachidonic acid and PET.
Article in Journal of nuclear medicine : official publication, Society of Nuclear Medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 180 citations in OpenAlex.
- Investigation of the Brain Biodistribution of the Lipoprotein-Associated Phospholipase AMolecular imaging and biology · 2017Trial
- The effect of APOE genotype on the delivery of DHA to cerebrospinal fluid in Alzheimer's disease.Alzheimer's research & therapy · 2016Trial
- The utility of (11)C-arachidonate PET to study in vivo dopaminergic neurotransmission in humans.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Trial
- Associations of fatty acids in cerebrospinal fluid with peripheral glucose concentrations and energy metabolism.PloS one · 2012Trial
- A perspective: PLA2G4A as drug target for vascular inflammation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Exploration of circulating metabolites in infants with abusive head trauma.Current research in neurobiology · 2025Article
- Exploring the Aβ Plaque Microenvironment in Alzheimer's Disease Model Mice by Multimodal Lipid-Protein-Histology Imaging on a Benchtop Mass Spectrometer.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Effects of APOE4 on omega-3 brain metabolism across the lifespan.Trends in endocrinology and metabolism: TEM · 2024Review
- Arachidonic Acid Mobilization and Peroxidation Promote Microglial Dysfunction in Aβ Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Imaging neuroinflammation in individuals with substance use disorders.The Journal of clinical investigation · 2024Review
- Article
- Neuroinflammation and Mitochondrial Dysfunction in Parkinson's Disease: Connecting Neuroimaging with Pathophysiology.Antioxidants (Basel, Switzerland) · 2023Review
- Origins of nervous tissue susceptibility to ferroptosis.Cell insight · 2023Review
- Positron Emission Tomography of Neuroimmune Responses in Humans: Insights and Intricacies.Seminars in nuclear medicine · 2023Review
- Nutritional metabolism and cerebral bioenergetics in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Review
- Neuroglia Cells Transcriptomic in Brain Development, Aging and Neurodegenerative Diseases.Aging and disease · 2023Review
- PET molecular imaging for pathophysiological visualization in Alzheimer's disease.European journal of nuclear medicine and molecular imaging · 2023Review
- Radiosynthesis, Preclinical, and Clinical Positron Emission Tomography Studies of Carbon-11 Labeled Endogenous and Natural Exogenous Compounds.Chemical reviews · 2023Review
- Radiosynthesis of 20-[Prostaglandins, leukotrienes, and essential fatty acids · 2022Article
- Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
Abstract
unlabelledIncorporation coefficients (K*) of arachidonic acid (AA) in the brain are increased in a rat model of neuroinflammation, as are other markers of AA metabolism. Data also indicate that neuroinflammation contributes to Alzheimer's disease (AD). On the basis of these observations, K* for AA was hypothesized to be elevated in patients with AD.
methodsA total of 8 patients with AD with an average (+/-SD) Mini-Mental State Examination score of 14.7+/-8.4 (mean age, 71.7+/-11.2 y) and 9 controls with a normal Mini-Mental State Examination score (mean age, 68.7+/-5.6 y) were studied. Each subject received a (15)O-water PET scan of regional cerebral blood flow, followed after 15 min by a 1-(11)C-AA scan of regional K* for AA.
resultsIn the patients with AD, compared with control subjects, global gray matter K* for AA (corrected or uncorrected for the partial-volume error [PVE]) was significantly elevated, whereas only PVE-uncorrected global cerebral blood flow was reduced significantly (P<0.05). A false-discovery-rate procedure indicated that PVE-corrected K* for AA was increased in 78 of 90 identified hemispheric gray matter regions. PVE-corrected regional cerebral blood flow, although decreased in 12 regions at P<0.01 by an unpaired t test, did not survive the false-discovery-rate procedure. The surviving K* increments were widespread in the neocortex but were absent in caudate, pallidum, and thalamic regions.
conclusionThese preliminary results show that K* for AA is widely elevated in the AD brain, particularly in regions reported to have high densities of senile (neuritic) plaques with activated microglia. To the extent that the elevations represent upregulated AA metabolism associated with neuroinflammation, PET with 1-(11)C-AA could be used to examine neuroinflammation in patients with AD and other brain diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.