Cited by 737Amyotrophic Lateral Sclerosis ResearchNeuroinflammation and Neurodegeneration MechanismsMultiple Sclerosis Research Studies

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Evidence of widespread cerebral microglial activation in amyotrophic lateral sclerosis: an [11C](R)-PK11195 positron emission tomography study

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Turner, M.R, Cagnin, A, Turkheimer, F.E, Miller, C.C.J, Shaw, C.E, Brooks, D.J, Leigh, P.N, Banati, R.B·2004·Neurobiology of Disease

DOI 10.1016/j.nbd.2003.12.012

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Abstract

Microglial activation is implicated in the pathogenesis of ALS and can be detected in animal models of the disease that demonstrate increased survival when treated with anti-inflammatory drugs. PK11195 is a ligand for the "peripheral benzodiazepine binding site" expressed by activated microglia. Ten ALS patients and 14 healthy controls underwent [(11)C](R)-PK11195 PET of the brain. Volumes of interest were defined to obtain [(11)C](R)-PK11195 regional binding potential values for motor and "extra-motor" regions. Significantly increased binding was found in motor cortex (P = 0.003), pons (P = 0.004), dorsolateral prefrontal cortex (P = 0.010) and thalamus (P = 0.005) in the ALS patients, with significant correlation between binding in the motor cortex and the burden of upper motor neuron signs clinically (r = 0.73, P = 0.009). These findings indicate that cerebral microglial activation can be detected in vivo during the evolution of ALS, and support the previous observations that cerebral pathology is widespread. They also argue for the development of therapeutic strategies aimed at inflammatory pathways.

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Authors: Turner, M. R., Cagnin, A., Turkheimer, F. E., Miller, C. C. J., Shaw, C. E., Brooks, D. J., Leigh, P. N., & Banati, R. B.
Affiliations: King's College London (GB)
University of Padua (IT)
Hammersmith Hospital (GB)
Corresponding author: Turner, M.R
ORCID: Turner, M.R
Turkheimer, F.E
Miller, C.C.J
Shaw, C.E
Brooks, D.J
Banati, R.B
Venue: Neurobiology of Disease
Publisher: Elsevier BV
Published: 2004-04
Volume: 15
Issue: 3
Pages: 601-609
ISSN: 0969-9961 (ISSN-L)
DOI: 10.1016/j.nbd.2003.12.012
OpenAlex: W2019706623
Cited by: 737
References: 90
Citations by year: 2026: 15 · 2025: 23 · 2024: 37 · 2023: 31 · 2022: 40 · 2021: 52 · 2020: 52 · 2019: 43 · 2018: 43 · 2017: 44 · 2016: 42 · 2015: 42 · 2014: 47 · 2013: 42 · 2012: 27
FWCI: 15.87
Type: journal article
Language: en
Open access: green
doaj.org
Licence: cc-by-sa
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Neurobiology of Disease (publishedVersion)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Research Portal (King's College London) (submittedVersion)
Padua Research Archive (University of Padova) (submittedVersion, other-oa)
Topics: Health Sciences › Medicine › Clinical Neurology › Amyotrophic Lateral Sclerosis Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
Keywords: amyotrophic lateral sclerosis, microglial activation, [11C]PK11195, positron emission tomography, translocator protein (TSPO), motor cortex, passive optical networks, dorsolateral prefrontal cortex, thalamus, upper motor neuron signs, neuroinflammation, neuropathology
MeSH terms: Adult, Amyotrophic Lateral Sclerosis, Brain, Female, Humans, Isoquinolines, Male, Middle Aged, Tomography, Emission-Computed, Microglia

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Evidence of widespread cerebral microglial activation in amyotrophic lateral sclerosis: an [11C](R)-PK11195 positron emission tomography study

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