In-vivo measurement of activated microglia in dementia.

By A. Cagnin, D. Brooks, A. M. Kennedy, Roger N. Gunn, R. Myers, Federico E. Turkheimer, T. Jones, R. Banati. The Lancet, 2001

1,089 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/307d78442cf7164e150975d730616ac19533b238

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. M. Block
2. Jau-Shyong Hong
3. T. Wyss‐Coray

In Neurology

1. M. Block
2. Jau-Shyong Hong
3. Manuel B. Graeber
4. T. Wyss‐Coray
5. J. Rogers
6. David J. Loane
7. P. Whitton
8. Melinda E Lull

In Physiology

1. M. Block
2. J. Rogers
3. Manuel B. Graeber
4. Jau-Shyong Hong
5. T. Wyss‐Coray
6. Wolfgang Streit
7. G. Wenk

Citations in the corpus

• Inflammation in Alzheimer disease: driving force, bystander or beneficial response? (2006, methodology): “, the use of a refined method led to the observation of increased binding in the entorhinal, temporoparietal and cingulate cortex in those with mild to moderate Alzheimer diseas”
• Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature. (2012, background): “Positron emission tomography (PET) using benzodiazepine ligands for activated microglia has shown increasing signal for these cells in living AD versus control subjects (Cagnin et al. 2001; Edison et al. 2008), and an inverse correlation between benzodiazepine-positive microglial load and cognitive ”
• Microglia-mediated neurotoxicity: uncovering the molecular mechanisms (2007, background): “In fact, microglial overactivation is an early pathogenic event that precedes neuropil destruction in patients with Alzheimer's diseas”
• Neuropathologic changes in Alzheimer's disease. (2003, background): “In vivo detection of increased binding in Alzheimer’s type dementia suggests that microglial activation is an early event in the pathogenesis of Alzheimer’s disease that appears in brain regions that later show the greatest degree of atrophy.(15)”
• Inflammatory processes in Alzheimer's disease. (2007, neutral): “In support of this hypothesis, a clinical study detected microglial activation at very early stages of AD, comparing PET and volumetric magnetic resonance imaging of the brain in patients with mild to moderate dementia to healthy individuals (Cagnin et al., 2001).”
• Neuroinflammation after traumatic brain injury: opportunities for therapeutic intervention. (2012, neutral): “vated microglia cluster at sites of aggregated Ab and penetrate the neuritic plaques (Cagnin et al., 2001; McGeer et al., 1987).”